# Hunt v. Secretary of Health and Human Services

> United States Court of Federal Claims · June 3, 2026

URL: https://www.frixlaw.com/law-library/cases/11337588

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** June 3, 2026
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Herbrina D S Young
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/11337588

## How later opinions describe it (automated extraction)

- stating that an idiopathic diagnosis cannot be a “factor unrelated,” as it is idiopathic
- explaining that “a temporal relationship alone will not demonstrate the requisite causal link and that [P]etitioner must posit a medical theory causally connecting the vaccine and injury”
- recognizing that a court may find that there is a gap between the data and the opinion
- explaining that respondent’s burden is to show that the “factor unrelated” was the “sole substantial factor” in causing the injury

## Opinion text

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.
28
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
29
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.

30
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:
31
(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
32
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.

33
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

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/11337588. Public record. Not legal advice.