Hunt v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: May 8, 2026

* * * * * * * * * * * * * * *

STEPHEN R. HUNT, *

*

*

Petitioner, * No. 21-1379V

*

v. * Special Master Young

*

SECRETARY OF HEALTH *

AND HUMAN SERVICES, *

*

Respondent. *

* * * * * * * * * * * * * * *

Richard H. Moeller, Moore, Heffernan, et al., Sioux City, IA, for Petitioner

Austin Joel Egan, United States Department of Justice, Washington, DC, for Respondent

DECISION ON ENTITLEMENT 1

On May 20, 2021, Stephen Hunt (“Petitioner”) filed a petition for compensation under the

National Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”), 42 U.S.C. §

300aa-10 et seq. (2018). 2 Pet., ECF No. 1. He alleged that after receipt of a pneumococcal

conjugate (“Prevnar 13”) vaccine on May 21, 2018, “he experienced, and continues to experience,

pain, illnesses, disabilities, injuries, and conditions which are a result of or caused in fact by the

vaccine.” Id. at 1. Petitioner’s brief in support of his motion for a ruling on the record clarified that

Petitioner “sustained illnesses, disabilities, injuries, and conditions, including Guillain Barré

Syndrome [(“GBS”) 3], which were caused-in-fact by the Prevnar 13 vaccine.” Pet’r’s Mot., ECF

No. 58 at 1. Respondent argued against compensation, asserting that Petitioner could not establish

vaccine causation by a preponderance of the evidence. Resp’t’s Rept. at 11, ECF No. 31.

1

Because this Decision contains a reasoned explanation for the action taken in this case, it must be made

publicly accessible and will be posted on the United States Court of Federal Claims’ website, and/or at

https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government Act

of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic Government

Services). This means the Decision will be available to anyone with access to the internet. In accordance

with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact medical or other information,

the disclosure of which would constitute an unwarranted invasion of privacy. If, upon review, I agree that

the identified material fits within this definition, I will redact such material from public access.

2

National Childhood Vaccine Injury Act of 1986, Pub L. No. 99-660, 100 Stat. 3755. Hereinafter, for

ease of citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. §

300aa (2018).

3

GBS is a “rapidly progressive ascending motor neuron paralysis of unknown etiology, frequently seen

after an enteric or respiratory infection.” Guillain-Barré Syndrome, DORLAND’S MED. DICTIONARY

ONLINE, https://www.dorlandsonline.com/dorland/definition?id=110689 (hereinafter, “DORLAND’S”).

A careful analysis and weighing of all the evidence presented in this case in accordance

with the applicable legal standards 4 reveals that Petitioner has failed to provide preponderant

evidence that the Prevnar 13 vaccine he received on May 21, 2018, was the cause-in-fact of his

GBS. Accordingly, Petitioner is not entitled to an award of compensation.

I. Procedural History

Petitioner filed his petition, an affidavit, and medical records on May 20, 2021. Pet., Pet’r’s

Exs. 1–16, ECF No. 1. Petitioner filed additional medical records and a statement of completion

between July 7, 2021, and August 25, 2021. Pet’r’s Exs. 17–18, ECF No. 7; Pet’r’s Exs. 19–29,

ECF No. 9; Pet’r’s Ex. 30, ECF No. 11; ECF No. 13. Petitioner filed additional medical records

and another statement of completion on January 3, 2022. Pet’r’s Exs. 32–34, ECF No. 16; ECF

No. 18.

On May 11, 2022, this case was referred for alternative dispute resolution (“ADR”)

proceedings with Special Master Gowen. ECF Nos. 26–27. Special Master Gowen held an ADR

conference between the parties on July 12, 2022, where Respondent indicated his intention to

continue defending the case. See Min. Entry, docketed July 12, 2022; see also ECF No. 29. The

same day Special Master Gowen entered an order removing the case from ADR and restoring it to

my active docket. ECF No. 29.

Respondent filed his Rule 4(c) report, opposing compensation, on September 14, 2022.

Resp’t’s Rept. Petitioner filed additional medical records on February 23, 2023. Pet’r’s Exs. 36–

41, ECF No. 35. On March 13, 2023, Petitioner filed an expert report from Lawrence Steinman,

M.D., and his curriculum vitae (“CV”). Pet’r’s Exs. 42–43, ECF No. 36. Petitioner filed supporting

medical literature on April 3, 2023. Pet’r’s Exs. 44–84, ECF No. 39. Respondent filed responsive

expert reports from Dara Jamieson, M.D., and J. Lindsay Whitton, M.B., Ch.B., Ph.D., on

September 15, 2023, along with their CVs and supporting literature. Resp’t’s Ex. A, Tabs 1–15,

Resp’t’s Ex. B, ECF No. 41; Resp’t’s Ex. C, Tabs 1–33, Resp’t’s Ex. D, ECF No. 42.

Petitioner filed a supplemental report from Dr. Steinman on December 11, 2023, and

supporting medical literature on December 14, 2023. Pet’r’s Ex. 85, ECF No. 44; Pet’r’s Exs. 86–

95, ECF No. 45. Respondent filed a supplemental report from Dr. Jamieson, along with supporting

literature, on March 29, 2024. Resp’t’s Ex. E, Tab 1, ECF No. 46. Respondent also filed a

supplemental report and supporting literature from Dr. Whitton on May 8, 2024. Resp’t’s Ex. F,

Tabs 1–4, ECF No. 48. Petitioner filed a final supplemental report from Dr. Steinman and

supporting literature on July 2, 2024. Pet’r’s Exs. 96–97, ECF No. 50.

On September 16, 2024, Petitioner filed a motion for a ruling on the record and additional

medical literature. Pet’r’s Mot.; Pet’r’s Ex. 102, ECF No. 59. Respondent filed his response on

4

While I have reviewed all of the information filed in this case, only those filings and records that are

most relevant to the Ruling will be discussed. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322,

1328 (Fed. Cir. 2016) (“We generally presume that a special master considered the relevant record

evidence even though he does not explicitly reference such evidence in his decision.”) (citation omitted);

see also Paterek v. Sec’y of Health & Hum. Servs., 527 F. App’x 875, 884 (Fed. Cir. 2013) (“Finding

certain information not relevant does not lead to—and likely undermines—the conclusion that it was not

considered.”).

2

November 12, 2024, and Petitioner filed his reply on December 4, 2024. Resp’t’s Resp., ECF No.

62; Pet’r’s Reply, ECF No. 64.

This matter is now ripe for consideration.

II. Medical Evidence

Petitioner’s pre-vaccination medical history is significant for cervical and lumbar

degeneration and diabetes. Pet’r’s Ex 4 at 72; Pet’r’s Ex. 5 at 45. Petitioner received his Prevnar

13 vaccination on May 21, 2018. Pet’r’s Ex. 2 at 3. Approximately two and a half weeks later, on

June 7, 2018, he presented to the Ohio Health Emergency Department (“ED”) for neck, back, and

midthoracic pain. Pet’r’s Ex. 4 at 82. Petitioner described how several days prior, while planting

and lifting, he experienced numbness or tingling in all four of his extremities. Id. Petitioner denied

any cough, runny nose, ear pain, sore throat, recent fall, or injury. Id. Petitioner reported

“significant pain,” which was “highly unusual” to him. Id. The attending physician noted that

Petitioner’s computed tomography (“CT”) scan showed multiple abnormal findings, including

cervical and lumbar degenerative changes, prostate enlargement, and abnormal bladder. Id. at 86.

On June 8, 2018, Petitioner returned to the ED for neck pain, back pain, numbness, tingling,

and loss of strength. Pet’r’s Ex. 4 at 64. His neurological examination was marked as “normal.”

Id. at 69. Physician notes mentioned Petitioner’s cervical and lumbar degenerative changes,

weakness in his upper extremities, numbness in his lower extremities, and Petitioner’s inability to

get comfortable. Id.at 72. Petitioner was then transferred to Riverside Methodist Hospital (“RMH”)

and hospitalized until June 11, 2018. Id.; Pet’r’s Ex. 5 at 17. Upon arrival, Petitioner had full

strength in all four extremities, but the nurse’s notes also recorded radiculopathy, numbness,

tingling, and moderate discomfort that was worse with movement. Pet’r’s Ex. 5 at 14; Pet’r’s Ex.

6 at 16. On June 9, 2018, Petitioner underwent a neurosurgery consultation for his back pain and

radiculopathy. Pet’r’s Ex. 5 at 26. Upon examination, Petitioner had intermittent numbness in both

hands and feet, a negative Hoffman’s sign, and normal strength in his extremities. Id. at 28. On

June 10, 2018, Petitioner underwent magnetic resonance imaging (“MRI”) of his thoracic spine,

which revealed an anterior displacement of the thoracic spinal cord. Id. at 79. Later that day, a

hospitalist discussed diabetes management with Petitioner and stated that diabetic neuropathy

could be contributing to the pain, numbness, and tingling in his feet. Id. at 45. On June 11, 2018,

a neurosurgeon reviewed the MRI and concluded that Petitioner had a T4 posterior subarachnoid

cyst that was not “acutely surgical” and that Petitioner’s lower extremities were not myelopathic.

Id. at 44. Later that day, Petitioner was discharged and stated his back pain was completely

resolved. Id.

Petitioner returned to the ED on June 12, 2018, complaining of tingling and weakness in

his upper extremities and progressive tingling and weakness in his lower extremities. Pet’r’s Ex.

4 at 34. The treating physician considered a diagnosis of GBS given the “progression of symptoms

and [felt the] need to reimage for progression of compressive phenomenon as well as consideration

of [GBS] or other nonmechanical etiologies of progressive lower greater than upper weakness and

paresthesias.” Id. at 43. From June 13, 2018, to June 23, 2018, Petitioner was hospitalized at RMH.

Pet’r’s Ex. 38 at 65; Pet’r’s Ex. 39 at 33. Upon arrival, he was too weak to walk. Pet’r’s Ex. 38 at

65. The attending physician noted Petitioner had newly onset facial droop and acute back pain in

addition to twenty years of chronic back pain. Id. at 93. Petitioner underwent a brain MRI with

3

and without contrast, which showed an asymmetric effacement of the right facial nerve compatible

with Bell’s palsy. 5 Pet’r’s Ex. 39 at 98. On June 14, 2018, a physiatrist performed an

electromyogram (“EMG”) examination and concluded Petitioner’s condition was consistent with

acute inflammatory demyelinating polyradiculopathy (“AIDP”), which is otherwise known as

GBS. Pet’r’s Ex. 38 at 111, 114. The hospitalist assessed GBS and transferred Petitioner to the

intensive care unit. Id. at 117.

During his hospitalization, Petitioner was seen by neurologist Dr. Jacqueline Nicholas.

Pet’r’s Ex. 38 at 65. She agreed with his AIDP/GBS diagnosis and added that “[h]is [r]ight facial

weakness raises consideration of possible Miller Fisher Variant,[6] Bickerstaff encephalitis.” Id.

She planned to treat “the AIDP and [f]acial palsy as one and not separate out the facial weakness

as [B]ell’s palsy.” Id. at 66. In her assessment, Dr. Nicholas noted that Petitioner had a recent

urinary tract infection (“URI”) and Prevnar 13 vaccination prior to presenting to the hospital with

mid-back pain. She noted that his AIDP “could explain his radicular back pain.” Id.

Petitioner’s consulting neurologist reviewed Petitioner’s MRI imaging and EMG study and

concluded that the imaging and studies suggested GBS. Pet’r’s Ex. 38 at 119–20. A lumbar

puncture was performed, and intravenous immunoglobulin (“IVIG”) was ordered pending the

results of Petitioner’s IgA levels. Id. at 122; Pet’r’s Ex. 39 at 100. The nurse practitioner also noted

the etiology of Petitioner’s right Bell’s palsy was a “recent [URI], possible extension of AIDP.

Facial nerve involvement noted on EMG and thought to be part of AIDP.” Pet’r’s Ex. 38 at 122.

IVIG was initiated, and on June 16, 2018, the neurologic nurse practitioner noted Petitioner

showed improved strength in his upper extremities but remained weak in his lower extremities. Id.

at 129. Petitioner could not dorsiflex his toes, and his reflexes remained absent in his lower

extremities and were diminished in his upper extremities. Id. at 131. Petitioner reported his back

pain improved, and the neurology nurse practitioner attributed the back pain to AIDP. Id. at 128–

29.

On June 17, 2018, Petitioner received his cerebrospinal fluid (“CSF”) tests results from his

lumbar puncture, which included the presence of xanthochromia, elevated protein, and elevated

white blood cells. Pet’r’s Ex. 39 at 40–42. The neurologist concluded that Petitioner had AIDP but

was unsure of the etiology of Petitioner’s right facial weakness, noting the possibility of Bell’s

palsy, the Miller Fisher variant of GBS, and Bickerstaff encephalitis. Id. at 142. The neurologist

also concluded that, based upon the xanthochromia found in the CSF, Petitioner had a thoracic

arachnoid web. Id.

On June 19, 2018, the neurologic nurse practitioner noted Petitioner’s strength was slowly

improving, and Petitioner completed his fifth and final dose of IVIG. Pet’r’s Ex. 38 at 149.

Petitioner’s prior medical history on a June 20, 2018 visit record noted that Petitioner had a recent

URI and a pneumonia vaccine on May 21, 2018. Id. at 159. During the examination, Petitioner had

no movement in his feet, trace movement in the hips and knees, and weak movement in the upper

extremities and shoulders. Id. at 161. On June 21 and June 22, 2018, occupational therapists

evaluated Petitioner for discharge to inpatient rehabilitation. Pet’r’s Ex. 39 at 17, 21. The

5

Bell palsy is “unilateral facial paralysis of sudden onset, due to lesion of the facial nerve and resulting in

characteristic distortion of the face.” Bell Palsy, DORLAND’S.

6

Miller Fisher Syndrome is “a variant of [GBS] characterized by areflexia, ataxia, and ophthalmoplegia.”

Fisher Syndrome, DORLAND’S.

4

occupational therapists noted that Petitioner needed assistance for many activities of daily living.

Id. at 17–18, 21–22. By June 23, 2018, Petitioner’s GBS had improved following treatment, and

he was discharged to inpatient rehabilitation. Id. at 32–33. Petitioner’s discharge diagnoses were

AIDP, right facial weakness, hyponatremia, posterior arachnoid cyst, encephalopathy,

hypertensive urgence, constipation, and Type 2 diabetes mellitus. Id. Petitioner was admitted to

Ohio Health Rehabilitation Hospital on the night of June 23, 2018, for GBS, weakness, and

numbness. Pet’r’s Ex. 10 at 175. The physical medicine and rehabilitation specialist noted

Petitioner’s GBS was past its nadir and Petitioner was improving clinically. Id. at 178.

On October 30, 2018, Petitioner saw neurologist Douglass Woo for his AIDP. Pet’r’s Ex.

18 at 46. Petitioner’s facial weakness resolved but still had significant weakness in his legs. Id. In

his impression of Petitioner’s AIDP, Dr. Woo stated that it was idiopathic, closely improving, and

would continue to be monitored. Id. at 45. On February 21, 2019, Petitioner returned to Dr. Woo,

who noted Petitioner demonstrated steady improvement since his visit in October. Id. at 34. Dr.

Woo stated that Petitioner’s AIDP “remain[ed] idiopathic,” continued to improve, and would

continue to be monitored. Id. at 30. On June 29, 2020, Petitioner saw an oncologist for his sepsis,

and his medical history noted Petitioner’s history of GBS that was preceded by his Prevnar13

vaccination. Pet’r’s Ex. 3 at 12. Under “Allergens,” the oncologist listed “Prevnar 13 – [GBS].”

Id. at 14.

No other relevant medical records were filed.

III. Petitioner’s Affidavit

On May 20, 2021, Petitioner filed a brief affidavit. Pet’r’s Ex. 1. He recounted receipt of

his Prevnar 13 vaccine on May 21, 2018, at seventy years old. Id. at ¶ 2. Shortly thereafter,

“[s]ometime during the Memorial Day weekend, [Petitioner and his wife] were visiting at the home

of [his brother-in-law] when [he] felt numbness in [his] calves and lower legs, and tingling in [his]

feet.” Id. at ¶ 3. The next morning, Petitioner’s legs gave out and a few days later, the numbness

and tingling in his legs continued to progress and then it started in his hands. Id. at ¶ 4. Petitioner

recalled being taken to the ED on or about June 5, 2021, and staying overnight. Id. at ¶ 5. He went

to several emergency rooms over a period of weeks in June and was eventually told that he had

GBS during his hospitalization at RMH. Id. at ¶¶ 6–9.

Following his diagnosis, Petitioner underwent inpatient rehabilitation and various

therapies, including physical, occupational, and speech. Pet’r’s Ex. 1 at ¶¶ 10–13. Prior to his

vaccination, Petitioner described himself as “in generally good health and physically fit.” Id. at ¶

17.

IV. Experts

A. Expert Qualifications

1. Petitioner’s Expert, Dr. Lawrence Steinman, M.D.

Dr. Steinman is a board-certified neurologist and currently serves as a Professor of

Neurology at Stanford University. Pet’r’s Ex. 42 at 1. He received his M.D. from Harvard

5

University and completed his medical internship and residencies in pediatric and adult neurology

at Stanford University Hospital. Pet’r’s Ex. 43 at 1. Throughout his clinical career Dr. Steinman

has “cared for hundreds of adults and children with various forms of inflammatory neuropathy,”

including GBS. Pet’r’s Ex. 42 at 1. Dr. Steinman has published 12 articles in the field of molecular

mimicry, in addition to numerous other publications. Id. He has also received several awards for

his work in the field of neuro-immunology. Id. at 2–4.

2. Respondent’s Expert, Dr. Dara Jamieson, M.D.

Dr. Jameison is a board-certified neurologist and currently serves as a Clinical Associate

Professor of Neurology at Weill Cornell Medicine. Resp’t’s Ex. A at 1. She received her M.D.

from the University of Pennsylvania School of Medicine, where she also completed her medical

internship, neurology residency, and research fellowship. Resp’t’s Ex. B at 1. She has over 30

years of clinical neurology experience and has “authored many papers published in peer reviewed

journals, and authored two books, as well as book chapters and review articles of multiple

neurological topics.” Resp’t’s Ex. A at 1–2.

3. Respondent’s Expert, Dr. J. Lindsay Whitton, M.B., Ch.B., 7 Ph.D.

Dr. Whitton is an Emeritus Professor of the Department of Immunology and Microbiology

at the Scripps Research Institute in La Jolla, California. Resp’t’s Ex. D at 1. He is not licensed to

practice in the United States and is not board-certified in the United States. Resp’t’s Ex. C at 3. He

received his M.B., Ch.B. and Ph.D. in virology from the University of Glasgow. Resp’t’s Ex. D at

1. Throughout his career he has held several academic teaching and research positions in the United

Kingdom and in the United States. Id. He has also “published both on the adaptive and innate

immune responses, and on molecular mimicry.” Resp’t’s Ex. C at 1.

B. Expert Reports

1. Diagnosis

Petitioner’s diagnosis was confirmed throughout the medical records. See generally, Pet’r’s

Exs. 6, 7, 38. Additionally, Petitioner’s expert, Dr. Steinman and Respondent’s expert, Dr.

Jamieson, both agreed that Petitioner suffered from AIDP consistent with GBS. Pet’r’s Ex. 42 at

42, Resp’t’s Ex. A at 11. In his initial expert report, Dr. Steinman asserted that “[b]ased on the

medical record and opinions of the treating physicians the diagnosis here is [GBS].” Id. at 14. Dr.

Steinman referenced an explanation from The National Institute of Neurological Disorders and

Stroke that in GBS patients, “the immune system starts to destroy the myelin sheath that surrounds

the axons of many peripheral nerves, or even the axons themselves.” Pet’r’s Ex. 42 at 14 (citing

Pet’r’s Ex. 52). 8 Dr. Jamieson agreed that “it is more likely than not that [Petitioner] had

GBS/AIDP.” Resp’t’s Ex. A at 11. In her initial report, Dr. Jamieson also defined GBS and

explained that it is “a group of autoimmune disorders that present as an acute, monophasic illness

and that cause neurological deficits due to peripheral nerve injury.” Id. at 6. Dr. Jamieson

continued that AIDP is the most common subtype of GBS, and it is characterized by “progressive,

7

An M.B., Ch.B., is the United Kingdom equivalent to an M.D. in the United States.

8

Guillain-Barré Syndrome Fact Sheet, NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND

STROKE, https://www.ninds.nigh.gov/disorders/gbs/detail_gbs.htm (last visited April 3, 2023).

6

symmetric, leg followed by arm, distal to proximal, weakness with absent or depressed deep

tendon reflexes.” Id.

2. Causation

a. Dr. Steinman’s Initial Report

Dr. Steinman explained that the National Institute of Neurological Disorders and Stroke

defines GBS as a rare syndrome that usually “occurs a few days or weeks after the patient has had

symptoms of a respiratory or gastrointestinal viral infection.” Pet’r’s Ex. 42 at 14. He noted that

occasionally, it is triggered by surgery and “[i]n rare instances vaccinations may increase the risk

of GBS.” Id. Acknowledging that Petitioner’s medical records mention a recent URI, Dr. Steinman

asserted that otherwise they do not “provide any detail of a diagnosis of [URI] or illness temporally

related to the onset of AIDP.” Id. He continued that “[t]he only record of [a URI], before the onset

of AIDP, appears to be [from a medical visit] on March 15, 2018, [67] days prior to vaccination

and approximately 11 to 12 weeks prior to onset of AIDP.” Id.

The 17-day interval between Petitioner’s Prevnar 13 vaccine and the onset of his GBS

symptoms is more indicative, according to Dr. Steinman, of a causal relationship based on a “study

from [the Centers for Disease Control (“CDC”)] on the swine flu vaccine and GBS.” Pet’r’s Ex.

42 at 42 (citing Pet’r’s Ex. 84). 9 This seminal 1979 paper by the CDC revealed epidemiologic

evidence that “[w]hen compared to the unvaccinated population, the vaccinated population had a

significantly elevated attack rate in every adult age group.” Pet’r’s Ex. 84 at 1. Dr. Steinman

extrapolated that paper’s findings of a “period of increased risk [] concentrated primarily within

the [five]-week period after vaccination,” to identify an appropriate temporal relationship between

Prevnar 13 vaccination and GBS. Id. Dr. Steinman compared this five-week period to the findings

in the Haber et al. 10 paper that documented 11 cases of GBS following Prevnar 13 vaccination.

Pet’r’s Ex. 83. The symptom onset interval was two to 43 days with a median of nine days. Id. at

4. Dr. Steinman noted that of the 11 patients, only one “had [a URI] 16 days prior to GBS.” Pet’r’s

Ex. 42 at 42. Ultimately, the researchers concluded that “evidence of a possible association of GBS

with inactivated seasonal influenza vaccines has been inconsistent[, and] data mining analysis

noted no disproportionate reporting for GBS.” Pet’r’s Ex. 84 at 5. However, Dr. Steinman argued

that Petitioner’s chronology is consistent with the timing for the interval between vaccination and

GBS in the 1976 swine flu studies, and “[a] a showing of a proximate temporal relationship

between vaccination and injury is fulfilled.” Pet’r’s Ex. 42 at 42.

Dr. Steinman opined that Petitioner’s GBS was caused by his Prevnar 13 vaccine via

molecular mimicry. Pet’r’s Ex. 42 at 11. Referring to a self-authored article in 1993, he explained

that generally during this process, “shared structures on a virus or bacteria or in a vaccine can

trigger a cross-reactive response to self.” Id. at 15 (citing Pet’r’s Ex. 48). 11 Dr. Steinman identified

9

Lawrence B. Schonberger et al., Guillain-Barre Syndrome Following Vaccination in the National

Influenza Immunization Program, United States, 1976–77, 110 AM. J. EPIDEMIOLOGY 105 (1979).

10

Penina Haber et al., Post-Licensure Surveillance of 13-Valent Pneumococcal Conjugate Vaccine

(PCV13) in Adults Aged ≥ 19 Years Old in the United States, Vaccine Adverse Event Reporting System

(VAERS), June 1, 2012–December 31, 2015, 34 VACCINE 6330 (2016).

11

Lawrence Steinman, The Discovery of Natalizumab, A Potent Therapeutic for Multiple

Sclerosis, 199 J. Cell Biology 413 (2012).

7

several potential cross-reactive components of the Prevnar 13 vaccine, including the CRM197

carrier protein, polysorbate 80, a succinate buffer, an aluminum phosphate adjuvant, and two of

the 13 Streptococcus pneumoniae serotypes, specifically the 18C and 23F saccharides. 12 Id. at 16.

He explained that the 18C capsular polysaccharide, 13 for example, contains a glycerol-phosphate14

group that “must be preserved for conserving adequate antigenicity of the [serotype] within the

Prevnar 13 vaccine.” Id. at 19.

As evidence of homology sufficient for cross reactivity between vaccine and host

components, Dr. Steinman cited to multiple sclerosis 15 (“MS”) studies to explain that

“phospholipids[16] are components of the myelin sheath in humans, and [] they are targeted by

antibodies in neuroinflammation.” Pet’r’s Ex. 42 at 16. He continued that he and other researchers

had “identif[ied] bona fide lipid targets of the autoimmune response in [a human] MS brain, and

an animal model of MS to explore the role of identified lipids in autoimmune demyelination.” Id.

For example, Kanter et al., 17 which includes Dr. Steinman as a co-author, is styled as a “large-

scale multiplex analysis of antibody responses to lipids in [MS].” Pet’r’s 50 at 1. The authors

sought to “show that antibodies to sulfatide and other lipids are present in CSF samples from

individuals with [MS] and in sera from mice with experimental autoimmune encephalitis

[(“EAE”)].” Id. Their “observations suggest that autoimmune responses directed against

sulfatide[18] and other lipids contribute to the pathogenesis of autoimmune demyelinating disease.”

Id. at 5. Dr. Steinman also cited the Ho et al. 19 article asserting “that ‘[l]ipids constitute 70% of

the myelin sheath, and autoantibodies against lipids may contribute to the demyelination that

characterizes [MS].’” Pet’r’s Ex. 42 at 16. (quoting Pet’r’s Ex. 51 at 1). Further, the authors were

able “to identify bona fide lipid targets of the autoimmune response in MS brain,” specifically, a

phosphate group in phosphatidylserine 20 and oxidized phosphatidylcholine 21 derivatives. Id. Dr.

12

A saccharide is “one of a series of carbohydrates, including the sugars. The saccharides are divided into

monosaccharides, oligosaccharides, and polysaccharides, according to the number of monosaccharaide

groups [] composing them.” Saccharide, DORLAND’S. A monosaccharide is “a simple sugar; a

carbohydrate that cannot be decomposed by hydrolysis.” Monosaccharide, DORLAND’S.

13

A polysaccharide is “a carbohydrate that on hydrolysis yields a large number of monosaccharides

(variously defined as five or more to eleven or more).” Polysaccharide, DORLAND’S.

14

Glycerol Phosphate is “an intermediate in the glycerol phosphate shuttle, in the utilizations of glycerol,

and in the biosynthesis of lipids.” Glycerol Phosphate, DORLAND’S.

15

MS is “a disease in which there are foci of demyelination throughout the white matter of the central

nervous system, sometimes extending into the gray matter.” Multiple Sclerosis, DORLAND’S.

16

A phospholipid is “any lipid that contains phosphorus, including those with a glycerol backbone.”

Phospholipid, DORLAND’S.

17

Jennifer L. Kanter et al., Lipid Microarrays Identify Key Mediators of Autoimmune Brain Inflammation,

12 NATURE MEDICINE 138 (2006).

18

Sulfatide are “any of the cerebrosides esterified with a sulfate residue at the C-6 of the sugar; they are

found largely in the medullated nerve fibers.” Sulfatide, DORLAND’S.

19

Peggy P. Ho et al., Identification of Naturally Occurring Fatty Acids of the Myelin Sheath That Resolve

Neuroinflammation, 4 SCI. TRANSNAT’L MED. 73 (2012).

20

Phosphatidylserine is “a phospholipid in which serine is attached to the phosphate group of

phosphatidic acid by an ester linkage . . . and is localized preferentially in the inner surface of the plasma

membrane.” Phosphatidylserine, DORLAND’S.

21

Phosphatidylcholine is “a phospholipid in which choline is attached to the phosphate group of

phosphatidic acid by an ester linkage . . . and is localized preferentially in the outer surface of the plasma

membrane.” Phosphatidylcholine, DORLAND’S.

8

Steinman then cited to Nakos et al. 22 and noted that “phospholipid antibodies were found in

patients with GBS,” but not in the controls. Id. (citing Pet’r’s Ex. 55).

The Nakos et al. article noted that GBS “is an acute inflammatory polyneuropathy related

to autoimmunity. However, no conclusive etiological concept has yet been found.” Pet’r’s Ex. 55

at 1. The authors sought to measure antibodies levels before, during, and after treatment to

determine useful indicators of treatment efficacy. Id. Noting the “close association between GBS

and preceding infection,” the article stated that “[a]pproximately 15–50% of patients with GBS

develop anti-gangliosidic antibodies that target glycolipids.” 23 Id. at 2. The authors stated that

“[l]ipopolysaccharides[24] of [Campylobacter jejuni (“C. jejuni”)] share structural similarity with

epitopes in gangliosides,” 25 and suggest cross-reactivity could occur between antibodies against

the bacteria and host myelin sheaths. Id. The study revealed “a wide range of anti-phospholipid

antibodies in patients with idiopathic GBS,” and the authors stressed the importance of an

investigation into this relationship. Id. at 5.

Dr. Steinman also cited to Chang et al., 26 which noted that “phosphoglycerol is present in

serotypes 18C and in 23F in the Prevnar 13 vaccine.” Pet’r’s Ex. 42 at 20 (citing Pet’r’s Ex. 56).

Dr. Steinman asserted that “phosphoglycerol is directly targeted by the core of the two human

antibodies targeting 23F.” Pet’r’s Ex. 42 at 21. He inserted two schematics of 23F into his report

with the phosphoglycerol central to the antibody binding site identified. The first figure is

reproduced from the Bryson et al. 27 article. See Pet’r’s Ex. 59. The second was taken from Yu et

al. 28 See Pet’r’s Ex. 60.

22

G. Nakos et al., Anti-Phospholipid Antibodies in Serum From Patients with Guillain-Barré Syndrome,

31 Intensive Care Med. 1401 (2005).

23

A glycolipid is “a lipid containing carbohydrate groups, usually galactose but also glucose, inositol, or

others . . . the term is used almost exclusively to denote the sphingosine derivatives lacking phosphate

groups.” Glycolipid, DORLAND’S.

24

A lipopolysaccharide is “a complex of lipid and polysaccharide” and “a major component of the cell

wall of gram-negative bacteria.” Lipopolysaccharide, DORLAND’S.

25

A ganglioside is “any group of glycosphingolipids in which the polar head group on ceramide is a sialic

acid-containing oligosaccharide linked via glucose residue; they occur predominantly in tissues of the

[CNS].” Ganglioside, DORLAND’S.

26

Janoi Chang, Relevance of O-Acetyl and Phosphoglycerol Groups for the Antigenicity of Streptococcus

Pneumoniae Serotype 18C Capsular Polysaccharide, 30 Vaccine 7090 (2012).

27

Steve Bryson et al., Structures of Preferred Human IgV Genes-Based Protective Antibodies Identify

How Conserved Residues Contact Diverse Antigens and Assigned Source of Specificity to CDR3 Loop

Variation, 196 J. IMMUNOLOGY 4723 (2016).

28

Kang Yu et al., Synthesis of the Biological Repeating Unit of Streptococcus Pneumoniae Serotype 24F

Capsular Polysaccharide, 14 ORGANIC & BIOMOLECULAR CHEMISTRY 11462 (2016).

9

Pet’r’s Ex. 59, Figure 2; Pet’r’s Ex. 60, Figure 1.

Yu et al. explained and illustrated “[a]n efficient synthesis of the 3-aminopropyl

glycoside[29] of the biological repeating unit of Streptococcus pneumoniae serotype 23F capsular

polysaccharide.” Pet’r’s Ex. 60 at 1. This breakthrough, the authors opined, “has laid the

foundation for accessing homogeneous and structurally well-defined bacterial [capsular

polysaccharide] analogs . . . useful for structure–activity relationships and many other biological

studies.” Id. at 4. Bryson et al. “illuminate[d] the centrality of the phosphate in glycerophosphate

in a human antibody response to 23F after the human received a pneumococcal vaccine intended

to elicit antibodies to 23F[, but t]he study was done with Pneumovax 23.” Pet’r’s Ex. 42 at 24

(citing Pet’r’s Ex. 59). Dr. Steinman asserted that the “data from the Bryson [et al.] article

demonstrates UNEQUIVOCALLY that the immune response to the serotype 23F component of

Pneumovax 23 targets the phosphoglycerol in serotype 23F.” Id. at 24 (emphasis in original). He

acknowledged that Pneumovax 23 is a different vaccine but asserted that Prevnar 13 contains the

same sugars as Pneumovax 23. Id. He mused that “[if] only there were such pictures with a study

on Prevnar 13, it would be a ‘perfect fit,’ but [asserted that] in searching for evidence that is ‘sound

and reliable,’ this is the best the Petitioner can do at the present time. Id. Dr. Steinman then argued

that “Prevnar 13 is also designed to generate an immune response to serotype 23F.” Id. He

concluded that “[s]ince the 23F and 18C components of Prevnar 13 also contain[] the

phosphoglycerol moiety[30] that is targeted by the antibodies generated by Pneumovax, it is very

likely that the immune response to 23F and 18C components of Prevnar 13 vaccine also targets

the phosphoglycerol moiety.” Id. at 24–25.

Dr. Steinman identified CRM197 as one part of a second molecular mimicry homology.

Pet’r’s Ex. 42 at 25. CRM197 is “used to conjugate the pneumococcal polysaccharides in the

Prevnar 13 vaccine to an immunogenic protein carrier.” Id. Dr. Steinman then identified contactin-

1 as the potential target, based on the Devaux et al. 31 paper that found “[i]n eight patients with

GBS or CIDP, we identified that IgG antibodies recognized the native extracellular domain of

NF186, gliomedin, or contactin.” Id. (citing Pet’r’s Ex. 63) The National Library of Medicine

defines contactin-1 as a “glycosylphosphatidylinositol-anchored neuronal membrane protein that

29

A glycoside is “any compound that contains a carbohydrate molecule (sugar), particularly any such

natural product in plants, convertible by hydrolytic cleavage, into sugar and a nonsugar component

(aglycon), and named specifically for the sugar contained, as glucoside (glucose).” Glycoside,

DORLAND’S.

30

A moiety is defined as “any equal part; a half; also any part or portion.” Moiety, DORLAND’S.

31

Jerome Devaux et al., Nodal Proteins are Target Antigens in Guillain-Barré Syndrome, 17 J.

PERIPHERAL NERVOUS SYSTEM 62 (2012).

10

functions as a cell adhesion molecule. It may play a role in the formation of axon connections in

the developing nervous system.” 32

The Devaux et al. study sought to “investigate[] the prevalence of antibodies against nodal

adhesion molecules in patients with GBS or chronic inflammatory demyelinating polyneuropathy

(“CIDP”).” Pet’r’s Ex. 63 at 1. The study “identified NF186, gliomedin, and contactin as the

immune targets of autoantibodies.” Id. at 6. The authors further suggested that “autoantibodies to

nodal adhesion molecules are more prevalent in GBS forms and are not related to secondary

immune reactions against demyelinated or damaged myelinated fibers.” Id. at 8. The results

indicated that “the prevalence of these autoantibodies in [MS] may vary considerably.” Id.

Additionally, the authors warned that “[t]he causes generating these autoantibodies in GBS remain

[] unknown.” Id. While “[t]he presence of autoantibodies did not correlate with any antecedent

illnesses in particular,” the authors noted “that infectious agents showing molecular mimicry with

nodal proteins may trigger the development of autoantibodies against

NF186/gliomedin/contactin/NrCAM and simultaneously the development of IgM against

gangliosides.” Id. They then warned that they “did not detect IgM deposition at nodes or paranodes,

albeit many patients showed IgM antibodies against gliomedin, NF186, contactin, or NrCAM. The

importance of IgM against nodal adhesion molecules in GBS pathology is therefore uncertain.” Id.

Dr. Steinman “used the NIH BLAST search tool and performed BLAST searches to align

contactin-1 with the components of the CRM197” in Prevnar 13. Pet’r’s Ex. 42 at 25. The

parameters that Dr. Steinman set for the search were based on his on research that demonstrated

“a viral peptide with homology at just [five] amino acids with a self-peptide can induce clinical

signs of EAE in mice,” even when nonconsecutive, “but there cannot be a gap in the alignment of

the proteins on the BLAST search.” Id. Dr. Steinman again relied on research done in the context

of MS to show how “a molecular mimic between EBNA1[, Epstein-Barr virus (“EBV”)

transcription factor] and a [central nervous system (“CNS”)] protein called GlialCAM, triggers”

the disease. Id. at 26. The identified homology consisted of “a stretch of 12 amino acids where

there are five” that are identical. Id. at 27. The results of the CRM197 and contactin-1 BLAST

revealed “[t]he sequence WEQAKALSVE has five of [10] identical amino acids, and thus would

be a region that [Gautam et al. (1992), 33 Gautam et al. (1994), 34 Gautam et al. (1998), 35 and Lanz

et al. 36] indicate might be capable of inducing a neuroinflammatory disease.” Id. at 32. (citing

Pet’r’s Exs. 21–24).

32

CNTN1 Contactin 1 [Homo Sapiens (Human)], National Library of Medicine, https://www.ncbi.nlm.

nih.gov/gene/1272 (last visited May 1, 2026).

33

Anand M. Gautam et al., A polyalanine Peptide Containing Only Five Native Myelin Basic Protein

Residues Induces Autoimmune Encephalomyelitis, 176 J. EXPERIMENTAL MED. 605 (1992). Although Dr.

Steinman drew conclusions from this article, it was not filed by Petitioner. Instead, Petitioner filed a

screenshot of one table from this article and filed it as Petitioner’s Exhibit 21.

34

Anand M. Gautam et al., Minimum Structural Requirements for Peptide Presentation by Major

Histocompatibility Complex Class II Molecules: Implications in Induction of Autoimmunity, 91

IMMUNOLOGY 767 (1994).

35

Anand M. Gautam et al., A Viral Peptide with Limited Homology to a Self Peptide Can Induce Clinical

Signs of Experimental Autoimmune Encephalomyelitis, 161 J. IMMUNOLOGY 60 (1998).

36

Tobias V. Lanz et al., Clonally Expanded B Cells in Multiple Sclerosis Bind EBV EBNA1 and

GlialCAM, 603 NATURE 321 (2022).

11

Following his BLAST search, Dr. Steinman cross-referenced the relevant results to the

Immune Epitope Database (“IEDB”) and Alignment Resource, both publicly available online.

Pet’r’s Ex. 42 at 32. He described the IEDB as a “freely available resource funded by NIAID. It

catalogs experimental data on antibody and T cell epitopes studied in humans, non-human

primates, and other animal species in the context of infectious disease, allergy, autoimmunity, and

transplantation.” Id. Dr. Steinman noted that the sequence he identified, WEQAKALSVE, “is an

epitope in diphtheria toxin, which has only one amino acid difference from CRM197.” Id. at 33.

He continued that “[h]umans have been shown to mount T cell responses to these regions of the

diphtheria molecule.” Id. at 35. Dr. Steinman summarized his process:

These congruent findings between 1) Petitioner’s various searches on public

databases, 2) the three steps of filtration using peer reviewed journals as one

criterion, 3) searches on different US government-financed search tools (BLAST,

and IEDB), and now step 4) showing a correlation with detailed studies on the

human immune response to diphtheria toxin, differing in only one amino acid from

CRM, continue to make a compelling theory, that is sound and reliable, for how

molecular mimics in Prevnar 13 can cause GBS.

Id. at 36.

Additionally, Dr. Steinman discovered “an alignment between the CRM197 component of

the Prevnar 13 vaccine and Caspr2, an antigen targeted in GBS.” Pet’r’s Ex. 42 at 36. A second

BLAST search comparing diphtheria toxin and Caspr2 revealed a region sharing seven of nine

identical amino acids. Id. at 37. Dr. Steinman concluded that phosphoglycerol and a CRM197

region are two molecular mimics in the Prevnar 13 vaccine.

In anticipation of criticisms of his theory by Respondent’s expert(s), Dr. Steinman included

a “frequently asked questions” section to his initial report. Pet’r’s Ex. 42 at 39. First, he explained

why, under this theory, “the immune system would target phosphoglycerol in peripheral nerves

and not in other places where it is present in the body.” Id. Dr. Steinman noted that “antibody to

gangliosides results in GBS in some individuals, even though gangliosides are all over the body.”

Id. He continued that when GBS manifests following C. jejuni infection, the immune system

responds to gangliosides in the peripheral nervous system and “not to any diseases of erythrocytes,

intestine, liver, spleen and/or testis.” Id.

b. Dr. Whitton’s Initial Report

Dr. Whitton began by defining relevant terms and explaining general processes. Resp’t’s

Ex. C at 3. He characterized the structure of S. pneumoniae as a bacterial pathogen “surrounded

by a capsule made up of [sugar molecules]” and the Prevnar 13 vaccine as protection against 13

of the near 100 strains of pneumococcus. Id. He continued that these sugars, known as

polysaccharides when they are linked in molecules of 12 more together, are extremely diverse and

occur in mammals, plants, and bacteria. Id. Their diversity is rooted in the relatively large number

of monosaccharides, similar to protein chains where there are 20 different amino acid building

blocks. Id. at 4. An important difference between proteins and sugars however, Dr. Whitton

asserted, is “the chemical nature of their linkages.” Id. Unlike amino acid chains that are always

built head-to-tail in a chain, “monosaccharides can join to each other in different molecular

12

orientations.” Id. This results in an exponentially larger number of ways to connect the same

components. Id. Dr. Whitton then explained the difference between proteins and polysaccharides

by comparing the former to a string of pearls and the later to branches of a tree. Id. He wrote, “each

monosaccharide has several different points at which it can link to other monosaccharides; thus,

not only can they build an up/down zigzagging chain, they also can grow branches; and each

branch can itself sprout ‘daughter’ branches.” Id.

Next, Dr. Whitton noted the importance of the differences in the molecular composition of

each of the 13 polysaccharides comprising Prevnar 13. Resp’t’s Ex. C at 5. Each of “these different

bacterial polysaccharides trigger different immune responses and, consequently, our immune

system can distinguish among the many different strains of S. pneumoniae based on the

polysaccharides that each strain has in its capsule.” Id. This is why Prevnar 13, for example, only

protects against 13 specific strains. Id. Dr. Whitton asserted that many factors determine the

virulence of a bacterial pathogen; “most relevant to matter at hand, one factor that is related to

virulence is the polysaccharide capsule by which each bacterium is surrounded.” Id. Because each

strain has a different capsule, these “difference[s] form the basis by which the many different

pneumococcal strains are distinguished.” Id. These strains are referred to as serotypes, based on

“how it is recognized by the antibody response.” Id.

So, if you take a single S. pneumoniae bacterium, the antibody response against the

capsule of that bacterium recognizes only that bacterium and its progeny (so, we

could define that bacterium as “serotype #1” pneumococcus). However, those

antibodies would not recognize other strains of S. pneumoniae that carry different

polysaccharide capsules. The converse also holds true; antibodies against a

different S. pneumoniae isolate would define that bacterium as “serotype #2” and

those antibodies would not recognize bacteria of serotype #1 (nor bacteria of

serotypes #3, #4, etc...).

Id.

Dr. Whitton cited two articles, Haber et al. and Tseng et al., 37 to highlight the safety of

Prevnar 13. Resp’t’s Ex. C at 7. Haber et al. was described by the authors as “the first post-

marketing safety review of [Prevnar 13] in adults.” Resp’t’s Ex. A, Tab 5 at 4. The study reviewed

Vaccine Adverse Events Reporting System (“VAERS”) submissions based on an inoculation

period that covered approximately 16 million vaccine doses. Id. There were 11 reports of verified

GBS “with symptom onset within 42 days of [Prevnar 13] vaccination.” Id. The Tseng et al. cohort

study examined adults at least 65 years of age “for risk of adverse events requiring medical

attention following vaccination with [Prevnar 13] as compared with vaccination with [Pneumovax

23].” Resp’t’s Ex. A, Tab 13 at 1. A review of “313,136 doses of [Prevnar 13] and 232,591 doses

of [Pneumovax 23]” revealed four adverse events of GBS following the former group and eight

following the later. Id. at 4, 6. These “results indicate that there is no significantly elevated risk of

[GBS].” Id. at 7. Dr. Whitton also summarized the Baxter et al. 38 study that was “not directly

evaluating Prevnar 13, [but] did include two vaccines (Tdap and Td) that contain diphtheria toxin

37

Hung Fu Tseng et al., Pneumococcal Conjugate Vaccine Safety in Elderly Adults, 5 OPEN FORUM

INFECTIOUS DISEASES 100 (2018).

38

Roger Baxter et al., Lack of Association of Guillain-Barré Syndrome With Vaccinations, 57 CLINICAL

INFECTIOUS DISEASES 197 (2013).

13

(DT), and the authors found no association with an increased risk of GBS.” Resp’t’s Ex. C at 8

(citing Resp’t’s Ex. A, Tab 1). A study of 415 GBS patients did not find “an association between

influenza vaccine or any other vaccine and development of GBS withing six weeks following

vaccination.” Resp’t’s Ex. A, Tab 1 at 8. The article did note that the authors “had limited power

to fully assess the risk of GBS following vaccination due to the rarity of the outcome.” Id.

According to Dr. Whitton, Dr. Steinman’s two asserted causation theories “depend on

molecular mimicry.” Resp’t’s Ex. C at 12. Dr. Whitton distilled molecular mimicry down to three

steps: 1) an induced immune response, 2) a cross-reaction to host material, and 3) pathogenesis.

Resp’t’s Ex. C at 12–13. While acknowledging that molecular mimicry does occur, particularly in

animals, Dr. Whitton quoted expert immunologist Dr. Noel Rose: “There are, however, no clear

examples of a human disease caused by molecular mimicry.” Id. at 14. Dr. Whitton explained how

difficult it was to cause disease this way in mice, including the need for predisposed mice that

were bred because “they mounted a strong immune response to the viral protein.” Id. at 15.

In the context of this case, Dr. Whitton noted that in Prevnar 13, two of “S. pneumoniae

polysaccharides [(18C and 23F)] contain modifications, [specifically] the chemical linkage of . . .

a small molecule named glycerophosphate/phosphoglycerol.” Resp’t’s Ex. C at 20.

Because Dr. Steinman’s primary causation theory relies on the cross reactivity of

phosphoglycerol, Dr. Whitton thought it important to discuss generally. Resp’t’s Ex. C at 17. He

provided a figure of the chemical structure of phosphoglycerol and noted its very small size. Id.

With an average mass of approximately 154 Da, it is incredible that a single phosphoglycerol

molecule could trigger an immune response, given that “the rule of thumb is that the cutoff is about

3000 Da.” Id. Dr. Whitton then explained that small molecules (hapten) can trigger an immune

response to produce antibodies if they are attached to a larger “carrier” molecule. Id. A bacterial

polysaccharide is such a carrier, whereby “the epitope recognized by such an antibody would not

be phosphoglycerol alone; rather, it would be a larger structure comprising phosphoglycerol +

bacterial polysaccharide.” Id. Dr. Whitton then noted that in the Bryson et al. article, the authors

noted the high specificity of the antibodies detected. Id. at 18. He argued that these antibodies “are

not specific for phosphoglycerol alone (as Dr. Steinman appears to imply), they are specific for a

larger epitope that comprises phosphoglycerol + 23F polysaccharide.” Id. By way of illustration,

Dr. Whitton reproduced a figure from Bryson et al. that “showed the points of electrostatic contact

between individual amino-acids on the antibody, and components of the 23F epitope.” Id. at 19.

He noted that “of the nine contact points between the antibody and the epitope, eight are between

various amino acids in the antibody, and the saccharide residues on the 23F structure.” Id. The

only contact between the antibody and the phosphoglycerol “contacts an oxygen atom that is

attached to the phosphate.” Id. Dr. Whitton asserted that these antibodies “recognize mainly the

sugar residue” and only on 23F, “but not the 18C polysaccharide, even though it also has an

attached phosphoglycerol. Id. He further noted that other S. pneumoniae strains, such as 11A and

15B also contain phosphoglycerol-containing polysaccharides. Id. at 20.

He summarized Dr. Steinman’s first theory of causation as follows: “(i) a phosphoglycerol-

containing polysaccharide in Prevnar 13 induces an antibody response against the

phosphoglycerol, and (ii) this antibody causes GBS.” Resp’t’s Ex. C at 6. As an initial matter, Dr.

Whitton noted that these phosphoglycerol-containing polysaccharides are also present in S.

pneumoniae; therefore for Dr. Steinman’s theory to be valid, “S. pneumoniae strains 18C and 23F

14

should cause GBS.” Id. Dr. Whitton argued that this extrapolation does not hold and cited to

writing by Dr. Eric Gershwin that discusses infectious triggers of GBS. Id. at 9 (citing Resp’t’s

Ex. C, Tab 19). 39 Dr. Gershwin noted that “[o]ver two-thirds of patients with GBS refer symptoms

of respiratory or digestive infections within [six] weeks of onset.” Id. He then identified at least 40

infectious organisms thought capable of triggering GBS, most notably, C. jejuni. Id. at 10. C.

jejuni, for example, expresses molecules with ganglioside-like structures that induce antibodies,

which then go on to attack host gangliosides on neurons, causing GBS. Id. Dr. Whitton highlighted

the absence of S. pneumoniae from Dr. Gershwin’s list. Id.

The difference between these bacteria capable of triggering GBS and S. pneumoniae,

according to Dr. Whitton, is the composition of the bacterial cell wall. Resp’t’s Ex. C at 11.

Bacteria with a thin wall, or gram-negative, are “surrounded by an outer membrane, in the surface

of which are embedded the molecules that are thought to be involved in GBS.” Id. This is the

ganglioside-like material that cross-reacts with host neuron cells. Id. Conversely, S. pneumoniae

is gram positive with a thick cellular wall. Id. “It has a very thick capsule, composed mainly of the

polysaccharides that are used in the Prevnar 13 vaccine. S. pneumoniae does not have an outer

membrane, and it does not express the molecules that are thought to trigger GBS.” Id.

The cross-reactivity that Dr. Steinman asserted in this case is between phosphoglycerol +

polysaccharide in the vaccine and phosphoglycerol that is present in phospholipids within the host

myelin sheath. Resp’t’s Ex. C at 21. Dr. Whitton began by noting that Dr. Steinman asserted this

theory based on MS studies. Id. Dr. Whitton argued that this is “not appropriate” to use as a model

for GBS because the diseases differ in their pathogenesis as evidenced by their different treatment

regimens. Id. Differences notwithstanding, Dr. Whitton acknowledged that antiphospholipid

antibodies are present in some cases of GBS. Id. at 22. However, “as [he has] consistently opined,

autoantibodies (i) may be the cause of disease, (ii) may be the result of the disease; or (iii) may be

irrelevant to the disease.” Id. In support of this contention, Dr. Whitton quoted the Nakos et al.

paper relied on by Steinman: “It is not well understood whether these anti-phospholipid antibodies

play a role in the pathogenesis of the polyneuropathy or represent a part of a more extensive

immunoreaction that takes place in the GBS.” Id. (citing Pet’r’s Ex. 55 at 6). He also referred to

Gilburd et al., 40 a 1993 study of “the reactivity of GBS sera with various phospholipids which are

known to be important constituents of myelin, and serve as autoantigens in other autoimmune

conditions.” Resp’t’s Ex. C, Tab 26 at 1. “[O]ur results do not show a significant increase in any

specific antiphospholipid antibody. . . . However, some patients [] produce a variety of

antiphospholipid . . . antibodies, probably as a result of the myelin damage or as a result of cross

reaction with other anti-myelin antibodies.” Id. at 5.

Next, Dr. Whitton discussed the difference between polysaccharides and phospholipids.

Resp’t’s Ex. C at 23. Citing Hughes et al., 41 Dr. Whitton noted that the discussion of GBS

pathogenesis is always in the context of gangliosides and not phospholipids. Id. (citing Resp’t’s

Ex. C, Tab 27). He asserted that the word phospholipid is not mentioned at all. Id. “[T]here is no

39

Anil K. Jasti et al., Guillain-Barré Syndrome: Causes, Immunopathogenic Mechanisms and Treatment,

12 EXPERT REV. CLINICAL IMMUNOLOGY 1175 (2016).

40

B. Gilburd et al., Autoantibodies to Phospholipids and Brain Extract in Patients With the Guillain-

Barre Syndrome: Cross-Reactive or Pathogenic?, 16 AUTOIMMUNITY 23 (1993).

41

Richard A. C. Hughes et al., Guillain-Barré Syndrome in the 100 Years Since Its Description by

Guillain, Barré, and Strohl, 139 BRAIN 3041 (2016).

15

credible reason to believe that the antibodies described in Bryson [et al.], which recognize a

phosphoglycerol + 23F polysaccharide epitope, could also recognize a very different structure,

comprising phosphoglycerol remnant + lipid.” Id. Furthermore, Dr. Whitton asserted that Dr.

Steinman shifted from a phosphoglycerol target to phosphocholine, the polar head group on the

phospholipid phosphatidyl choline. Resp’t’s Ex. C at 24. He argued that “[t]he phosphocholine

head group is, chemically, very different from phosphoglycerol.” Id. Dr. Whitton continued,

explaining that Ho et al., co-authored by Dr. Steinman, “do[es] not even mention phosphoglycerol

or glycerophosphate.” Id. Dr. Whitton questioned that if the phosphate group that exists in

phospholipids is the sole target of these phosphate-specific antibodies, what about the other

identical phospholipids “present on the membrane of essentially every cell in our body.” Id. at 26.

Even more problematic, according to Dr. Whitton, is his contention that “[t]he

phospholipids that are the alleged target of autoantibody attack do not contain phosphoglycerol.”

Resp’t’s Ex. C at 28. Instead, the relevant phospholipids (in which phosphoglycerol is used as a

building block) are incorporated in larger glycerophospholipids to become the targets that Dr.

Steinman described. Id. Dr. Whitton explained that it is similar to comparing the raw ingredients

for a baked good to a completed cake, wherein flour, sugar, butter, and eggs “become involved in

complex chemical interactions, which change their chemical structure.” Id.

Many free phosphoglycerol molecules exist inside a cell, and some will be

exploited when assembling molecules such as glycerophospholipids. But when a

free phosphoglycerol molecule moves through this biochemical assembly-line, it is

irreversibly altered; it is no longer phosphoglycerol.

Id. Dr. Whitton continued to stress the importance of precise terminology. Resp’t’s Ex. C

at 29. He asserted that “when a phosphoglycerol (or glycerophosphate) molecule is used

… to build a glycerophospholipid, that molecule is consumed [ ]: (i) it loses both of its

hydroxy groups, which (ii) are replaced by very different molecules, called long-chain fatty

acids.” Id. He cautioned that “the three carbons remain as part of the glycerophospholipid

and, given their origin, those carbons are often referred to as the “glycerol backbone” of

the phospholipid.” Id. However, “this nomenclature is ‘misleading,’” and “very different

from the starting brick, phosphoglycerol/glycerophosphate.” Id. Dr. Whitton provided

diagrams for phosphoglycerol and glycerophosphate. Id.at 26.

16

Resp’t’s Ex. C at 26, Figure 3.

Dr. Whitton argued that Dr. Steinman’s theory depends on “the alleged antibody

response induced by a phosphoglycerol + polysaccharide epitope [that] must recognize

(cross-react with) a very different proposed epitope that comprises phosphoglycerol + lipid

that, he speculates, exists in specific host phospholipids,” such as phosphatidyl-choline.

Resp’t’s Ex. C at 30.

Resp’t’s Ex. C at 30, Figure 4.

He then used figures from Dr. Steinman’s report to illustrate these two epitopes.

Resp’t’s Ex. C. at 31. “The point being made here is []: regardless of what term you employ,

be it phosphoglycerol or glycerophosphate, neither of those chemical compounds is

present, intact, in the phospholipids; only vestiges remain.” Id. Dr. Whitton agreed with

Dr. Steinman’s referral to Chang et al. that “chemically modifying the phosphoglycerol

side chain of the 18C polysaccharide abrogates that polysaccharide’s immunogenicity.” Id.

Therefore, he argued that it is unreasonable that the phosphoglycerol remnant in

17

phosphatidyl choline (for example) “must have the same antigenicity as the (relatively

intact) phosphoglycerol that is present in a few of the S. pneumoniae polysaccharides.” Id.

Even when comparing phospholipids where the phosphoglycerol remnants are

“identical,” Dr. Whitton questioned why there are some that Dr. Steinman labeled reactive,

or recognized by the antiphospholipid antibodies, and nonreactive, which are not. Resp’t’s

Ex. C at 32.

Dr. Whitton generally restated Dr. Steinman’s second theory of causation “that antibody

responses against the CRM197 protein can cause GBS.” Resp’t’s Ex. C at 8. He noted that Dr.

Steinman’s conclusions are based largely from a layered homology analysis using BLAST

searches. Id. Immediately, Dr. Whitton stated that “whenever two average-length proteins are

properly compared, short homologies will inevitably be found.” Id. at 36. Indeed, these homologies

are “commonplace,” and of little importance. Id. Dr. Whitton referred to the 2006 Silvanovich et

al. 42 paper that sought “to assess whether or not short peptide matches were valuable in predicting

whether or not a protein was allergenic.” Id. at 38 (citing Resp’t’s Ex C, Tab 30). The paper’s

abstract ended with the statement that “searches for short amino acid sequence matches of eight

amino acids or fewer to identify proteins as potential cross-reactive allergens is a product of chance

and adds little value to allergy assessments for newly expressed proteins.” Resp’t’s Ex. C, Tab 30

at 1. Dr. Whitton asserted that due to the number of short homologies between two proteins of

average length, cross-reactivity can be asserted with respect to any host target. Resp’t’s Ex. C at

39.

Thus, regardless of the disease from which a petitioner suffers, Dr. Steinman will

always be able to identify short homologies between a disease-related host protein,

and a protein in the relevant vaccine. It works in the other direction, too: not only

can Dr. Steinman select the host protein that best fits the petitioner’s alleged

disease, he also can apply his approach to any vaccine; he will always be able to

find homologies. So, if a petitioner has received Prevnar 13 then, irrespective of the

alleged disease (be it GBS, narcolepsy, transverse myelitis, or whatever), a proper

comparison of CRM197 against a chosen host protein will always find homologies.

In other words, Dr. Steinman’s BLAST approach will always achieve his desired

outcome; he will identify homologies regardless of the alleged disease, and

regardless of the vaccine that he claims caused it.

Id.

In the present case, Dr. Whitton explained that the polysaccharides from the 13 serotypes

found in Prevnar 13 are individually cross-linked to CRM197, “a mutated variant of diphtheria

toxin.” Resp’t’s Ex. C at 6–7. He clarified, “CRM197 is not “used to conjugate the pneumococcal

polysaccharides in Prevnar 13 to an immunogenic protein carrier, [as Dr. Steinman alleged, but

rather], CRM197 is the immunogenic protein carrier.” Id. at 40. Dr. Whitton then analyzed the

BLAST results from CRM197 and contactin-1. Id. He relied on the 2006 Silvanovich et al.

approach because “this is the only approved use of BLAST for identifying protein sequences of

possible immunological relevance.” Id. at 42. The two criteria both must be met or exceeded for

42

Andre Silvanovich et al., The Value of Short Amino Acid Sequence Matches for Prediction of Protein

Allergenicity, 90 TOXICOLOGICAL SCI. 252 (2006).

18

possible immunological relevance for an identified homology. Id. “[F]irst, the length of the

homology must be at least 80 amino acids; and, second, after the sequences are aligned, at least 28

of the 80 amino acids (28/80 = 35%) must be identical.” Id. These criteria can be applied to linear

antibody epitopes or discontinuous, but following identification, there is a “very stringent criteria

[that is applied] before claiming to have identified a potentially immunologically relevant

sequence.” Id. at 43.

Dr. Whitton identified the Expect (“E”) value as “a parameter that describes the number of

hits one can ‘expect’ to see by chance when searching a database of a particular size.” Resp’t’s

Ex. C at 43. He then asked, what is a possible meaningful E value for immunologically significant

homologies? Id. at 44. According to Dr. Whitton, Silvanovich et al. answered that question: below

3.9 x 10-7. Id. The 2009 Silvanovich et al. 43 paper identified the threshold for identifying potential

allergenic cross-reactivity of transgene encoded proteins in genetically enhanced crops when using

BLAST searches. Resp’t’s Ex. C, Tab 32 at 1. A threshold of 3.9E-07 “has a potential false positive

rate as high as 95% for the identification of known allergens. Yet, it is of sufficient sensitivity that

it will discriminate against the majority of alignments that [exhibit] protein composition bias.” Id.

at 5.

Of the four homologies that Dr. Steinman identified, Dr. Whitton focused on the homology

noted between the CRM197 sequence WEQAKALSVE and the contactin-1 sequence

WDHVVALSNE. Resp’t’s Ex. C at 45. Dr. Whitton noted that the sequences compared were

longer in order to argue that the results are cherry picked. Id.

Id. (citing Pet’r’s Ex. 42 at 31).

Next. Dr. Whitton attacked Dr. Steinman’s “assum[ption] that any immune response that

recognizes WEQAKALSVE must also recognize WDHVVALSNE.” Resp’t’s Ex. C at 46.

Because these sequences and the identified homology does not meet any of the three Silvanovich

et al. criteria, Dr. Whitton argued that there is no evidence that this homology occurs for any reason

other than by chance. Id. Dr. Whitton argued further that Dr. Steinman’s filter funnel does not

provide evidence of immunogenicity. Id. at 50. First, Dr. Whitton argued that the CRM107

sequence, “WEQAKALSVE[,] is not a known epitope” identified in the IEDB. Id. Dr. Steinman

associated this sequence to the IEDB “by changing the default setting, Exact Match, to a lower-

stringency search, termed ‘BLAST Option: 70%.’” Id. at 50 (citing Pet’r’s Ex. 42 at 35). Dr.

Whitton identified this sequence within the database as a part of a larger, 20-amino-acid-long

sequence that “could activate some human CD4+ T cells.” Id. at 52. He added that “we do not

know what part of the 20 amino acid long [sequence] is responsible for activating the T cells.” Id.

at 51. Additionally, the contactin-1 sequence, WDHVVALSNE, “returned no hits, even when

carried out using the low-stringency BLAST approach.” Id. Therefore, “there is no evidence that

the alleged target sequence in contactin-1, WDHVVALSNE, is recognized by the human immune

system.” Id. Dr. Whitton continued that even if these two chains were molecular mimics, Dr.

Andre Silvanovich et al., The Use of E-Scores to Determine the Quality of Protein Alignments, 54

43

REGULATORY TOXICOLOGY & PHARMACOLOGY 26 (2009).

19

Steinman would still need to “show that both peptides can be recognized by the same antibody or

by the same T cell.” Id.

Although Dr. Whitton disagreed with Dr. Steinman’s assertion that that WEQAKALSVE

within contactin-1 is immunogenic, he conducted a BLAST search to identify “better homologies

in many other human proteins because . . . those other human proteins – and the tissues that express

them – should be the target of autoimmune assault by the CRM197-induced antibodies.” Resp’t’s

Ex. C at 54. He noted that “thousands of proteins were identified” but “contactin was not among

[them].” Id. at 54–55. As a control, Dr. Whitton ran a search of the WDHVVALSNE peptide

sequence and “contactin-1 was at the top, with an E-value of 3 x 10-4.” Id. at 55. Dr. Whitton

argued that this result is evidence that BLAST searches do work to identify homology, “if they

exist.” Id. “This validates [Dr. Whitton’s] conclusion regarding the WEQAKALSVE-based

BLAST search; no homology with contactin-1 was found, indicating that no meaningful homology

exists.” Id. Dr. Whitton reiterated that “Dr. Steinman’s BLAST search did not identify

[WEQAKALSVE], Dr. Steinman’s BLAST search identified an 18 amino-acid long peptide as

being partially homologous with contactin-1. Dr. Steinman then cherry-picked the shorter

sequence” contained within. Id.

Dr. Whitton conceded “that short peptides can, occasionally, be involved in molecular

mimicry.” Resp’t’s Ex. C at 58. However, he attacked Dr. Steinman’s use of literature, some of

which is self-authored, to support molecular mimicry as a mechanism for Prevnar 13 vaccine-

caused GBS. Id. First, Dr. Whitton asserted that Dr. Steinman overstated the conclusion in Lanz

et al. Id. (citing Pet’r’s Ex. 67). Evidence that “some individuals with MS have antibodies that can

cross-react with both EBNA-1 and GlialCAM . . . most certainly does not demonstrate that this

cross-reactivity causes MS!” Id. He quoted the conclusion of the paper, which stated that “[o]ur

results provide a mechanistic link for the association between MS and EBV, and could guide the

development of novel MS therapies.” Id.

Second, Dr. Whitton stressed that many of the studies, including Lanz et al., are related to

EBV and MS, neither of which are present in this case. Id. He described the Bjornevik et al. 44 as

“tour de force of epidemiology, involving ~10 million people and carried out over ~20 years[ that]

appear[s] to have demonstrated that [MS] is caused by EBV.” Id. at 57 (citing Resp’t’s Ex. C, Tab

33). He continued that EBV is a live virus, compared to Prevnar 13, a non-live vaccine against a

bacterium; and MS is a different disease characterized by differences in diagnostic criteria,

duration, and treatment. Id. at 58.

The end of Dr. Whitton’s report is a summary of criticisms of Dr. Steinman’s arguments

and restatements of some of his asserted inconsistencies in Dr. Steinman’s theories. Resp’t’s Ex.

C at 63. He noted generally, that despite Dr. Steinman’s heavy reliance on molecular mimicry as

a mechanism for GBS by comparison to MS, his own article “make[s] no mention whatsoever of

phosphoglycerol or phospholipids as possible targets of autoimmune attack causing MS.” Id. at

62.

44

Kjetil Bjornevik et al., Longitudinal Analysis Reveals High Prevalence of Epstein-Barr Virus

Associated with Multiple Sclerosis, 375 SCIENCE 296 (2022).

20

c. Dr. Steinman’s Supplemental Report

Dr. Steinman responded directly to Dr. Whitton’s report starting with the conclusion from

his own professional experience that molecular mimics can cause “widespread unwanted immune

reactions” and “provoke neuroinflammatory disease” in humans. Pet’r’s Ex. 85 at 4. Next, Dr.

Steinman explained that “the components of the entire [S. pneumoniae] bacterium contain various

proteins, sugars and lipids which serve to subvert the human immune system.” Id. at 4–5. He

clarified that his cross-reactivity theory is based on the fact that the sugars in Prevnar 13 are

combined with CRM197 and formulated with alum. Id. These additions, according to Dr.

Steinman, were deemed “necessary to get adequate immunity to the sugars.” Id. Furthermore, they

distinguish the infection from the vaccine in a way that explains the latter’s cross-reactivity. Id.

This cross-reactivity, Dr. Steinman maintained, occurs because “the antibody binds to the

phosphoglycerol moiety of the sugar as well as to the sugars” in the 23F and 18C components of

Prevnar 13 that “is also central to the composition of the phospholipids in myelin.” Id. at 5–6. He

argued that Ho et al. established “a strong attraction for binding to these phosphate moiety,

independent of what is attached to it.” Id. at 6. Dr. Steinman also cited to Barbar et al. 45 to assert

“that binding to the phosphate group was retained, no matter what the structure was that was

attached to it.” Id. (citing Pet’r’s Ex. 88).

The Barbar et al. article began by stating that “current procedures to produce hapten-carrier

protein conjugates . . . disallow[] determination of specific structural details of antigen-antibody

interactions.” Pet’r’s Ex. 88 at 1. The authors “sought to analyze the carrier contribution to hapten

binding by utilizing small, homogeneous amino acid-hapten conjugates.” Id. They noted at the

outset that “[t]he hapten phosphocholine is immunogenic when coupled to protein carriers.” Id.

Building from that, Barbar et al. “synthesized a series of haptenated carriers made from amino

acids and peptides,” and found that “[t]he affinity for hapten was shown to be modulated by the

identity of the carrier molecule.” Id. at 2. Additionally, “[t]he bound confirmations of at least some

of the carriers were found to be influenced by antibody.” Id. The authors concluded “that binding

involves specific interactions that change the conformation of both the hapten and antibody. . . .

Thus there is a conformational distortion of the carrier as well.” Id. at 9. They noted that

“conformational mobility of the antibody combining site has been proposed as a possible

mechanism for cross-reactivity.” Id. at 10. Barbar et al. also suggested that this “mechanism may

be common.” Id. Ultimately, “the differences in I50[46] values and binding affinities of the hapten

when coupled to various small carriers are not attributable to changes in the orientation of the

hapten in the combining site, but rather to interactions with the carrier.” Id. Dr. Steinman

analogized binding of a phosphate group to the hook on an aircraft carrier attaching to a fighter

jet. Pet’r’s Ex. 85 at 8.

Upon landing, there is contact of the wheels under the nose of the plane and under

the wings with the deck. However, the primary binding is to the arresting hook on

the deck of the carrier: “A tailhook, arresting hook, or arrester hook is a device

attached to the empennage (rear) of some military fixed-wing aircraft. The hook is

45

Elisar Barbar et al., Binding of Phenylphosphocholine–Carrier Conjugates to the Combining Site of

Antibodies Maintains a Confirmation of the Hapten, 35 BIOCHEMISTRY 2958 (1996).

46

I50 values correspond to the hapten concentration needed to inhibit 50% of the antibody binding to

phosphocholine-histone. See Pet’r’s Ex. 80 at 3 (Sven Jarius et al., Neuromyelitis Optica, 6 NATURE

REVIEWS 85 (2020)).

21

used to achieve rapid deceleration during routine landings aboard aircraft carrier

flight decks at sea.”

Id. The hook, “all important in landing the plane and keeping it on deck,” is analogous to the

phosphate group. Id. Dr. Steinman opined that the autoantibodies targeting the phosphate groups

in MS “is exceptionally close to what [] would constitute certainty on the question of whether

humans who receive a pneumococcal vaccine make antibodies that target phosphoglycerol.” Id. at

8.

Next, Dr. Steinman directly addressed Dr. Whitton’s contention that the Ho et al. article

does not mention phosphoglycerol or glycerophosphate. Pet’r’s Ex. 82 at 8. “Similarities are seen

with binding to phospholipids in myelin in the Ho et al. paper.” Id. Ho et al. was an analytical

study done to “discover[] autoimmune targets and developing therapeutic strategies for MS.”

Pet’r’s Ex. 51 at 1. To determine whether the autoantibody targeted lipids have a role in

autoimmune demyelination, the authors tested the effect of select lipids on EAE, a mouse model

of MS. Id. at 2. The lipids selected included myelin lipids (gangliosides), membrane lipids

(phosphatidylcholine), microbial lipids (lipopolysaccharide), and oxidized lipids (1-palmitoyl2-

glutaroyl-sn-glycero-3-phosphocholine (“PGPC”) and its derivatives). Id. Dorland’s Online

Dictionary provides definitions for three of the four subgroups. First, ganglioside is defined as

“any of a group of [glycolipids] in which the polar head group on ceramide is a sialic acid–

containing oligosaccharide linked via a glucose residue; they occur predominantly in tissues of the

central nervous system.” Ganglioside, DORLAND’S. Glycolipids contain carbohydrates and the

term “is used almost exclusively to denote the lack of a phosphate group.” Glycolipid, DORLAND’S.

Second, phosphatidylcholine is “a phospholipid in which choline is attached to the phosphate

group of phosphatidic acid by an ester linkage; it is a major component of cell membranes and is

localized preferentially in the outer surface of the plasma membrane.” Phosphatidylcholine,

DORLAND’S. Phospholipids are further defined as “the major form of lipid in all cell membranes.”

Phospholipid, DORLAND’S. Third, a lipopolysaccharide is “a complex of lipid and polysaccharide”

that is “a major component of the cell wall of gram-negative bacteria.” Lipopolysaccharide,

DORLAND’S. The fourth type of lipid studied by Ho et al., PGPC is defined by the authors as “a

derivative of oxidized phosphatidylcholine.” Pet’r’s Ex. 51 at 3. The authors were particularly

interested in PGPC “because antibodies for oxidized phosphatidylcholine are present in MS brain

lesions.” Id. Additionally, “unlike the other lipids tested, PGPC attenuated the development of

EAE and ameliorated EAE after onset. A reduction in T cell activation, a process important in MS

pathogenesis, accompanied the PGPC-induced attenuation of EAE.” Id. These findings caused the

authors to investigate “autoantibody targeting of seven lipids that have a glycero-3-phosphocholine

backbone in common with PGPC, as well as targeting of other structurally similar lipids . . .

including a phosphate head group with one or two nonpolar side chains.” Id. Of the seven, three

glycerol-3-phosphocholine–containing lipids exhibited autoantibody reactivity during microarray

analysis. Id. The authors hypothesized “that autoantibodies present in [relapse-remitting MS

patient] CSF target the phospholipids’ phosphate head group and that the affinity of antibody-lipid

binding is not specific to a particular phospholipid.” Id. Further support of this idea is evidenced

by autoantibodies not targeting myelin lipids without the phosphate polar head. Id. The authors

noted that the “binding of [relapse-remitting MS] CSF autoantibodies to these lipids is dependent

on the presence of (i) a nonbulky polar head group such as a phosphate group and (ii) at least one

long hydrocarbon side chain.” Id. Ultimately, “[w]hereas the polar head groups are the lipid

22

components targeted by the autoantibodies, the fatty acid side chains are the components that

mediate the lipids’ anti-inflammatory effects.” Id. at 9.

The discussion section of the Ho et al. article posed several suggestions about the

pathogenesis of MS based on the studies of these autoantibodies. Pet’r’s Ex. 51 at 9. Notably that

“[t]he destruction of myelin involves anti-lipid autoantibodies, which can induce demyelination

and prevent remyelination in mouse models of MS.” Id. Additionally, the results of this study

suggest that “the antibodies to oxidized phosphatidylcholine derivatives that we detect in CSF [are

generated as part of the pathological process of autoimmune demyelination and] can bind their

lipid targets in MS brain.” Id. Dr. Steinman then asserted that the phospholipids in the myelin of

MS patients discussed in Ho et al. “are identical in many cases to the phospholipids” in Nakos et

al. Pet’r’s Ex. 85 at 9. He noted that Al-Temeemi et al. 47 “[m]easur[ed] immunoglobulin G and

immunoglobulin M antiphospholipid antibodies of incidental untreated GBS patients and

compar[ed] them with that of normal population.” Id. at 14 (citing Pet’r’s Ex. 89). He noted the

authors’ findings that “GBS cases have statistically significant higher [immunoglobulin M

antiphospholipid antibodies] titers during the first week and the first two weeks of illness than

healthy controls, and [antiphospholipid antibodies] may have a protective effect in GBS.” Id.

(citing Pet’r’s Ex. 89). Nakos et al. also suggested “that antibody mediated injury is a predominant

disorder in the demyelinating form of GBS.” Pet’r’s Ex. 55 at 6–7. They described GBS pathology

as an “extensive immune reaction” that “is directed against components of Schwann cell[48]

membrane and is accompanied by the characteristic feature of vesicular demyelination.” Id. at 7.

In conclusion, they asserted that “it is crucial to investigate how anti-phospholipid antibodies are

related to specific antigens in Schwann cell membrane.” Id. Dr. Steinman strongly disagreed with

Dr. Whitton’s opinion of the significance of Nakos et al., explaining that he “think[s] that Dr.

Whitton is reading the Nakos paper rather selectively. But that is why two experts debate these

details.” Pet’r’s Ex. 85 at 14.

Returning to Ho et al., Dr. Steinman directly challenged Dr. Whitton’s contention that his

article did not mention phosphoglycerol or glycerophosphate. Pet’r’s Ex. 85 at 15. He reproduced

Figure 2C, depicting “antibody reactivity to various glycerol-3-phosphocholine lipids in CSF

samples from patients with [relapsing remitting] MS and from control patients with [other

noninflammatory, neurological disease].” Id. (citing Pet’r’s 51 at 4). Dr. Steinman asserted that

“panel C speaks in English to the actual chemical structures shown in this sound and reliable paper.

We have …Glycero-3[phospho…] repeated in English in six lines in a row.” Id. Noting that he

was a co-author, Dr. Steinman wrote, “[w]e found autoantibodies in MS target a phosphate group

in phosphatidylserine and oxidized phosphatidylcholine derivatives.” Id. Indeed, Dr. Steinman

asserted “the phosphoglycerol backbone is a critical constituent of many of the phospholipids

described in Ho et al.,” including the glycerol- 3-phosphoethanolamine and glycerol-3-phosphoL-

Serine. Id. at 16. Lastly, as it relates to his phosphoglycerol theory, Dr. Steinman noted that Dr.

Whitton’s other critiques were addressed in his initial report. Id.

47

Temeem M. Al-Temeemi et al., Antiphospholipid Antibody in Serum of Guillain-Barre Syndrome

Patients, 10 IRAQI J. MED. SCI. 191 (2012).

48

Schwann cells are “any of the large nucleated cells whose cell membrane spirally enwraps the axons of

myelinated peripheral neurons and is the source of myelin; a single Schwann cell supplies the myelin

sheath between two nodes of Ranvier.” Schwann Cell, DORLAND’S.

23

The second part of Dr. Steinman’s responsive report discussed Dr. Whitton’s opinions

related to his BLAST search and conclusions. Pet’r’s Ex. 85 at 18. He argued that Dr. Whitton’s

criteria are based on “searches over much longer stretches of protein-80 amino acids and does not

address the chunks of protein in an immunological epitope.” Id. Dr. Steinman relied on the Raju

et al. 49 paper to explain that “the immune system is probed with [shorter] peptides of 10 to 20

amino acids.” Pet’r’s Ex. 85 at 18 (citing Pet’r’s Ex. 74). He also cited the Lanz et al. paper to

assert that “peptides of length 10 to 20 amino acids are recognized by the immune system.” Id.

(citing Pet’r’s Ex. 67).

In Raju et al., the authors suggested that “[i]dentification of [immunodominant region

sequences] might facilitate the design of peptide vaccines for immunoprophylaxis of diphtheria.”

Pet’r’s Ex. 74 at 8. Diphtheria toxin (“DTX”) is made up of a single chain of 535 amino acids. Id.

at 1. The authors broke that chain “into fragments . . . leading to arrest of protein synthesis.” Id. at

2. They then used these peptide chains “to identify sequence regions recognized by CD4+ cells of

seven healthy humans.” Id. The study included fragments of “53 peptides, 20 residues long and

overlapping by [ten] residues, corresponding to the complete DTX sequence.” Id. at 2–3. The

authors explained this “length was chosen because, although class II-restricted epitopes are only

13-17 residues long the presence of extra residues does not interfere with epitope presentation.”

Id. at 3. The authors cautioned that they “do not know which residues within the [immunodominant

region sequences] interact with the different class II molecules, and [] cannot identify structural

correlates between the sequence of the IRS peptides and their ability to bind to different presenting

molecules” Id. at 8. However, “the binding motifs identified for peptide binding to [HLA-]DRl,

and different [HLA-]DR4 subtypes are present in most or all the DTX immunodominant region

sequences.” Id.

In 2022, Lanz et al. published an article “demonstrat[ing] high-affinity molecular mimicry

between the EBV transcription factor EBV nuclear antigen 1 (EBNA1) and the [CNS] protein glial

cell adhesion molecule (GlialCAM) and provid[ing] structural and in vivo functional evidence for

its relevance.” Pet’r’s Ex. 67 at 1. Monoclonal antibody 50 MS39p2w174 is an immunoglobulin

superfamily cell adhesion molecule expressed in the CNS that binds with GlialCAM. Id. at 4.

MS39p2w174 also bound to the EBNA1 protein and the EBNA1AA386–405 peptide, but “its

binding affinity for the native peptide GlialCAMAA370–389 was three orders of magnitude lower

than for GlialCAM protein.” Id. at 5. “MS39p2w174 did not demonstrate high enrichment for any

single peptide, which suggests that it has low affinity for multiple native peptides.” Id. at 5.

The 2023 Lanz et al. 51 article was described by the authors as “a roadmap for what may be

studied next in understanding how EBV triggers MS.” Pet’r’s Ex. 82 at 3. They believed that their

research “may also illuminate parallel mechanisms in other diseases including systemic lupus

49

Raghavanpillai Raju et al., Epitopes for Human CD4+ Cells on Diphtheria Toxin: Structural Features

of Sequence Segments Forming Epitopes Recognized by Most Subjects, 25 EUR. J. IMMUNOLOGY 3207

(1995).

50

Monoclonal antibodies are “chemically and immunologically homogenous antibodies produced by

hybridomas, used as laboratory reagents in radioimmunoassays, ELISA, and immunofluorescence

assays.” Monoclonal Antibody, DORLAND’S.

51

Tobias V. Lanz et al., Roadmap for Understanding Mechanisms on How Epstein-Barr Virus

Triggers Multiple Sclerosis and for Translating These Discoveries in Clinical Trials, 23

CLINICAL & TRANSLATIONAL IMMUNOLOGY 1438 (2023).

24

erythematosus, rheumatoid arthritis, Sjogren’s syndrome, Long COVID and even myalgic

encephalomyelitis/ chronic fatigue syndrome.” Id. The authors identified the region of the peptide

of EBNA-1 between amino acids 365 and 420 that shared homology with GlialCAM. Id. at 4.

Within that region, “[c]lonally expanded antibodies isolated from the cerebrospinal fluid of MS

patients target EBNA-1 residues 386–405 that cross-react with the CNS cell adhesion molecule

GlialCAM and are associated with CD4 and CD8 T cell responses targeting GlialCAM.” Id. The

authors focused on “the molecular mechanisms underlying how clonal antibody in the CSF

emanates in widespread molecular mimicry to key antigens in the nervous system including

GlialCAM, a protein associated with chloride channels.” Id. at 3.

The epitopes, EBNA 1 AA386-405 and GlialCAM AA370-389, consist of 19 amino acids

and “show[] that the landing pad for an antibody is a small domain of the protein of 10-20 amino

acids.” Pet’r’s Ex. 85 at 19. Dr. Steinman argued that “[t]he mimic, where [five] identical amino

acids in a stretch of 12 between EBNA 1 and GlialCAM, also was tested in the EAE model, where

it worsened disease.” Id. at 20. He noted that “[i]n some cases alignment is extensive and e-values

approach zero.” Id. at 21. To account for this, Dr. Steinman reiterated that the BLAST search is

followed by his multi-step, filter funnel to support molecular mimicry once homology has been

identified. Id. at 23.

d. Dr. Whitton’s Supplemental Report

Dr. Whitton’s second filed report sought to address Dr. Steinman’s direct responses to the

criticisms and concerns that Dr. Whitton detailed in his initial report. Resp’t’s Ex. F at 4. Dr.

Whitton asserted that Dr. Steinman has modified one of the identified molecular mimics asserted

in this case. Id. Dr. Whitton stated that initially “Dr. Steinman hypothesized that a phosphoglycerol

molecule that is attached to some S. pneumoniae polysaccharides in Prevnar 13 can induce

antibodies that can cross-react with a phosphoglycerol that is present in phospholipids, and that

this results in GBS.” Id. In response to Dr. Steinman’s second report, Dr. Whitton stated that the

theory is now based “on recognition of a phosphate residue that just happens to be on a

phosphoglycerol molecule (or on a remnant thereof).” Id. Dr. Whitton wrote “if the proposed target

is actually phosphate, rather than phosphoglycerol, then I agree that these phospholipids do contain

a phosphate moiety.” Id. Consequently, Dr. Whitton did not direct any further attention to whether

the phospholipids identified by Dr. Steinman contain intact phosphoglycerol. Id.

Instead, Dr. Whitton noted Dr. Steinman’s reliance on Barbar et al. and criticized his

“attempt to convince us that the antibodies can recognize phosphate alone.” Resp’t’s Ex. F at 6.

Dr. Whitton made several observations about the substance of the Barbar et al. study. Id. at 7. He

noted that “[t]he antibodies [studied by Barbar et al.] are specific for a molecule named

phenylphosphocholine, not for phosphate;” and they, along with “the target structures, [] have no

relationship to S. pneumoniae polysaccharides.” Id. Additionally, the researchers “do not attempt

to induce antibodies using very small molecules; rather, they use synthesized (preexisting)

antibodies, and determine what ‘shapes’ those antibodies can recognize.” Id. Dr. Whitton also

noted that “even the largest of the materials attached to [phenylphosphocholine] is far smaller than

the bacterial polysaccharides to which the phosphate groups are linked in some S. pneumoniae

polysaccharides.” Id.

25

Expanding on Dr. Steinman’s use of a fighter jet analogy, Dr. Whitton countered with his

own interpretation: “in allowing the plane to land, the carrier does not rely solely on the interaction

between the wire rope and the arresting hook.” Resp’t’s Ex. F at 8. He explained:

In summary, the carrier’s deck (the Bryson antibody) captures the plane (the

phosphate + 23F polysaccharide epitope) when (i) the wire rope grabs the arresting

hook (the phosphate moiety) and (ii) the rest of the deck accepts the plane’s wheels

(the eight points of contact with S. pneumoniae sugars).

Id. Because each epitope has a different polysaccharide, “the fighter with ‘18C wheels’ can land

only on the aircraft carrier (antibody) that can accept those wheels.” Id. Dr. Whitton argued that

this makes his point that the hook is not a sufficient point of recognition because “even though the

23F deck has a wire rope to accept the fighter’s arresting hook, that deck does not have the correct

surface configuration to capture the 18C fighter’s wheels.” Id.

Dr. Whitton next clarified the significance of linear versus discontinuous chains of amino

acids. Resp’t’s Ex. F at 14. He argued that in order for most amino acid chains “to achieve

biological activity, [they] must fold up into a 3D structure.” Id. Dr. Whitton noted that a folded

protein can contain a linear epitope, but most epitopes are discontinuous, i.e., made from shorter

chains of amino acids that are “scattered” throughout a longer sequence and “brought together by

protein folding.” Id. Each antibody epitope is made up of amino acids sequences present along the

“surface of the protein; many other amino acids are buried in the middle of the structure and . . .

invisible to antibodies.” Id. Dr. Whitton opined that the short homologies identified by Dr.

Steinman’s BLAST searches are too short to “contain an antibody epitope because the great

majority of antibody epitopes are discontinuous, and span lengths far longer than 10-12 amino

acids.” Id. In the cases that Dr. Steinman does provide examples of short homologies, such as the

one identified in the Fujinami & Oldstone52 paper, the amino acid sequence from myelin basic

protein (“MBP”) “was already known to be a molecular mimic, and was already known to cause

disease (EAE).” Id. at 18 (citing Pet’r’s Ex. 76). That sequence was then used to find homology in

viral protein. Id. at 19. The corresponding sequence “was found in hepatitis B virus polymerase

(HBVP); . . . and it shares [six] identical amino acids with the MBP.” Id. Dr. Whitton argued that

this type of comparison is “completely different” and only “similar because they both use a

computer search.” Id.

V. Applicable Legal Standards

To receive compensation under the Vaccine Act, a petitioner must demonstrate either that:

(1) the petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently

developing a listed injury within the timeframe prescribed by the Vaccine Injury Table set forth at

42 U.S.C. § 300aa-14, as modified by 42 C.F.R. § 100.3; or (2) that the petitioner suffered an “off-

Table injury,” one not listed on the Table, as a result of him receiving a covered vaccine. See §

11(c)(1)(C); Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010);

Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1319–20 (Fed. Cir. 2006). In this

case, GBS is not a Table injury associated with the Prevnar 13 vaccine, and thus Petitioner must

prove by preponderant evidence that his injury was caused-in-fact by a Table vaccine.

52

Robert S. Fujinami & Michael B. A. Oldstone, Amino Acid Homology Between the Encephalitogenic

Site of Myelin Basic Protein and Virus: Mechanism for Autoimmunity, 230 SCIENCE 1044 (1985).

26

A. Factual Issues

A petitioner must prove, by a preponderance of the evidence, the factual circumstances

surrounding his claim. § 13(a)(1)(A). To resolve factual issues, the special master must weigh the

evidence presented, which may include contemporaneous medical records and testimony. See

Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a special

master must decide what weight to give evidence including oral testimony and contemporaneous

medical records). Contemporaneous medical records, “in general, warrant consideration as

trustworthy evidence.” Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir.

1993); but see Kirby v. Sec’y of Health & Hum. Servs., 997 F.3d 1378, 1382 (Fed. Cir. 2021)

(rejection the presumption that “medical records are accurate and complete as to all the patient’s

physical conditions”); Shapiro v. Sec’y of Health & Hum. Servs., 101 Fed. Cl. 532, 538 (2001)

(“[T]he absence of a reference to a condition or circumstance is much less significant than a

reference which negates the existence of the condition or circumstance.”).

B. Causation-In-Fact

To establish causation-in-fact, a petitioner must demonstrate by a preponderance of the

evidence that the vaccine was the cause of the injury. § 13(a)(1)(A). A petitioner is required to

prove that the vaccine was “not only a but-for cause of the injury but also a substantial factor in

bringing about the injury.” Moberly, 592 F.3d at 1321–22 (quoting Shyface v. Sec’y of Health &

Hum. Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999).

In the seminal case of Althen v. Sec’y of Health & Hum. Servs., the Federal Circuit set forth

a three-pronged test used to determine whether a petitioner has established a causal link between

a vaccine and the claimed injury. See 418 F.3d 1274, 1278–79 (Fed. Cir. 2005). The Althen test

requires petitioners to set forth: “(1) a medical theory causally connecting the vaccination and the

injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for

the injury; and (3) a showing of a proximate temporal relationship between vaccination and

injury.” Id. at 1278. To establish entitlement to compensation under the Program, a petitioner is

required to establish each of the three prongs of Althen by a preponderance of the evidence. Id.

“[C]lose calls regarding causation are resolved in favor of injured claimants.” Id. at 1280. Further,

evidence used to satisfy one prong of the test may overlap to satisfy another prong. Capizzano,

440 F.3d at 1326.

Under the first prong of Althen, a petitioner must offer a scientific or medical theory that

answers in the affirmative the question: “can the vaccine[] at issue cause the type of injury

alleged?” See Pafford v. Sec’y of Health & Hum. Servs., No. 01-0165V, 2004 WL 1717359, at *4

(Fed. Cl. Spec. Mstr. July 16, 2004), mot. for rev. den’d, 64 Fed. Cl. 19 (2005), aff’d, 451 F.3d

1352 (Fed. Cir. 2006). To satisfy this prong, a petitioner’s theory must be based on a “sound and

reliable medical or scientific explanation.” Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d

543, 548 (Fed. Cir. 1994). Such theory must only be “legally probable, not medically or

scientifically certain.” Id. at 548–49. Petitioners are not required to identify “specific biological

mechanisms” to establish causation, nor are they required to present “epidemiologic studies,

rechallenge[] the presence of pathological markers or genetic disposition, or general acceptance in

the scientific or medical communities.” Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at

1280). Scientific and “objective confirmation” of the medical theory with additional medical

documentation is unnecessary. Althen, 418 F.3d at 1278–81; see also Moberly, 592 F.3d at 1322.

However, as the Federal Circuit has made clear, “simply identifying a ‘plausible’ theory of

27

causation is insufficient for a petitioner to meet her burden of proof.” LaLonde v. Sec’y of Health

& Hum. Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014) (citing Moberly, 592 F.3d at 1322). Indeed,

the Federal Circuit has “consistently rejected theories that the vaccine only ‘likely caused’ the

injury and reiterated that a ‘plausible’ or ‘possible’ causal theory does not satisfy the standard.”

Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1360 (Fed. Cir. 2019) (citing Moberly,

592 F.3d at 1322; LaLonde, 746 F.3d at 1339); see also Cerrone v. Sec’y of Health & Hum. Servs.,

146 F.4th 1113, 1121 (Fed. Cir. 2025) (explaining that “simply identifying a plausible theory of

causation is insufficient for a petitioner to meet her burden of proof.” (internal quotes omitted)).

Rather, “[a] petitioner must provide a reputable medical or scientific explanation that pertains

specifically to the petitioner’s case.” Moberly, 592 F.3d at 1322. In general, “the statutory standard

of preponderance of the evidence requires a petitioner to demonstrate that the vaccine more likely

than not caused the condition alleged.” LaLonde, 746 F.3d at 1339.

Furthermore, establishing a sound and reliable medical theory connecting the vaccine to

the injury often requires a petitioner to present expert testimony in support of his claim. Lampe v.

Sec’y of Health & Hum. Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). The Supreme Court’s

opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993) requires that courts

determine the reliability of an expert opinion before it may be considered as evidence. However,

in the Vaccine Program, the Daubert factors are used in the weighing of the reliability of scientific

evidence proffered. Davis v. Sec’y of Health & Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010)

(“[U]niquely in this Circuit, the Daubert factors have been employed also as an acceptable

evidentiary-gauging tool with respect to the persuasiveness of expert testimony already

admitted.”); see also Cedillo v. Sec’y of health & Hum. Servs., 617 F.3d 1328, 1339 (Fed. Cir.

2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999)). It

is also not required that special masters utilize Daubert when weighing the reliability of expert

testimony. See Boatmon, 941 F.3d at 1359 (“Special masters may, but are not required to, analyze

expert testimony according to Daubert.” (emphasis in original)). Under Daubert, the

Factors for analyzing the reliability of testimony are: (1) whether a theory or

technique can be (and has been) tested; (2) whether the theory or technique has

been subjected to peer review and publication; (3) whether there is a known or

potential rate of error and whether there are standards for controlling the error; and

(4) whether the theory or technique enjoys general acceptance within a relevant

scientific community.

Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592–95).

The Daubert factors are “meant to be helpful, not definitive.” Kumho Tire Co. v.

Carmichael, 526 U.S. 137, 151 (1999). The factors do not “constitute a ‘definitive checklist or

test’” and may be applied differently depending on the facts of a particular case. Id. at 150 (quoting

Daubert, 509 U.S. at 593).

“In short, the requirement that an expert’s testimony pertain to ‘scientific knowledge’

establish a standard of evidentiary reliability.” Daubert, 509 U.S. at 590 (citation omitted). Thus,

for Vaccine Act claims, a “special master is entitled to require some indicia of reliability to support

the assertion of the expert witness.” Moberly, 592 F.3d at 1324. Nothing requires the acceptance

of an expert’s conclusion “connected to existing data only by the ipse dixit of the expert,”

especially if “there is simply too great an analytical gap between the data and the opinion

proffered.” Synder v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen.

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Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also D’Tiole v. Sec’y of Health & Hum. Servs.,

No. 15-085V, 2016 WL 7664475, at *24 (Fed. Cl. Spec. Mstr. Nov. 28, 2016) (stating that the

Vaccine Act “require[s] a chain of reliable propositions supporting [a] petitioner’s theory”).

Under the second prong of Althen, a petitioner must prove that the vaccine actually did

cause the alleged injury in a particular case. See Pafford, 2004 WL 1717359, at *4; Althen, 418

F.3d at 1279. The second Althen prong requires proof of a logical sequence of cause and effect,

usually supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278;

Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956 F.2d 1144, 1148 (Fed.

Cir. 1992). A petitioner does not meet this obligation by showing only a temporal association

between the vaccination and the injury; instead, the petitioner “must explain how and why the

injury occurred.” Pafford, 2004 WL 1717359, at *4 (emphasis in original). The special master in

Pafford noted petitioners “must prove [] both that her vaccinations were a substantial factor in

causing the illness . . . and that the harm would not have occurred in the absence of the

vaccination.” 2004 WL 1717359, at *4 (citing Shyface, 165 F.3d at 1352). A reputable medical or

scientific explanation must support this logical sequence of cause and effect. Hodges v. Sec’y of

Health & Hum. Servs., 9 F.3d 958, 961 (Fed. Cir. 1993) (citation omitted). Nevertheless,

“[r]equiring epidemiologic studies . . . or general acceptance in the scientific or medical

communities . . . impermissibly raises a claimant’s burden under the Vaccine Act and hinders the

system created by Congress.” Capizzano, 440 F.3d at 1325–26. “[C]lose calls regarding causation

are resolved in favor of injured claimants.” Althen 418 F.3d at 1280.

In Program cases, contemporaneous medical records and the opinions of treating

physicians are favored. Capizzano, 440 F.3d at 1326 (citing Althen, 418 F.3d at 1280). Indeed,

when reviewing the record, a special master must consider the opinions of treating physicians.

Capizzano, 440 F.3d at 1326. This is because “treating physicians are likely to be in the best

position to determine whether ‘a logical sequence of cause and effect show[s] that the vaccination

was the reason for the injury.’” Id. In addition, “[m]edical records, in general, warrant

consideration as trustworthy evidence. The records contain information supplied to or by health

professionals to facilitate diagnosis and treatment of medical conditions. With proper treatment

hanging in the balance, accuracy has an extra premium. These records are also generally

contemporaneous to the medical events.” Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d

1525, 1528 (Fed. Cir. 1993). However, there is no “presumption that medical records are accurate

and complete as to all of the patient’s physical conditions.” Kirby v. Sec’y of Health & Hum. Servs.,

997 F.3d 1378, 1383 (Fed. Cir. 2021) (finding that a special master must consider the context of a

medical encounter before concluding that it constitutes evidence regarding the absence of a

condition). While a special master must consider these opinions and records, they are not “binding

on the special master or court.” § 13(b)(1). Rather, when “evaluating the weight to be afforded to

any such . . . [evidence], the special master . . . shall consider the entire record.” Id.

To satisfy the third Althen prong, a petitioner must establish a “proximate temporal

relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This

“requires preponderant proof that the onset of symptoms occurred within a timeframe for which,

given the medical understanding of the disorder’s etiology, it is medically acceptable to finger

causation-in-fact.” de Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir.

2008). Typically, “a petitioner’s failure to satisfy the proximate temporal relationship prong is due

to the fact that onset was too late after the administration of a vaccine for the vaccine to be the

cause.” Id. However, “cases in which onset is too soon” also fail this prong; “in either case, the

temporal relationship is not such that it is medically acceptable to conclude that the vaccination

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and the injury are causally linked.” Id.; see also Locane v. Sec’y of Health & Hum. Servs., 685

F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the illness was present before the vaccine was administered,

logically, the vaccine could not have caused the illness.”).

Although a temporal association alone is insufficient to establish causation, under the third

prong of Althen, a petitioner must show that the timing of the injury fits with the causal theory.

See Althen, 418 F.3d at 1278. The special master cannot infer causation from temporal proximity

alone. See Thibaudeau v. Sec’y of Health & Hum. Servs., 24 Cl. Ct. 400, 403–04 (1991); see also

Grant, 956 F.2d at 1148 (“[T]he inoculation is not the cause of every event that occurs within the

ten[-]day period . . . [w]ithout more, this proximate temporal relationship will not support a finding

of causation.” (quoting Hasler v. United States, 718 F.2d 202, 205 (6th Cir. 1983))).

A petitioner who satisfies all three prongs of the Althen test has established a prima facie

showing of causation. Hammitt v. Sec’y of Health & Hum. Servs., 98 Fed. Cl. 719, 726 (2011). A

petitioner who demonstrates by a preponderance of the evidence that he suffered an injury caused

by vaccination is entitled to compensation unless the respondent can demonstrate by a

preponderance of the evidence that the injury was caused by factors unrelated to the vaccination.

See Althen, 418 F.3d at 1278; Knudsen, 35 F.3d at 547. In such a case, the government must not

merely prove the existence of an alternative cause, but that such an alternative actually caused the

injury. Kundsen, 35 F.3d at 549. Consequently, when and if the petitioner establishes a prima facie

case, the burden the shifts to the government to prove that an alternative cause, unrelated to the

administration of the vaccine, was the “sole substantial factor” in causing the alleged injury. See

de Bazan, 539 F.3d at 1354; see also Hammitt, 98 Fed. Cl. at 726 (explaining that respondent’s

burden is to show that the “factor unrelated” was the “sole substantial factor” in causing the injury).

Additionally, a factor unrelated “may not include ‘any idiopathic, unexplained, unknown,

hypothetical, or undocumentable cause, factor, injury, illness or condition.’” § 13(a)(2); see also

Doe v. Sec’y of Health & Hum. Servs., 601 F.3d 1349 (Fed. Cir. 2010) (stating that an idiopathic

diagnosis cannot be a “factor unrelated,” as it is idiopathic).

VI. Analysis

A. Prior Claims

In the past few years, there have been several Program cases that have alleged a GBS injury

following Prevnar 13 vaccination with split results from the special masters. In cases where there

is disagreement among special masters regarding asserted causation theories, the presiding special

masters will often distinguish the most recent decision from previous decisions. These varying

perspectives are not necessarily problematic as “Congress desired the special masters to have very

wide discretion with respect to the evidence they would consider and the weight to be assigned

that evidence.” Whitecotton v. Sec’y of Health & Hum. Servs., 81 F.3d 1099, 1108 (Fed. Cir. 1996).

Furthermore, this is done notwithstanding the Circuit’s reaffirmance in Gamboa-Avila that “it was

not arbitrary and capricious for a special master to make no attempt to distinguish the instant case

from the other cases reaching opposite conclusions.” Gamboa-Avila v. Sec’y of Health & Hum.

Servs., 166 F.4th 1318, 1323 (Fed. Cir. 2026) (citing Boatmon, 941 F.3d at 1358). It is also worth

noting, as I have done here, that many cases alleging the same vaccine/injury cause-and-effect

were done with experts that may overlap but are not the same on both sides; sharing theories that

are similar but not identical; and using literature that has been at times, novel, outdated, updated,

or even abandoned.

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Several special masters have found in favor of petitioners relying on Dr. Steinman’s

phosphoglycerol theory or some variation thereof.

1. Koller v. Sec’y of Health & Hum. Servs

In Koller, Dr. Steinman opined that the petitioner’s Miller Fisher variant of GBS was

caused by Prevnar 13. Koller v. Sec’y of Health & Hum. Servs., No. 16-439V, 2021 WL 5027947,

at *8 (Fed. Cl. Spec. Mstr. Oct. 8, 2021). Specifically, Dr. Steinman asserted that “it’s molecular

mimicry to the phosphoglycerol that is connected to the polysaccharide structure of the vaccine

that gives rise to GBS.” Id. Dr. Steinman continued that “[p]hosphoglycerol is the scaffold for the

fatty acids that adorn the anus of the three carbon molecules of phosphoglycerol. Phosphoglycerol

is thus a building block of the vaccine and also of the phospholipid” in myelin.” Id. at *9. The

special master found unpersuasive the argument presented by Respondent’s expert, Dr. Leist, that

“there is “no reliable medical literature supporting,” petitioner’s theory.” Id. at *19. He noted that

identification and proof of specific biological mechanisms is not needed and found Dr. Steinman’s

theory to be based on a sound and reliable scientific explanation. Id. at *20.

2. Parker v. Sec’y of Health & Hum. Servs.

In Parker, the petitioner’s expert, Dr. Gershwin, relied on Dr. Steinman’s molecular

mimicry theory articulated in Koller, “as a springboard to review the literature cited and arrive at

his own conclusions.” Parker v. Sec’y of Health & Hum. Servs., No. 20-411V, 2023 WL 9261248,

at *10 (Fed. Cl. Spec. Mstr. Dec. 20, 2023). Dr. Gershwin opined that “the mimic is the

phosphoglycerol structure within at least two serotypes of Prevnar, 18C and 23F. The cross-

reactive mimic is phospholipid found within the myelin sheath of peripheral nerves, causing GBS.”

Id. at *12. Respondent’s expert, Dr. He, argued that the lack of epidemiologic and mechanistic

evidence was fatal to Dr. Gershwin’s theory. Id. In finding entitlement, the special master noted

that Dr. He did “not refute the scientific data or foundational evidence used by Dr. Gershwin to

support his theory.” Id. at *22. She noted that Dr. Gershwin relied on MS studies to show that

“myelin phospholipids are targeted by an immune response, . . . that myelin is comprised of

phospholipids, [] that phospholipids can serve as autoantigens in autoimmune disorders[, and] that

patients with GBS have autoantibodies to phospholipids.” Id. Taken together, this “is sound

support from reputable medical studies for the foundational aspects of Dr. Gershwin’s

phosphoglycerol theory.” Id.

3. Davison v. Sec’y of Health & Hum. Servs.

In the Davison case, the petitioner relied on Dr. Steinman who proposed two molecular

mimicry theories based on a phosphoglycerol theory and a CRM197 mimic, similar to the current

case. Davison v. Sec’y of Health & Hum. Servs., No. 19-1404V, 2025 WL 2692664, at *7 (Fed.

Cl. Spec. Mstr. Aug. 19, 2025). Again, the special master found in the petitioner’s favor, noting

that scientific certainty is not the evidentiary standard and “[w]ith regard to the application of

molecular mimicry, prior cases have expressed that the line must be drawn somewhere between

speculation and certainty.” Id. at *12 (citing Brayboy v. Sec’y of Health & Human Servs., No. 15-

183V, 2021 WL 4453146, at *19 (Fed. Cl. Spec. Mstr. Aug. 30, 2021)). The special master further

noted that Respondent’s immunology expert, Dr. Zhang, did “not specifically discuss any of Dr.

Steinman’s more specific observations regarding the potential pathogenicity of phospholipid

antibodies in GBS or any of the literature he relied upon.” Id. at *10. The special master found that

Dr. Steinman presented supporting evidence for his assertions:

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(1) the Prevnar 13 vaccine contains phosphoglycerol groups that are necessary to

the vaccine’s immunogenicity[;] . . . (2) the phosphate portion of the phospholipid

molecule has immune reactivity in myelin tissue, albeit demonstrated in the context

of a different demyelinating condition ([MS])[;] . . . (3) GBS patients develop

antiphospholipid antibodies[;] . . . and (4) these antibodies are cross-reactive with

phospholipids present in myelin tissue.

Id. at *12. In response, Dr. Zhang’s rebuttal was focused on “fact that the wild S.

pneumoniae infection has not been shown to cause GBS,” and the lack of epidemiological studies.

Id. at *15. In his decision, the special master noted that “evidence of parallels to nature infection

[] is never sufficient to either accept or reject a causal relationship.” Id. at *14 (citing Gaskin v.

Sec’y of Health & Human Servs., No. 21-835V, 2025 WL 786306 at *12 (Fed. Cl. Spec. Mstr.

Feb. 11, 2025)). He further noted that epidemiology is not necessary for a petitioner to be

successful. Id. (citing Capizzano, 440 F.3d at 1325).

4. Fee v. Sec’y of Health & Hum. Servs.

In the Fee case, the petitioner’s expert, Dr. DeAngelo, also presented the theory “that

molecular mimicry caused ‘a homologous interplay between the

phosphoglycerol/phosphorylcholine within the Prevnar 13 vaccine and the phospholipid

components in the human myelin sheath.’” Fee v. Sec’y of Health & Hum. Servs., No. 19-1979V,

2026 WL 700326, at *13 (Fed. Cl. Spec. Mstr. Feb. 13, 2026). As in Parker, Dr. He’s rebuttal

warned against the overreliance on molecular mimicry in Program cases. Id. at *9. He criticized

Dr. DeAngelo’s use of MS studies and the lack of supporting statistics. Id. Dr. He argued that it

was “unclear whether GBS patients have similar types of autoantibodies targeting

a phosphate group,” and there was “no evidence that these autoantibodies are the initiators of MS,

let alone GBS.” Id. at *14. Dr. He also referred to the Institute of Medicine (“IOM”) stating

“naturally occurring and postinfectious cross-reactive antibodies and T cells are relatively common

and most frequently not pathogenic, and can also be secondary to a nonspecific tissue injury.” Id.

In finding for petitioner, I noted that Dr. He “denounced molecular mimicry as a theory outright,

contending that if it were true, all vaccines could cross-react to induce all kinds of autoimmune

conditions.” Id. at *21. Dr. He did not refute the substance of Dr. DeAngelo’s theory, but instead

argued that without epidemiologic evidence, a traditional criterion sanctioned by the IOM to prove

molecular mimicry, the theory was insufficient. Id. I also noted that given the rare nature of many

of the conditions seen in the Program and lack of testing practicality, epidemiological studies are

not required. Id.

Other special masters have found this theory less persuasive.

5. Bielak v. Sec’y of Health & Hum. Servs.

In Bielak, the chief special master noted that molecular mimicry has been accepted as a

biological mechanism for flu-vaccine caused GBS, and that there are “several evidentiary

components” of causal association. Bielak v. Sec’y of Health & Hum. Servs., No. 18-761V, 2023

WL 35509, at *30 (Fed. Cl. Spec. Mstr. Jan. 3, 2023). First, “reliable science” has identified a

specific autoantibody generated in response to C. jejuni that can cross-react with myelin

gangliosides and cause autoimmune damage that manifests as motor axonal variant of GBS. Id.

This supports molecular mimicry as a potential mechanism for other forms of GBS, “[a]nd there

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is reliable evidence that the amino acid peptide sequences that make up different proteins could

mimic aspects of myelin basic protein.” Id. Lastly, there is epidemiological evidence of increased

GBS rates following a previously administered flu vaccine. Id. While this theory has since been

asserted by petitioners as a causal mechanism for other vaccines, Bielak noted that the flu vaccine

from the epidemiological study is an outlier, especially when compared to Prevnar 13. Id. at *31.

The chief special master noted the focus on “phospholipids common to the bacterial capsid

antigens and the lipid content of myelin, attempting further to show the potential for cross-reactive

harm by identifying antiphospholipid antibodies in the blood serum of GBS patients.” Bielak, 2023

WL 35509, at *33. Furthermore, Respondent’s expert, “Dr. Fujinami[,] did not dispute that some

homologic commonalities were demonstrated through this aspect of [p]etitioner’s case.” Id.

However, the chief special master ultimately found there was a lack of preponderant evidence 1)

that Prevnar 13 produces pathogenic antibodies, and 2) that the relevant antibodies detected in

GBS patients are caused by the disease as opposed to created by it. Id.

6. Gamboa-Avila v. Sec’y of Health & Hum. Servs.

The Federal Circuit weighed in on a later Prevnar 13/GBS opinion wherein the chief special

master denied entitlement. Gamboa-Avila, 166 F.4th 1318. While the decision was based in part

on “the absence of support in the medical literature for Dr. Steinman’s theories,” the Circuit

reiterated that “[a] special master may weigh the fact that a ‘proposed mechanism had never been

tested in any peer-reviewed study’ and may properly consider the weakness of medical literature

support when evaluating the overall reliability of scientific evidence.” Id. at 6 (quoting Moberly,

592 F.3d at 1324); see Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1350–

51(Fed. Cir. 2010). The chief special master identified very specific deficiencies in the asserted

theory that caused for speculation below a more likely than not threshold. Id. at 7. The Circuit

found that the chief “special master did not apply a standard inconsistent with [their decision in]

Althen,” and his decision was not arbitrary and capricious. Id. There was some concern in the

affirmance, however, regarding the “the inconsistent factual findings among the special masters

on central issues presented in this case.” Id. The petitioner argued on appeal that the “findings in

this case are inconsistent with those reached by other special masters on identical evidence in other

cases.” Id. The Circuit also noted that the inconsistency in assessments by different special masters

was noted in the entitlement denial. Id. at 8. The identity of the special master ultimately

determined the outcome in this case. Id. Special masters were encouraged to recommend a Claims

Court “related rule or other mechanisms to avoid inconsistent rulings.” Id.

7. Romine v. Sec’y of Health & Hum. Servs.

Since the Circuit’s finding in Gamboa-Avila, the Romine decision was published and

included additional analysis to address some of the concerns articulated on appeal. Romine v. Sec’y

of Health & Hum. Servs., No. 19-468V, 2026 WL 937898, at *7 (Fed. Cl. Spec. Mstr. Mar. 13,

2026). The special master began with analysis of the epidemiological evidence exploring possible

relationships between pneumococcal vaccines and GBS and between the bacteria pneumococcus

and GBS. Id. at *7–11. The special master found that “four large-scale epidemiological studies

have looked for an increased risk of GBS after vaccines against S[.] pneumoniae[ and] did not find

an increased risk.” Id. at *11. Additionally, the evidence submitted contained “no reports of a wild

S[.] pneumoniae infection preceding GBS.” Id.

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Dr. Steinman was also the petitioner’s expert in Romine, and he proposed a homology that

he identified through BLAST searches. Romine, 2026 WL 937898, at *13–17. The special master

held that the reliability standard for potentially relevant homologies was too generous based on the

evidence. Id. at *16. Therefore, “any ensuing steps that follow from the BLAST searches are also

problematic.” Id. Dr. Steinman reasoned that the body’s reaction to diphtheria toxin, a pathogen,

would be similar to the protein CRM197 found in the Prevnar 13 because they share similar amino

acid sequences. Id. Again, the special master found that Dr. Steinman’s reliance on homology was

misplaced. Id. at *18. While CRM197, diphtheria toxin, and diphtheria toxoid have very similar

amino-acid sequences, the biophysical, immunological, structural, and chemical differences mean

that analyses of immune responses to diphtheria toxin/toxoid may not necessarily apply to

CRM197. Id. Because of the numerous other concerns with the fundamental methodology behind

Dr. Steinman’s reasoning, the decision did not reach the final step necessary for molecular

mimicry. Id. at *15. The question of whether cross reactivity between identified components in

Prevnar 13 and in human peripheral myelin “can contribute to the pathogenesis of GBS is not

required, [and] can be reserved for another day.” Id.

In Romine, as in the present case, Dr. Steinman presented a variation on molecular mimicry

in which “antibodies produced in response to a phosphate in the context of a polysaccharide[, a

component of Prevnar 13] can cross-react with a phosphate in the context of a phospholipid[, a

component of the myelin sheath].” Romine, 2026 WL 937898, at *29. The special master again

found there was a lack of evidence generally to support GBS pathogenesis and specifically to

support cross-reactivity. Id.

In an attempt to address the concerns expressed by the Circuit in Gamboa-Avila, the

Romine decision included a discussion of how special masters may have come to different

conclusions when presented with similar evidence in cases involving the same or similar vaccine

and injury combinations. Romine, 2026 WL 937898, at * 29–33. Over 25 years ago, the Terran

decision endorsed use of the Daubert factors “as a tool or framework for conducting the inquiry

into the reliability of the evidence.” Terran, 195 F.3d at 1316. The Federal Circuit has continued

to make clear that although peer reviewed studies are not required, “[a] special master may weigh

the fact that a proposed mechanism had never been tested in any peer-reviewed study and may

properly consider the weakness of medical literature support when evaluating the overall reliability

of scientific evidence.” Gamboa-Avila, 166 F.4th at 1323 (citing Moberly, 592 F.3d at 1324).

Indeed, in Romine, all four Daubert factors are articulated (testability, peer review, error rate, and

general acceptance); however, the unique nature of the Program creates difficulties for the

application of each one. Romine, 2026 WL 937898, at *33. While reiterating that “[t]he Daubert

criteria should be employed flexibly,” the special master found it “difficult to see how [Dr.

Steinman’s theories] pass[] any of the Daubert factors.” Id.

Various iterations of the two theories that Dr. Steinman has proposed in the present case

have been previously asserted successfully and unsuccessfully in the Program, as discussed above.

It is important to note that theory modifications based on a better understanding of how the immune

system works (e.g., newly published research), observations of documented temporal associations

between a specific vaccination and a specific injury (case studies), and consideration of specific

case facts (positive antibody testing results) may have contributed to different conclusions in these

cases. While I have considered the past findings of my colleagues and the evidence that they

considered as detailed in their respective decisions, this Petitioner’s claim will be adjudicated

based on the evidence contained within this case record.

34

We are cautious to not apply a one-size-fits-all approach in every case, because the nuance

matters. Indeed, as the Program has evolved, renowned experts have presented novel theories that

have been accepted or rejected based on the arguments and supporting literature presented to the

special masters. For example, where there may have been no epidemiology for a specific theory,

relevant studies have since been completed. See D’Tiole, 2016 WL 7664475 (the special master

denying entitlement, in part, based on a 2014 epidemiological study that found no cases of the

alleged injury, narcolepsy, following the relevant vaccine, FluMist). In another instance, ideas that

were presented as plausible were not sufficiently developed to be reliable. See D’Angiolini v. Sec’y

of Health & Hum. Servs., 122 Fed. Cl. 86, 101 (2015) (the Claims Court affirming the special

master’s rejection of the ASIA theory by “the world’s preeminent expert in autoimmunity,”

holding that the research is “still developing and currently incomplete”); see also Cerrone, 146

F.4th at 1121. There are however, many cases where the science is not proven, and yet we do not

require specific causation evidence, because Table criteria have been accepted by medical experts

retained by the United States government. Indeed, the Table, while efficient and consistent, is not

ideal to settle complex and evolving disagreements between esteemed medical experts in their

respective fields, that develop in real time. And so, a case-by-case analysis is needed. In such off-

Table cases, Petitioner’s theory “must be supported by a sound and reliable medical or scientific

explanation.” Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378 (Fed. Cir. 2009);

Knudsen, 35 F.3d at 548. Presently, the alleged vaccine-cause injury is not a Table claim, but

Petitioner draws many parallels between the Table flu/GBS injury and his off-Table claim to

establish many of the parameters foundational to his asserted causation theory.

B. Althen Prong One

All the medical professionals in this case, including Petitioner’s treaters and the experts

retained by Petitioner and Respondent, agree that the relevant condition is GBS. 53 Furthermore,

there is no dispute of the underlying facts regarding the timing, onset, and nature of Petitioner’s

symptoms. Indeed, the determinative issue in this case whether there is preponderant evidence of

a causal mechanism for GBS following Prevnar 13 vaccination.

Under Althen prong one, Petitioner must set forth a medical theory explaining how the

received vaccine could have caused or sustained injury. Andreu, 569 F.3d at 1375; Pafford, 451

F.3d at 1355–56. Petitioner’s theory of causation need not be medically or scientifically certain,

but it must be informed by a “sound and reliable” medical or scientific explanation. Boatmon, 941

F.3d at 1359; see also Knudsen, 35 F.3c at 548; Veryzer v. Sec’y of Health & Hum. Servs., 98 Fed.

Cl. 214, 223 (2011) (noting that special masters are bound by both § 13(b)(1) and Vaccine Rule

8(b)(1) to consider only evidence that is both “relevant” and “reliable”), aff’d 475 F. App’x 765

(Fed. Cir. 2012). If Petitioner relies upon a medical opinion to support his theory, the basis for the

opinion and the reliability of that basis must be considered in the determination of how much

weight to afford the offered opinion. See Broekelschen, 618 F.3d at 1347 (“The special master’s

decision oftentimes is based on the credibility of the experts and the relative persuasiveness of

their competing theories.”); Perriera v. Sec’y of Health & Hum. Servs., 33 F.3d 1375, 1377 n.6

(Fed. Cir. 1994) (stating that an “expert opinion is no better than the soundness of the reasons

supporting it” (citing Fehrs v. United States, 620 F.2d 255 (Ct. Cl. 1980))). Importantly, as the

Federal Circuit has made clear, “simply identifying a ‘plausible’ theory of causation is insufficient

53

Dr. Whitton noted that he is not a licensed doctor that diagnoses patients. He stated that “whenever I am

invited to review a case, prior to accepting I invariably ensure that a board-certified MD will be retained

to discuss the diagnosis and other clinical aspects of the case.” Resp’t’s Ex. C at 3.

35

for a petitioner to meet her burden of proof.” LaLonde, 746 F.3d at 1339. Instead, Petitioner must

show it was more likely than not that the vaccine caused the condition alleged. Id.

Dr. Steinman’s molecular mimicry theory can be broken down into two main branches that

he argues work together in this case, though both are capable of causing GBS independently. The

first iteration asserts that two of the Prevnar 13 viral serotypes (18C and 23F) contain a

phosphoglycerol moiety that is also central to the composition of phospholipids in the myelin that

is damaged in GBS. These homologous sequences are molecular mimics wherein

antibodies/autoantibodies can bind to either the antigen or the host tissue via the phosphate group.

Dr. Steinman argued that studies on GBS patients have revealed the presence of these antibodies,

thereby establishing a causal relationship with the disease. A birds-eye review of this theory

appears reasonable and easy to follow. However, a more discerning review of the details begs the

question: What evidence is there that antibodies produced to recognize specific pneumococcal

vaccine serotypes will mistakenly target myelin tissue?

1. Phosphate Moiety Molecular Mimicry

a. MS v. GBS

The studies that Dr. Steinman relied on are largely in the context of MS. Indeed, the

research on MS that Dr. Steinman and others have done has been nothing short of groundbreaking.

While not conceding that Dr. Steinman’s MS research supports molecular mimicry as a pathogenic

mechanism in humans, even Dr. Whitton acknowledged that “molecular mimicry can be found in

people with MS.” Resp’t’s Ex. F at 19. He argued that the only article that definitively identifies

molecular mimics, Lanz et al., found high affinity between EBNA1, a viral protein, and GlialCAM,

a glycoprotein found in the CNS. Pet’r’s Ex. 67 at 1. This evidence clearly demonstrates molecular

mimicry; however, the cross-reactivity between these two proteins is substantively different than

the reaction that Dr. Steinman proposed in this case.

Comparing decisions that accept and reject Dr. Steinman’s theory, a critical factor that

emerges is to what degree the evidence is found to support similarity between MS and GBS. In

Davison, the special master found that “[w]hile the Ho [et al.] study pertained to [MS], there is no

debate [] that [an] autoimmune attack on the myelin sheath is relevant to the pathogenesis of GBS[,

and Nakos et al.] demonstrated the presence of phospholipid antibodies within GBS patients, but

not controls.” Davison, 2025 WL 2692664, at *7. While antiganglioside antibodies are more

commonly associated with GBS, “[w]e do not actually know the full scope of the antibodies that

may be implicated in the pathology of GBS;” therefore, “the possibility of a glycolipid antigen

remains.” Id. at *13 (internal citations omitted). There are two assumptions that must be made to

complete this sequence. Pathogenic antibodies must be, at least in part, targeting the phospholipids

and not just gangliosides, and the phospholipid antibodies here must be the cause as opposed to a

result of demyelination. Dr. Whitton argued that the latter argument is directly undercut by the

Gilburd et al. conclusion that the antibodies are “probably [] a result of the myelin damage or as a

result of cross reaction with other anti-myelin antibodies.” Pet’r’s Ex. 55 at 6. This 30-year-old

study does not consider some of the breakthroughs that have led to more researchers, including

Dr. Steinman, questioning the role of antibodies in actual pathogenesis. However, even the most

current studies concede that this question has not been answered.

Conversely, in Romine, the special master was unable to accept Dr. Steinman’s

extrapolation of Ho et al. 2026 WL 937898, at *30. The special master noted that MS patients are

36

not routinely tested for anti-phospholipid antibodies and “the Lanz [et al.] paper proposes a protein

as the target of autoimmune attack in [MS] and does not mention phospholipids as a possible

target.” Id. at *25. The Ho et al. article noted that “lipids constitute 70% of the myelin sheath,” but

the authors only go so far as to say “autoantibodies against lipids may contribute to the

demyelination that characterizes [MS].” Pet’r’s Ex. 50 at 16 (emphasis added). Similarly, the

Nakos et al. article cautioned that “no conclusive etiological concept [for GBS] has yet been

found.” Pet’r’s Ex. 55 at 1. The authors were also very careful to note that that anti-phospholipid

antibodies were found in patients with GBS. Id. at 1 (emphasis added).

Dr. Whitton’s argument highlighting differences between MS and GBS undercuts the use

of MS research for GBS patients. MS is a CNS disease, while GBS is a peripheral neuropathy;

because the diseases differ in their duration, pathogenesis, and treatment, Dr. Whitton argued that

MS “is not appropriate to use [] as a model for GBS.” Resp’t’s Ex. C at 21. While the EBV/MS

causal mechanism provides a roadmap for pathogenic molecular mimicry, there is no one-size-

fits-all theory. Dr. Steinman’s theory is based on cross-reactivity between components in the

Prevnar 13 vaccine and GBS, a peripheral neuropathy.

Dr. Steinman strongly disagreed with Dr. Whitton’s reading of Nakos et al. He argued that

the quote, “It is not well understood whether these anti-phospholipid antibodies play a role in the

pathogenesis of the polyneuropathy or represent a part of a more extensive immunoreaction that

takes place in [] GBS,” was taken out of context. Pet’r’s Ex. 55 at 6. To put the quote in context, I

will provide the entire paragraph:

It is not well understood whether these anti-phospholipid antibodies play a role in

the pathogenesis of the polyneuropathy or represent a part of a more extensive

immunoreaction that takes place in [] GBS. However, immunopathology in

autopsies suggests that antibody mediated injury is a predominant disorder in the

demyelinating form of GBS. The immune attack is directed against components of

Schwann cell membrane and is accompanied by the characteristic feature of

vesicular demyelination. Therefore it is crucial to investigate how anti-

phospholipid antibodies are related to specific antigens in Schwann cell membrane.

Id. at 6–7. The article then identified the “prospective benefit[s]” of their findings: 1) “use [of]

anti-phospholipid antibodies as an early additional marker of diagnostic significance;” and 2) use

for “prognostic significance for GBS, as it may reflect the response to treatment.” Id. at 7. Notably,

the authors did not suggest their findings be used to identify an etiological source or construct a

theory of pathology. If this conclusion is as clear as Dr. Steinman suggests, the question begs, why

do the authors not share his level of certainty, or at least suggest that their findings support that

conclusion?

b. Prevnar 13 Target

According to Dr. Steinman, the antibody binds to “the phosphogylcerol moiety of the sugar

as well as the sugars” in the 23F and 18C components of Prevnar 13. Pet’r’s Ex. 85 at 5. This

assertion is one of the strongest areas of disagreement between him and Dr. Whitton. Dr. Whitton

asserted that the Bryson et al. article “indisputably proves that the antibody predominantly

recognizes the 23F bacterial polysaccharide, not the phosphoglycerol.” Resp’t’s Ex. C at 19. Both

experts appear to recognize the importance of the polysaccharide for antibody recognition;

however, Dr. Steinman argued that indeed “data from the Bryson [et al.] article demonstrates

37

UNEQUIVOCALLY that the immune response to the serotype 23F component of Pneumovax 23

targets the phosphoglycerol in serotype 23F.” Pet’r’s Ex. 85 at 6 (emphasis in original). Bryson et

al. found that “[t]he electron density for the phosphate group[ is] another major binding

determinant of the 23F polymer.” Pet’r’s Ex. 59 at 6. This result supports Dr. Steinman’s assertion

that the phosphate group is a necessary condition for antibody recognition and binding; however,

the authors further explained that “crystal structures of the [monosaccharide components of these

polysaccharide complexes] reveal the basis for the high specificity of these [antibodies for the

monosaccharide,] the key antigenic component of the [pneumococcal capsular polysaccharides]

of S. pneumoniae serotype 23F.” Id. This conclusion supports Dr. Whitton’s assertion that “the

epitope recognized by such an antibody would not be phosphoglycerol alone; rather, it would be a

larger structure comprising phosphoglycerol + bacterial polysaccharide.” Resp’t’s Ex. C at 18.

Figure two of the Bryson et al. article illustrates the “nine points of contact” between the 23F

epitope and the antibody, and is further support for a hapten + carrier recognition and binding.

Pet’r’s Ex. 42 at 24, Figure S1.

There is preponderant evidence supporting Dr. Steinman’s assertion: the antibody does

recognize the phosphate group. There is also preponderant evidence that the polysaccharide is the

predominant target. This is further supported by the need for multiple serotypes within the

conjugate vaccine to generate antibodies to different strains of S. pneumoniae.

c. Myelin Target

Dr. Steinman relied again on his MS research to opine that the phospholipids in the myelin

sheath are targeted by antibodies in neuroinflammation. The Kanter et al. study noted the lipid

specific autoimmunity in MS patients and hypothesized that “[t]he lipid molecules are thereby

oriented so that the polar regions, such as the sulfate group or glycan molecule, are accessible for

antibody binding.” Pet’r’s Ex. 50 at 6. They also noted that the “data suggest that sulfatide-specific

and other lipid-specific responses can contribute to the pathogenesis of autoimmune demyelinating

disease.” Id. Dr. Whitton quoted Dr. Steinman’s own research in rebuttal to this argument.

“Autoimmune responses directed against phospholipids and gangliosides contribute to the

pathogenesis in systemic lupus erythematosus and [GBS], respectively.” Id. at 1. In all of the

38

literature that Dr. Steinman submitted, including those on which he is a co-author, there is no

assertion that phospholipids are the targets in GBS patients. Dr. Steinman is a co-author on many

of these MS papers and his confidence in his own theory is undercut by no mention of GBS

transferability in any of these papers. Instead, Dr. Steinman responded “that for the phosphate head

group, [a central component to the antibodies and the phospholipids] there is a strong attraction

for binding to these phosphate moiety, independent of what is attached to it.” Pet’r’s Ex. 85 at 6.

He is again focused on the phosphate moiety and the ability of the antibodies to recognize it

whether attached to the bacterial polysaccharide or the phospholipid myelin sheath. The MS

studies that reveal anti-phospholipid antibodies are instructive for further study, but as stated

previously, the diseases are not the same and one cannot be wholesale substituted for the other. He

does not present direct evidence that the antibodies recognize any part of the phospholipid in GBS

patients.

There is an additional hurdle that must be overcome even if one assumes that the antibodies

are targeting phospholipids. Dr. Steinman quoted the Nakos et al. findings of phospholipid

antibodies in GBS patients to establish pathology. However, the authors were unwilling to opine

on the nature of the relationship between the antibodies and the disease and suggested additional

research “to investigate how anti-phospholipid antibodies are related to specific antigens in

Schwann cell membrane.” Pet’r’s 55 at 7. Indeed, there is no consensus in the medical community

concerning whether the antibodies cause or result from GBS. Dr. Steinman relied on the Ho et al.

article’s statement that “studies in EAE indicate that antibodies to oxidized phosphatidylcholine

are generated as part of the pathological process of autoimmune demyelination.” Pet’r’s Ex. 59 at

9. But this statement is less instructive than their finding that “autoantibody targeting of oxidized

phosphatidylcholine derivatives could conceivably contribute to MS pathogenesis by reducing the

levels or blocking the immunoregulatory activity of these protective lipids.” Id. At this point, there

is not preponderant evidence of causation.

d. Cross-Reactive Components

The next step in the first branch of Dr. Steinman’s theory after identifying the relevant

components is establishing cross-reactivity. The experts for both parties sought to define relevant

terms related to homologous groups. Initially, Dr. Steinman asserted that “phosphoglycerol is

directly targeted by the core of the two human antibodies targeting 23F.” Pet’r’s Ex. 42 at 21. Dr.

Whitton addressed this at length in his first report, and I included that analysis in an earlier section

to provide some background information and show the degree of care that was taken by both

experts to explain their positions thoroughly. Further discussion of that point is not necessary,

because Dr. Steinman ultimately clarified that the phosphate moiety is the common component.

He explained that “[t]he fact that the antibody binds to the phosphoglycerol moiety of the sugar as

well as to the sugars is the basis for why the antibody to 23F and to other sugars containing

phosphoglycerol, would trigger a ‘cross-reactive’ response to that component.” Pet’r’s Ex. 85 at

5–6. Put another way, Dr. Steinman appears to be saying that in Prevnar 13, the antibodies bind to

specific saccharides plus the phosphate group in specific bacterial serotypes; and in the host tissue,

the antibodies bind to the phosphoglycerol component of myelin lipids, such as

phosphatidylcholine.

For comparison, I have again included the 23F serotype illustration highlighting the

phosphoglycerol structure below, taken directly from the Bryson et al. article. This is followed by

the structure of phosphatidylcholine and the location of the polar head groups targeted by

antibodies, taken from Ho et al.

39

23F

Pet’r’s Ex. 59, Figure 2; Pet’r’s Ex. 51, Figure B.

A comparison of these two molecules reveals that they are similar but not the same. Dr.

Steinman addressed this by way of his fighter jet analogy. This analogy, however, is an

oversimplification of both processes and presents more questions than it answers. Dr. Steinman is

correct that the hook is essential to a jet landing and remaining on the deck of an aircraft carrier.

However, “[t]he carrier landing process involves the interaction of ship motions, the optical

landing system, the pilot/aircraft combination, air wake disturbances and the landing signal officer.

Therefore, the actual carrier approach is very demanding.” 54 In fact, without perfect

synchronization of all of these moving parts, the fighter jet would be unable to land. It is unclear

how the other essential landing gear would translate to the other components of Prevnar 13 or the

myelin sheath to ensure antibody binding. This process is more consistent with Dr. Whitton’s

explanation using the nine points of contact. And the Barbar et al. paper best makes the point that

“the affinity for the hapten was shown to be modulated by the identity of the carrier molecule.”

Pet’r’s Ex. 88 at 1. There is not preponderant evidence that the respective Prevnar 13 and myelin

sheath phosphate moieties are sufficiently immunogenic to attract the relevant antibodies

independent of the polysaccharide/lipid, nor that the phosphate moieties are sufficiently similar to

each other attract the same antibodies.

54

Luis Hernando & R Martinez-Val, Preliminary Suitability Analysis of Carrier Approach Guidance and

Recovery of Land-Based Aircraft, 230 J. AEROSPACE ENGINEERING 906 (2016).

40

e. Known Cross-Reactivity

Molecular mimicry involving vaccination inevitably raises the question about the

corresponding wild antigen’s association with the relevant condition. In the most cited examples,

the flu and COVID vaccines, both viral infections were linked to an increased rate of GBS. Dr.

Whitton noted that many infections have been associated with GBS, but not S. pneumoniae. He

explained that this may be because the bacteria identified as infectious triggers of GBS are gram

negative with “outer membrane[s] in the surface of which are embedded the molecule that are

thought to be involved to be in GBS.” Pet’r’s 42 at 11. S. pneumoniae is a gram-positive bacteria

with a thick cellular wall and no outer membrane. This point is significant because the

phosphoglycerol-containing polysaccharides that are targeted by the antibodies and induce GBS

are also present in the bacterial strains. Dr. Steinman had no explanation for the significance or

lack thereof of an outer membrane. Stepping back from the minutia of molecular mimicry, the

relationship between a vaccine and the infection that it was designed to protect against is something

that any lay person can understand. Instead of directly addressing this point, Dr. Steinman argued

that vaccines are different from their corresponding bacteria, with the former acting as an immune

system stimulus and the latter designed to “subvert the human immune system.” Pet’r’s 85 at 5. A

more targeted response by Dr. Steinman could have done away with a point that would not have

been fatal on its own, but is persuasive supporting evidence that the pieces of this theory may not

fit.

Dr. Steinman emphasized that “sugars in the formulation of Prevnar 13 are combined with

a foreign protein CRM197, that has one amino acid different than diphtheria toxin, and the sugars

and the CRM197 are formulated with alum, a well-known adjuvant, added to boost the immune

response.” Pet’r’s Ex. 85 at 4. Dr. Steinman does not provide persuasive evidence to explain how

the alum component contributes to the development of GBS. Indeed, the vaccines commonly

associated with GBS, seasonal flu vaccines, 55 and the Janssen Covid vaccine, do not contain an

aluminum adjuvant. He does, in the second branch of his molecular mimicry theory, explain cross-

reactivity involving CRM197.

2. BLAST Theory

a. Methodology

BLAST search-based cross-reactivity has been asserted in the Program by Dr. Steinman

over the years with varying degrees of success. The criticism, largely the same, is also asserted

here by Dr. Whitton. Dr. Whitton conceded that the Lanz et al. paper “confirms that short peptides

can – sometimes – be recognized in a cross-reactive manner (something we have known for

decades).” Resp’t’s Ex. F at 19. While homology can be evidence of cross-reactivity, even with

short peptide chains, there must be some evidence that said cross-reactivity was harmful to the

host in order to establish vaccine-caused disease via molecular mimicry. Dr. Whitton’s discussion

of linear versus discontinuous antibody epitopes illustrated how short homologous chains can be

folded into a 3D structure to form functional proteins “recognized by biologically-relevant

antibodies.” Resp’t’s Ex. F at 13. In short, it is not how big the chain is, but how much it sparkles.

55

Fluad is an inactivated, adjuvanted flu vaccine approved for people 65 years and older to help create a

stronger immune response. Different Types of Flu Vaccines, Centers for Disease Control, https://www.cdc

.gov/flu/vaccine-types (last visited May 1, 2026).

41

Dr. Whitton attacked Dr. Steinman’s methodology as overbroad and cherry picked. He

explained that Dr. Steinman’s search parameters for his BLASTs were so inclusive, the results are

all identified by the search engine as “chance findings.” Resp’t’s Ex. C at 49. Dr. Steinman does

not dispute the commonality problem that presents itself when you conduct short searches. He

countered this criticism with an explanation of his multi-step filtration process to identify and

disregard false positives. Dr. Steinman’s starting point is not his end result. The fact that he begins

with a broad set of parameters could ensure that he does not miss relevant sequences. This initial

screening does not render his process unreliable. Aside from the argument that Dr. Steinman can

always find homology because his parameters are too generous, Dr. Whitton also took issue with

his methodology for immunological relevance. This step of the process is the deciding factor for

identifying epitopes capable of pathological cross-reactivity. It is there that Dr. Steinman’s

explanation of the process is less persuasive.

b. Mimic Identification

Dr. Steinman began with CRM197, and Dr. Whitton agreed with the immunogenic

relevance of CRM197, despite the disagreement over the type of molecule and its purpose.

Although Dr. Steinman focused on contactin-1 as the mimic, in a supplemental report he also

discussed GlialCAM. “The paranodal proteins, contactin, contactin-associated protein and

neurofascin are members of this family and share significant homology with GlialCAM.” Pet’r’s

Ex. 85 at 21. Dr. Whitton pointed out that in his published papers, “Dr. Steinman and colleagues

are telling the world that GlialCAM protein is the target of autoimmune assault, triggering MS;

while in the Court, Dr. Steinman asserts that phosphoglycerol, phospholipids, and phosphate are

the targets in MS (and therefore, he claims, in GBS).” Resp’t’s Ex. C at 62. These papers, Dr.

Steinman further noted, reported that antibodies to paranodal proteins are found in GBS patients.

Pet’r’s Ex. 85 at 21. The Lanz et al. article provided evidence that GlialCAM cross-reacts with

EBNA1 to potentially cause MS. The Bjornevik et al. “findings strongly suggest that the

occurrence of EBV infection, detectable by the elicited immune response, is a cause and not a

consequence of MS.” Pet’r’s Ex. 69 at 3. This reference to MS carries the same assumptions

inherent in the first iteration of his theory that the two diseases are inherently similar enough that

the molecular mimicry process would rely on the same sequences. The application of this study is

further complicated by the fact that the mimic is a peptide in a viral protein (EBNA 1) versus a

bacterial serotype within a conjugated vaccine (S. pneumoniae). Dr. Steinman’s sequence of cause

and effect begins with 1) a causal relationship between EBV and MS (established by Bjornevik et

al.) that is the foundation for asserting that 2) the antibodies in MS patients that cross react to

EBNA1 and GlialCAM (Lanz et al.) are evidence of a molecular mimicry pathogenesis. These

antibodies would also, pursuant to Dr. Steinman’s theory, 3) bind to other paranodal proteins,

including contactin because of their shared homology and 4) result in GBS. Repeatedly, Dr.

Steinman appears to conflate cross-reactivity with pathology without evidence to support such a

conclusion. He does not dispute Dr. Whitton’s assertion that benign cross-reactivity is common.

He also does not dispute that antibodies are not always the harbingers of disease. While the

evidentiary standard that petitioners must meet is deliberately and significantly lower than what is

necessary within the medical field for certainty, Dr. Steinman’s theory demands several leaps of

reason that may be possible but are currently based on speculative proclamations.

c. WEQAKALSVE

Using a Pubmed BLAST search algorithm, Dr. Steinman queried contactin-1 versus

CRM197 and discovered “[t]he sequence WEQAKALSVE has five of ten identical amino acids,

42

and thus would be a region that [] might be capable of inducing a neuroinflammatory disease.”

Pet’r’s Ex. 85 at 29. Dr. Steinman identified another sequence, WDHVVALSNE, but Dr. Whitton

argued that he “fails to present any immunological information regarding the contactin-1 sequence

WDHVVALSNE, which differs by [five] amino acids from the CRM197 sequence.” Resp’t’s Ex.

C at 45. He argued that “Dr. Steinman appears to simply assume (and to ask the Court to assume)

that any immune response that recognizes WEQAKALSVE must also recognize

WDHVVALSNE.” Id. at 46. Without further explanations from Dr. Steinman, this is yet another

gap that must be filled by speculation.

d. Immunogenicity

Dr. Steinman asserted that his BLAST search and filtration process not only identifies

relevant homologous epitopes but also provides evidence of immunogenicity necessary for

pathogenesis. In order to establish that homologous parts of the mimics he found in CRM197 and

contactin-1 were relevant immunogenic epitopes, Dr. Steinman “filtered his results through the

IEDB tool.” Pet’r’s Ex. 85 at 31. Dr. Steinman’s process revealed that the WEQAKALSVE

sequence “is an epitope in diphtheria toxin, which has only one amino acid difference from

CRM197.” Id. Dr. Whitton argued that the sequences selected by Dr. Steinman to compare were

not actual sequences that had been shown to activate the human immune system. Instead,

WDHVVALSNE was not categorized by the BLAST search tool as an immunogenic sequence at

all. Eventually, the BLAST search tool revealed that WEQAKALSVE was contained within a 20-

amino-acid-long sequence that did not, in total, share meaningful homology with contactin-1. Dr.

Whitton arrived at a 20-amino-acid-long sequence (NNWEQAKALSVELEINFETR) which Raju

et al. determined “could activate some human CD4+ T cells.” Resp’t’s Ex. C at 50 (citing Pet’r’s

Ex. 74). However, Dr. Steinman did not explain why these specific homologous sections that he

selected are the immunologically significant acids within the complete, immunologically

significant epitope. His assertion that the WEQAKLALSVE is itself an epitope is disproven by

Dr. Whitton’s illustrative BLAST search results. After entering the sequence into the entry box,

with settings to search for linear epitopes, there were “No Results to display.” Resp’t’s Ex. C at

50.

3. Epidemiological Studies

Within the medical community, epidemiological studies are considered among the best

types of evidence. In the Program, they have been used as a basis for Table claims, which when

specific criteria are met, provide a presumption of causation for the Petitioner that can then be

rebutted by Respondent. Due to the rare occurrence rate of many of the injuries that are examined

in the Vaccine Program, it is often difficult, if not impossible, to find relevant, large-scale studies

that prove or disprove vaccine causation. Consequently, “petitioners are not required to support

their claims with epidemiology.” Romine, 2026 WL 937898, at *35 (citing Althen at 1279–81).

However, to the extent that studies do exist, they can be used to support or rebut a theory that a

petitioner presents. Lampe, 219 F.3d at 1365; McCollum v. Sec’y of Health & Hum. Servs., 760

Fed App’x 1003, 1008 (Fed. Cir. 2019). In Romine, the special master noted that this is one of

those rare instances wherein there are multiple large-scale studies and suggested “if a

pneumococcal vaccine were increasing the incidence of GBS, one of these studies would have

detected an uptick.” Id. at *28. In the majority of cases, the lack of epidemiological studies

supporting Petitioner’s theory is a point that Respondent will mention, even as he acknowledges

that such studies are not required. This fact is rarely probative. However, “in a case like the present,

where a vaccine’s formulation bears heavily on Petitioner’s causation claim, and where Petitioner

43

wants to leverage findings about a different vaccine formulation, epidemiologic evidence relevant

to the version of the vaccine in dispute ought to be weighed against Petitioner’s proof in evaluating

whether he has carried his overall burden.” D’Tiole, 2016 WL 7664475, at *22; see W.C. v. Sec’y

of Health & Hum. Servs., 704 F.3d 1352, 1361 (Fed. Cir. 2013) (holding the special master was

not arbitrary in denying compensation and noting that the special master properly relied on several

epidemiological studies in reaching his decision). While the Haber et al. and Tseng et al. studies

are not determinative, these two articles, as also noted in Romine, underscore why epidemiological

studies can be persuasive.

Dr. Steinman argued that while GBS is a common neuropathy, it is “a relatively rare

illness,” particularly following any vaccination. Pet’r’s Ex. 42 at 41. As a result, it is unlikely that

a causal relationship would be statistically detectable, in an epidemiological study. Dr. Steinman

also argued the relevant studies that have been done have been unable to definitively rule out a

causal relationship between Prevnar 13 and GBS. In his first report, Dr. Steinman included a

section entitled “Case Reports and Epidemiologic Studies,” and briefly discussed Haber et al. Id.

In a later section on timing, Dr. Steinman acknowledged that “there is no [] detailed epidemiologic

data specific to Prevnar 13 and GBS for the Petitioner to show.” Id. at 42. Instead, he relied on

large scale studies of the swine flu vaccine/GBS and EBV/MS relationships. See id. at 26–28;

Pet’r’s Ex. 85 at 40. Dr. Whitton asserted that there are no epidemiological studi

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