Alqulissi v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: March 16, 2026

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

MUHAMMAD ALQULISSI, * PUBLISHED

*

Petitioner, * No. 22-1511V

*

v. * Special Master Nora Beth Dorsey

*

SECRETARY OF HEALTH * Dismissal; Influenza (“Flu”) Vaccine;

AND HUMAN SERVICES, * Rheumatoid Arthritis (“RA”); Causation-in-

* Fact.

Respondent. *

*

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

Sean Franks Greenwood, The Greenwood Law Firm, Houston, TX, for Petitioner.

Eleanor Hanson, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION 1

On October 13, 2022, Muhammad Alqulissi (“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 Petitioner alleges that an influenza (“flu”)

vaccination administered to him on November 11, 2019 “was the cause-in-fact” of his

seronegative rheumatoid arthritis (“RA”) and elevated erythrocyte sedimentation. Petition at

1

Because this Decision contains a reasoned explanation for the action in this case, the

undersigned is required to post it 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, the undersigned agrees that the

identified material fits within this definition, the undersigned will redact such material from

public access.

2

The National Vaccine Injury Compensation Program is set forth in Part 2 of the National

Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,

42 U.S.C. §§ 300aa-10 to -34 (2018) (“Vaccine Act” or “the Act”). All citations in this Decision

to individual sections of the Vaccine Act are to 42 U.S.C.A. § 300aa.

Preamble, ¶ 20 (ECF No. 1); Amended (“Am.”) Petition at Preamble, ¶ 31 (ECF No. 22). 3

Respondent argued against compensation, stating that “this case is not appropriate for

compensation under the terms of the Act.” Respondent’s Report (“Resp. Rept.”) at 1, 6 (ECF

No. 36) (emphasis omitted).

After carefully analyzing and weighing the evidence presented in this case in accordance

with the applicable legal standards, 4 the undersigned finds that Petitioner has failed to provide

preponderant evidence that his flu vaccine caused his seronegative RA, and thus has not satisfied

his burden of proof under Althen v. Secretary of Health & Human Services, 418 F.3d 1274, 1280

(Fed. Cir. 2005). Accordingly, Petitioner is not entitled to compensation.

I. ISSUES TO BE DECIDED

There are two issues in dispute. The first is whether Petitioner suffered a “medically

recognized injury” identified as RA. 5 Joint Status Rept. (“Joint Submission”), filed Jan. 14,

2025, at 1 (ECF No. 73). The second dispute is causation, specifically the parties disagree as to

whether Petitioner has provided preponderant evidence of all three Althen prongs. Id. at 1-2.

II. BACKGROUND

A. Medical Terminology

RA is a “systemic autoimmune disease characterized by inflammatory polyarthritis. The

hallmark of RA is symmetric synovial proliferation and tenderness in multiple joints, particularly

the small joints of the hands and feet.” Petitioner’s Exhibit (“Pet. Ex.”) 55 at 1. 6 Approximately

3

Petitioner’s amended petition added Petitioner’s pre-vaccination medical history and removed

“seronegative.” See Am. Petition.

4

While the undersigned has reviewed all the information filed in this case, only those filings and

records that are most relevant will be discussed. See 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 [s]he does not explicitly reference such evidence in

h[er] decision.”); Simanski v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 407, 436 (2014)

(“[A] Special Master is ‘not required to discuss every piece of evidence or testimony in her

decision.’” (citation omitted)), aff’d, 601 F. App’x 982 (Fed. Cir. 2015); 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.”).

5

Although his petition also alleged that he suffered elevated erythrocyte sedimentation, the

parties appropriately refined the alleged injury as RA in their Joint Submission.

6

Richard D. Brasington & Jonathan J. Miner, Clinical Features of Rheumatoid Arthritis, in

Rheumatology 760 (Marc C. Hochberg et al. eds., 7th ed. 2019).

2

80% of patients with RA test positive for rheumatoid factor (“RF”) 7 and/or anti-citrullinated

peptide antibodies (“ACPAs”). 8 Id.; Pet. Ex. 24 at 1. 9

Diagnostic criteria promulgated by the American College of Rheumatology (“ACR”) and

the European League Against Rheumatism (“EULAR”) in 2010 assess points based on an

algorithm which includes the following findings or serology results: “active synovitis in at least

one joint that cannot be better explained by another diagnosis,” ACPAs, RF, abnormal

inflammatory markers (erythrocyte sedimentation rate (“ESR”) 10 and C-reactive protein

(“CRP”)), 11 and duration of symptoms of six weeks or greater. Pet. Ex. 23 at 1, 2 tbl.92.1. 12

7

RF antibodies are “antibodies directed against antigenic determinants, i.e., Gm, in the Fc region

of the IgG class of immunoglobulins; these are found in the serum of about 80 percent of persons

with classical or definite [RA].” Rheumatoid Factor, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=74591 (last visited Mar. 12, 2026).

8

ACPAs are antibodies against cyclic citrullinated peptide, “a synthetic, citrulline-containing

peptide with a cyclic structure,” that are “highly specific for [RA].” Anti-CCP Antibody,

Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=

56787 (last visited Mar. 12, 2026); Cyclic Citrullinated Peptide, Dorland’s Med. Dictionary

Online, https://www.dorlandsonline.com/dorland/definition?id=97140 (last visited Mar. 12,

2026).

9

Chanchal Gera & Arti Muley, Classification Criteria for Seronegative Rheumatoid Arthritis

Based on Rheumatologist’s Practice and Experience, 19 Curr. Med. Issues 236 (2021).

10

ESR is “the rate at which erythrocytes precipitate out from a well-mixed specimen of venous

blood, measured by the distance the top of the column of erythrocytes falls in a given time

interval under specified conditions; an increase in rate is usually due to elevated levels of plasma

proteins, especially fibrinogen and immunoglobulins, which decrease the zeta potential on

erythrocytes by dielectric shielding and thus promote rouleau formation. It is increased in

monoclonal gammopathy, hypergammaglobulinemia due to inflammatory disease,

hyperfibrinogenemia, active inflammatory disease, and anemia.” Erythrocyte Sedimentation

Rate, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?

id=102146 (last visited Mar. 12, 2026).

11

CRP is “a globulin that forms a precipitate with the somatic C-polysaccharide of the

pneumococcus in vitro; it is the most predominant of the acute-phase proteins.” C-Reactive

Protein, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?

id=100489 (last visited Mar. 12, 2026).

12

Katherine P. Liao, Rheumatoid Arthritis: Classification and Epidemiology of Rheumatoid

Arthritis, in Rheumatology, supra note 6, at 747-53.

3

The cause of RA is not known. See, e.g., Pet. Ex. 30 at 1; 13 Pet. Ex. 58 at 2 (explaining

the “key biologic pathways that drive initial autoimmunity and then [] transition to a more

pathogenic stated and clinically identifiable [RA] are not known”); 14 Resp. Ex. A-2 at 1. 15 Risk

factors include family history, female sex, smoking, obesity, lung disease, and periodontal

inflammation. Pet. Ex. 23 at 3-5; Pet. Ex. 58 at 6 tbl.2; Resp. Ex. A-2 at 3-6. Genome studies

have shown associations between seropositive RA and the human leukocyte antigen (“HLA”)

region (HLA-DR alleles). 16 Resp. Ex. A-20 at 3, 5, 7; 17 see also Pet. Ex. 30 at 1-2 (discussing

the genetic basis of RA).

Studies have suggested that certain infectious pathogens may play a role in the etiology

of RA, notably Porphyromonas gingivalis (“P. gingivalis”) (periodontal disease), Proteus

mirabilis, Escherichia coli, and Epstein Barr Virus (“EBV”). Pet. Ex. 63 at 6. 18 Other infectious

agents have been associated with RA, including parvovirus, human immunodeficiency virus

(“HIV”), and hepatitis B and C viruses. Id. It has also been suggested that in the context of

infectious agents, molecular mimicry may play “a critical role” in the pathogenesis of RA. Id.

Lastly, “[i]t should be noted that in sharp contrast, seronegative RA is enigmatic and distinct

from seropositive RA.” Id.

13

Ernest Choy, Understanding the Dynamics: Pathways Involved in the Pathogenesis of

Rheumatoid Arthritis, 51 Rheumatology v3 (2012).

14

Kevin D. Deane & V. Michael Holers, Rheumatoid Arthritis Pathogenesis, Prediction, and

Prevention: An Emerging Paradigm Shift, 73 Arthritis & Rheumatol. 181 (2021).

15

Cynthia S. Crowson, Epidemiology of, Risk Factors for, and Possible Causes of Rheumatoid

Arthritis, UpToDate, https://www.uptodate.com/contents/epidemiology-of-risk-factors-for-and-

possible-causes-of-rheumatoid-arthritis (last updated Apr. 30, 2019).

16

HLA are “histocompatibility antigens governed by genes of the HLA complex (the human

major histocompatibility complex), a region on the short arm of chromosome 6 containing

several genetic loci, each having multiple alleles.” Human Leukocyte Antigens, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=56923 (last visited

Mar. 12, 2026). HLA-DR loci “are [] associated with antigenic determinants on class II antigen

molecules,” which are “major histocompatibility antigens found only on immunocompetent cells,

primarily B lymphocytes and macrophages; they are found on molecules consisting of two

noncovalently bound chains.” Class II Antigens, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=56885 (last visited Mar. 12, 2026).

17

Vivianne Malmström et al., The Immunopathogenesis of Seropositive Rheumatoid Arthritis:

From Triggering to Targeting, 17 Nature Revs. Immunol.60 (2017).

18

Manuel Rojas et al., Molecular Mimicry and Autoimmunity, 95 J. Autoimmun. 100 (2018).

4

B. Procedural History

Petitioner filed his petition on October 13, 2022. Petition. From October 2022 to April

2023, Petitioner filed medical records, 19 an affidavit from Petitioner, and an amended petition.

Pet. Exs. 1-18; Am. Petition. This case was assigned to the undersigned in June 2023. Notice of

Reassignment dated June 15, 2023 (ECF No. 26). Respondent filed his Rule 4(c) report arguing

against compensation on October 24, 2023. Resp. Rept. at 1, 6.

From December 2023 to June 2024, Petitioner filed expert reports from Dr. David

Axelrod and Respondent filed an expert report from Dr. Mehrdad Matloubian. Pet. Exs. 22, 53;

Resp. Ex. A.

On October 1, 2024, pursuant to the parties’ request, the undersigned held a Rule 5

conference. Rule 5 Order dated October 3, 2024 (ECF No. 66). The undersigned preliminarily

found Petitioner’s diagnosis to be seronegative RA. Id. at 2. The undersigned also preliminarily

found onset to be November 15, 2019, within four days of vaccination. Id. However, the

undersigned was unable to provide any preliminary opinions as to the Althen prongs. Id.

Thereafter, Respondent indicated he wished to defend the case, and the parties requested a

briefing schedule from the Court for resolution of entitlement on the record. Resp. Status Rept.,

filed Nov. 13, 2024 (ECF No. 68).

Petitioner filed a motion for a ruling on the record on February 3, 2025, and Respondent

filed a response on May 9, 2025. Pet. Mot. for Ruling on the Record (“Pet. Mot.”), filed Feb. 3,

2025 (ECF No. 77); 20 Resp. Response to Pet. Mot. (“Resp. Response”), filed May 9, 2025 (ECF

No. 81). Petitioner did not file a reply.

This matter is now ripe for adjudication.

C. Factual History

1. Medical History 21

Petitioner was thirty-six years old when he received a flu vaccination (Fluzone

Quadrivalent) on November 11, 2019 at a CVS Minute Clinic in Houston, Texas. Pet. Ex. 13 at

11-12. Petitioner’s medical history was significant for chronic microcytosis, fatty and mildly

19

Medical records were filed throughout litigation.

20

Petitioner, sua sponte, filed a brief in support of a damages award along with his motion for a

ruling on the record. See Pet. Supplemental Brief in Support of Damages Award, filed Feb. 3,

2025 (ECF No. 77-2). This brief was prematurely filed since entitlement to compensation was

not yet adjudicated. As such, it is not relevant to the issues in dispute resolved by this Decision.

21

This medical history is taken from Respondent’s Responsive Brief as the undersigned finds it

accurately reflects the medical records. See Resp. Response at 2-5. The undersigned has made

edits, deleted less relevant entries, and included additional information and definitions.

5

enlarged liver, ultrasound suggestive of thyrotoxic goiter, recurrent acute tonsillitis, hematuria,

and positive tests for Helicobacter pylori and gastroesophageal reflux disease (“GERD”). Pet.

Ex. 6 at 2, 9, 11, 31, 53-54, 56.

On December 3, 2019, Petitioner saw orthopedist, Steven Nolan, M.D., with complaints

of pain in his cervical spine, shoulders, hips, knees, and hands. Pet. Ex. 3 at 9. Petitioner stated

he noticed pain and weakness in both knees and hips “on occasion,” but his hips had improved,

and that most of his pain was now in his right knee, which would occasionally give way. Id. Dr.

Nolan noted that Petitioner had a previous X-ray on the right knee with normal results. Id. He

assessed Petitioner with a “probable torn meniscus of the right knee” and referred Petitioner for a

magnetic resonance imaging (“MRI”). Id.

Petitioner presented to his primary care physician (“PCP”), Chante Ellison-Hodges,

M.D., on December 5, 2019, complaining of pain “all over joints for the past few weeks.” Pet.

Ex. 19 at 266. He reported “severe aching pain” in his wrists, fingers, knees, and feet that was

worse in the morning. Id. He also had stiffness but no numbness or tingling. Id. Petitioner

advised that his mother was diagnosed with RA, and that he was seen by an orthopedist about

three weeks prior and given Motrin without relief. Id. at 267. A physical examination revealed

swelling in the fingers, tenderness of the interphalangeal (“IP”) joints of both thumbs and distal

IP (“DIP”) joints of both index fingers, as well as pain in all joints in both hands. Id. at 270. Dr.

Ellison-Hodges ordered laboratory tests, referred Petitioner to rheumatology, and ordered

dexamethasone tablets. Id.

The following day (December 6), Petitioner sent an email to Dr. Ellison-Hodges

regarding questions about possible thalassemia. 22 Pet. Ex. 19 at 261. He had never previously

been informed about thalassemia but had felt fatigued for the past three years and had shortness

of breath when he exercised. Id. Laboratory testing to evaluate Petitioner for thalassemia was

ordered. Id. Three days later (December 9), Petitioner emailed Dr. Ellison-Hodges to inquire

about laboratory testing for systemic lupus erythematosus (“lupus”), stating that his mother and

aunt were diagnosed with lupus. Id. at 248. Testing revealed Petitioner’s antinuclear antibody

(“ANA”) 23 results were negative. Id. at 248, 271-72.

On December 10, 2019, Petitioner presented to rheumatologist, Padma Chimata, M.D.,

for an initial evaluation. Pet. Ex. 4 at 23. Petitioner reported that most of his symptoms started

around the same time he received a flu vaccination and that he was worried that might have

triggered something. Id. Petitioner advised his symptoms began one-to-two months ago,

gradually starting with pain in his neck and shoulders, then hips, then knees and hands and feet.

22

Thalassemia is “a heterogeneous group of hereditary hemolytic anemias that have in common

a decreased rate of synthesis of one or more hemoglobin polypeptide chains.” Thalassemia,

Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=

49484 (last visited Mar. 12, 2026).

23

ANA are “antibodies directed against nuclear antigens” that “are frequently found in [RA].”

Antinuclear Antibodies, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition?id=56804 (last visited Mar. 12, 2026).

6

Id. Petitioner had joint pain in both hands, rated a 1/10, with redness, but no warmth or

tenderness. Id. Dr. Chimata noted that Petitioner’s CRP and ESR were abnormal, 24 and that

prior to the onset of Petitioner’s symptoms, he had a sore throat, “had taken flu shots [in]

November,” and had a strong family history of lupus and RA. Id. Dr. Chimata diagnosed

polyarthritis, noting that Petitioner was on steroids. Id. at 24. Dr. Chimata prescribed sulindac

(nonsteroidal anti-inflammatory) and famotidine. Id. at 25.

X-rays of Petitioner’s hands, wrists, knees, and pelvis were performed on December 13,

2019, and were noted to be unremarkable. Pet. Ex. 4 at 29. X-rays of the hands/wrists did not

show findings of inflammatory arthropathy. Id. X-ray of the bilateral knees revealed intact

alignment and no evidence of inflammatory arthropathy. Id. The same was true of the pelvis X-

ray. Id.

On January 8, 2020, Petitioner attended a follow-up appointment with Dr. Chimata to

discuss test results. Pet. Ex. 4 at 20-22. Dr. Chimata diagnosed Petitioner with seronegative RA.

Id. at 21. Petitioner’s RF and ACPA were normal. Pet. Ex. 19 at 276; Pet. Ex. 4 at 44. Dr.

Chimata prescribed methotrexate 25 and folic acid, refilled sulindac and famotidine, and advised

Petitioner to follow up in four to six weeks. Pet. Ex. 4 at 21-22. Petitioner attended a follow-up

appointment with Dr. Chimata on February 5, 2020, and no changes were noted. Id. at 17-19.

By June 11, 2020, when Petitioner returned to see Dr. Chimata, he reported he was

“doing much better.” Pet. Ex. 4 at 14. His laboratory results were also improved. Id. Petitioner

denied any aching, pain, or joint stiffness, but complained of fatigue. Id. Petitioner’s

prescription for methotrexate was discontinued, and he was started on Arava. 26 Id. Dr. Chimata

recommended he continue Sulindac as needed. Id.

Petitioner established care with Dr. Saiyada Mirza as his new PCP on June 24, 2020. Pet.

Ex. 19 at 217-18. At that time, Petitioner reported malaise/fatigue, weight loss, and joint pain.

Id. at 220. Dr. Mirza’s assessment included elevated red blood cells, low mean corpuscular

volume (“MCV”), hyperlipidemia, fatigue, and Vitamin D deficiency. Id. at 221-22. Petitioner

was referred to hematology/oncology specialist, Monica Desai, M.D., for further evaluation of

his MCV and red blood cell count, and for possible thalassemia. Id. at 154, 221-22.

24

His CRP (25; reference range 0-10 mg/L) and ESR (50; reference range 0-15 mm/hr) were

elevated. Pet. Ex. 19 at 273, 276-77.

25

Methotrexate is “a folic acid antagonist that acts by inhibiting synthesis of DNA, RNA,

thymidylate, and protein” and is “used as an antipsoriatic and antiarthritic in the treatment of

severe, recalcitrant, disabling psoriasis and severe [RA] and psoriatic arthritis.” Methotrexate,

Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=

30930 (last visited Mar. 12, 2026).

26

Arava (leflunomide) is “an immunomodulator that inhibits pyrimidine synthesis, used as a

disease-modifying antirheumatic drug in treatment of [RA].” Leflunomide, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=27821 (last visited

Mar. 12, 2026).

7

Petitioner’s next follow up with Dr. Chimata was September 9, 2020. Pet. Ex. 4 at 11.

He was doing well on Arava with minimal stiffness in the mornings. Id. His anemia was also

stable. Id. Dr. Chimata noted that Petitioner was seen by Dr. Desai who was also monitoring

Petitioner for thalassemia. Id.

On September 22, 2020, Petitioner underwent an MRI of his left knee which revealed a

chronic anterior cruciate ligament (“ACL”) tear. Pet. Ex. 5 at 28.

Petitioner attended a tele-health visit with Dr. Mirza on November 2, 2020, with

complaints of a sore throat and inflamed tonsils with pus. Pet. Ex. 19 at 132. He had

discontinued taking Arava due to this acute infection on instruction from his rheumatologist. Id.

at 133. Petitioner was diagnosed with tonsillitis and prescribed amoxicillin. Id. at 135-36.

On December 9, 2020, Petitioner attended a follow-up appointment with Dr. Chimata and

was reportedly doing well on Arava. Pet. Ex. 4 at 8. Dr. Chimata advised Petitioner he would

need to stop his medications for 90 days to plan a pregnancy, otherwise his treatment plan

remained unchanged. Id. at 8-10. He returned to see Dr. Chimata on March 10, 2021 for refills

and bloodwork. Id. at 5. He was noted to be stable. Id.

Petitioner received a Covid-19 vaccine on April 1, 2021. Pet. Ex. 5 at 1. He immediately

developed symptoms, including fever, fatigue, chest pain, and sore throat. Pet. Ex. 19 at 90-91.

He then began to develop abdominal pain, diarrhea, low grade fever, and chills three days post-

vaccination, followed by sore throat and fever. Id. at 91. He was seen by his PCP on April 9,

2021, complaining of nasal congestion, sore throat, cough, and right-sided chest pain and had a

temperature of 102.9ºF. Id. Physical examination was positive for erythema of the throat. Id. at

93. Petitioner tested positive for Covid-19. Id. at 120-21; Pet. Ex. 18 at 92. He received

monoclonal antibody infusions due to his immunosuppressant therapy (Arava). Pet. Ex. 18 at

12-81; Pet. Ex. 4 at 2.

On May 4, 2021, Petitioner followed up with Dr. Chimata. Pet. Ex. 4 at 2. Petitioner

reported his recent Covid vaccination and infection, for which he temporarily discontinued his

Arava, as well as increased fatigue. Id. His pain level was a 0/10. Id. He received refills of his

medications. Id.

Petitioner saw Dr. Mirza for his annual physical on June 10, 2021. Pet. Ex. 19 at 21.

Petitioner reported that he recovered well from Covid-19. Id. On that date, it was documented

that he continued to see Dr. Chimata for RA and that he took Arava daily. Id. at 21, 24. No

musculoskeletal complaints were noted on review of systems or physical examination. Id. at 24-

26. Assessment included seronegative RA. Id. at 27-28.

No additional relevant records have been filed.

8

2. Petitioner’s Declaration 27

Petitioner filed an undated declaration on October 14, 2022. Pet. Ex. 1. Petitioner

averred that he was born November 16, 1982. Id. at ¶ 1. He received the flu vaccination at issue

on November 11, 2019. Id. at ¶ 2. Approximately eight days later, he began to have “severe and

painful muscle and joint stiffness all over [his] body.” Id. at ¶ 3. His “arms, fingers, hands,

knees, shoulders, hips, thighs, legs, and feet were so stiff [he] had difficulty moving them.” Id.

His condition became progressively worse. Id. Petitioner sought care from an orthopedic

physician group and was diagnosed with a “possible torn meniscus.” Id. at ¶¶ 4-5. Since this

diagnosis did not explain his other pain, Petitioner sought a second opinion. Id. at ¶ 5.

On December 10, 2019, Petitioner saw rheumatologist Dr. Chimata and reported his

symptoms and the progression of his illness. Pet. Ex. 1 at ¶ 7. In January 2020, Dr. Chimata

diagnosed him with seronegative RA and elevated ESR. Id. at ¶ 9. She prescribed methotrexate

and sulindac. Id. Petitioner expressed his concern that the flu vaccine triggered his RA. Id. His

medication was changed to Arava and sulindac. Id. at ¶ 14.

Petitioner explained that he continues to suffer from “debilitating joint stiffness.” Pet.

Ex. 1 at ¶ 17. His illness “interferes with every aspect of his life.” Id. Because Arava causes a

risk of birth defects, in order to have another child, he will have to quit taking the medication.

Id. Further, he is unable to “enjoy vacationing at ski resorts because [his] physical limitations

are made worse in higher elevations and cold weather.” Id. His “immune system in also highly

compromised” and this makes him fearful of illnesses. Id. In conclusion, Petitioner averred that

his “vaccination injury has made [him] undergo painful, stressful, and devasting life

experiences” and “has deteriorated [his] quality of life.” Id.

Petitioner maintained that he did not experience any of these symptoms prior to his flu

vaccination, that his symptoms continued for more than six months, and continued to the day he

executed the declaration. Pet. Ex. 1 at ¶ 18.

D. Expert Reports 28

1. Petitioner’s Expert, Dr. David Axelrod 29

a. Background and Qualifications

Dr. Axelrod is a clinical immunologist board certified in internal medicine, adult

rheumatology, and allergy and immunology. Pet. Ex. 22 at 1. He received his M.D. at the

27

Although titled an affidavit, this document was not notarized, and therefore, it is referenced

herein as a declaration.

28

For the sake of brevity, the undersigned discusses only the most relevant portions of the expert

reports and only the most pertinent references.

29

Dr. Axelrod submitted two expert reports. Pet. Exs. 22, 53.

9

University of Michigan Medical School and his M.S. in Clinical Research Design and Statistical

Analysis at the University of Michigan School of Public Health. Id.; Pet. Ex. 48 at 1. He then

completed an internal medicine residency at University of Toronto School of Medicine and

William Beaumont Hospital. Pet. Ex. 48 at 1. Dr. Axelrod completed a fellowship in clinical

immunology, which included adult rheumatology, allergy and immunology, and medical

laboratory immunology, at McGill University. Id. He also worked as a medical staff fellow in

the clinical immunology laboratory at the National Institutes of Health (“NIH”). Id. Dr. Axelrod

held academic appointments from 1982 to 2010, as well as other non-academic positions

throughout his career before retiring in January 2018. Id. at 2. Although he is currently retired

from patient care, as a clinician he was “involved with the diagnosis and treatment of individuals

with drugs reactions (including to vaccines).” Pet. Ex. 22 at 1. Dr. Axelrod has authored or co-

authored several publications. Pet. Ex. 48 at 3-4.

b. Diagnosis

Dr. Axelrod defined RA as an “autoimmune disease that may result in destruction of

synovial joints, with resultant severe disability and premature mortality.” Pet. Ex. 22 at 7

(emphasis omitted). Although joint damage is not usually seen in the early stages of RA, as the

disease progresses, “the classification criteria tend to accumulate over time.” Id. Criteria for

diagnosis include “at least [one] joint with definite clinical synovitis (swelling)” that is “not

better explained by another disease.” Id.

Citing the 2010 ACR/EULAR diagnostic criteria, Dr. Axelrod explained that patients

with a score less than six (out of ten) do not have definite RA, but subsequent assessments may

establish criteria that are “fulfilled cumulatively over time.” Pet. Ex. 22 at 7 (citing Pet. Ex. 23

at 2 tbl.92.1). These criteria are set forth below:

Id. (citing Pet. Ex. 23 at 2 tbl.92.1).

Reviewing Petitioner’s medical records, Dr. Axelrod noted that on December 10, 2019,

Petitioner saw Dr. Chimata for joint pain. Pet. Ex. 22 at 8. Dr. Chimata noted wrist tenderness,

tenderness at the metacarpophalangeal (“MCP”) and proximal IP (“PIP”) joints of the first,

second, third, fourth and fifth digits, and swelling and tenderness at the metatarsophalangeal

(“MTP”) joints of both feet. Id. (emphasis omitted). Although Petitioner tested negative/normal

10

for RF and ACPA, he had elevated CRP and ESR levels. Id. Applying the 2010 ACR/EULAR

criteria, Dr. Axelrod calculated a score of 7, based on swelling of at least one joint, no other

disease implicated, more than 10 joints involved, elevated CRP and ESR, and duration of greater

than six weeks. Id. Thus, Dr. Axelrod opined that Petitioner met the diagnostic criteria for RA.

Id.; Pet. Ex. 53 at 5.

Dr. Axelrod further explained that Petitioner underwent a diagnostic work up, including

labs and X-rays, which was negative for an “alternative cause” of his synovitis. Pet. Ex. 22 at 8-

9. Dr. Axelrod acknowledged that while negative tests are not conclusive as to other causes,

they “provide[] a low probability” of alternative causes. Id. at 9.

Moving to the fact that Petitioner had seronegative RA, Dr. Axelrod described relevant

diagnostic criteria developed by Gera and Muley. Pet. Ex. 22 at 9 (citing Pet. Ex. 24). Gera and

Muley explained that the diagnosis of seronegative RA is challenging because “chronic synovitis

is nonspecific” and found in many diseases. Pet. Ex. 24 at 1. Due to this difficulty, and the need

to identify patients with seronegative RA early to institute treatment, the authors developed

classification criteria. Id. at 1-2. They sent questionnaires to rheumatologists to obtain

information about how they made the diagnosis of seronegative RA in their patients. Id. The

responses of 50 rheumatologists were analyzed and used to develop recommended diagnostic

criteria, which require (1) chronic inflammatory polyarthritis 30 (five or more joints on

examination), (2) elevated ESR and/or CRP, (3) absence of RF and ACPAs, and (4) one to three

of the following: (a) absence of spondyloarthropathy, 31 (b) synovitis confirmed by

ultrasonography or MRI, (c) absence of clinical features of connective tissue disease and

negative ANA, and (d) absence of hepatitis C virus, hepatitis B surface antigen, HIV,

tuberculosis, and leprosy. Id. at 3-4.

Dr. Axelrod opined Petitioner met the Gera and Muley diagnostic criteria. Pet. Ex. 22 at

10. Petitioner had chronic inflammatory polyarthritis in more than five 32 joints, he had elevated

CRP and ESR, he was negative for RF and ACPAs, and his records did not suggest

spondylarthritis, psoriasis, or connective tissue disease, his ANA was negative, and he did not

have hepatitis B or C, HIV, tuberculosis, or leprosy. Id.

30

Polyarthritis is “inflammation of several joints together.” Polyarthritis, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=40045 (last visited

Mar. 12, 2026).

31

Spondyloarthropathy is the “disease of the joints of the spine.” Spondyloarthropathy,

Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=

46736 (last visited Mar. 12, 2026).

32

Dr. Axelrod’s report stated Petitioner had “chronic inflammatory polyarthritis with

documented joint swelling of more than 4 joints on examination.” Pet. Ex. 22 at 10 (emphasis

added). This appears to be a typographical error. If it is not, this fact is not determinative to the

undersigned’s Decision.

11

Respondent’s expert, Dr. Matloubian, questioned the diagnosis of RA due to Petitioner’s

“atypical presentation.” Resp. Ex. A at 7-9. In response, Dr. Axelrod referenced portions of

Petitioner’s medical records showing the presence of joint swelling of the fingers, tenderness of

the IP joints of thumb and index fingers, and elevated CRP and ESR inflammatory markers. Pet.

Ex. 53 at 1. Petitioner had morning stiffness, especially in his feet and neck, indicating

inflammation. Id. Additionally, Petitioner had swelling of the knee and MTP joints of both feet.

Id. Dr. Axelrod also observed that Dr. Chimata documented that Petitioner’s small and medium

joints were involved, which is “typical of [RA]” and not osteoarthritis. Id.

Another point raised by Dr. Matloubian was the acute nature of Petitioner’s onset, which

he opined was not consistent with RA. Resp. Ex. A at 9. Dr. Axelrod disagreed and cited

Brasington and Miner, who noted that 10-25% of RA patients experience sudden onset instead of

gradual progression. Pet. Ex. 53 at 2 (citing Pet. Ex. 55 at 6 (“The clinical course of RA follows

an onset of disease that may be abrupt and acute, gradual and insidious, or subacute between

these extremes. A gradual onset is most common (at least 50% of cases); a sudden onset is much

less common (10%–25%).”)).

Dr. Matloubian also questioned Petitioner’s complaints of muscle pain, which he stated

was not typical of RA. Resp. Ex. A at 7. In response, Dr. Axelrod explained that RA can begin

with “an extra-articular or non-articular manifestation, such as myalgia (pain in the muscles).”

Pet. Ex. 53 at 2 (citing Pet. Ex. 55 at 6 (noting RA “may [] start as an extraarticular or

nonarticular manifestation”)).

Dr. Axelrod also disagreed with Dr. Matloubian’s opinion that that fact Petitioner’s

symptoms did not worsen when he stopped taking Arava undermined the diagnosis of RA. Resp.

Ex. A at 8-9; Pet. Ex. 53 at 2. Petitioner held Arava during periods he was ill with acute

streptococcal tonsilitis (diagnosed on November 2, 2020) and Covid-19 (April 2021). Resp. Ex.

A at 8-9; Pet. Ex. 53 at 2. Dr. Axelrod noted, however, that subsequent records show Petitioner

restarted Arava once his fever and infection symptoms subsided and he has continued to require

Arava, which he opined is evidence that Petitioner continued to require treatment for his RA.

Pet. Ex. 53 at 2.

c. Causation

i. Althen Prong One

Dr. Axelrod offered two mechanistic theories of causation. The first is “[v]accine

induced cytokine damage to the synovium.” Pet. Ex. 22 at 11. In his first expert report, Dr.

12

Axelrod did not discuss this theory and instead referenced six papers, discussed in more detail

below. 33 Id.

Choy explained the cause of RA is “unknown.” Pet. Ex. 30 at 1. The pathogenesis is

complex, involving “T cells, B cells[,] and the orchestrated interaction of pro-inflammatory

cytokines” including TNF-α and IL-6. Pet. Ex. 30 at 12. “These cytokines are messengers that

activate and differentiate effector cells that cause local and systemic symptoms associated with

the disease.” Id. at 7. IL-17 was also identified as a “potent cytokine that promotes synovitis.”

Id. at 1. Choy detailed the complex process whereby bones are destroyed in RA. Id. at 5. Choy

did not identify vaccines or the flu vaccine in his paper, nor specifically as a cause of RA or a

cause of cytokine induction.

Continuing with cytokines, Foti 34 described them as “cell-signaling proteins that affect

the biological function of cells and processes such as inflammation, a variety of immune

responses, and [] wound healing activity.” Pet. Ex. 27 at 1. Foti provided a brief description of

cytokine activity in RA and discussed the effectiveness of agents that block certain cytokines.

Id. at 19-23. Biologic agents that block cytokines IL-6 and TNF-α have had some success in the

treatment of RA; however, the results are not uniform. Id. at 19-21. Approximately “one-third

of patients with RA treated with anti-TNFα agents did not respond.” Id. Foti did not discuss

vaccines or offer an opinion about whether vaccines can induce or activate cytokines to cause

RA.

Yamaguchi et al. 35 examined the role of IL-6 in synovial fluid following the “induction

of ischemic osteonecrosis” in children with ischemic osteonecrosis of the femoral head. Pet. Ex.

29 at 1, 8. Hip MRIs revealed the presence of synovitis and additional studies showed elevated

33

Some studies were less relevant than others. Papoudas et al. described a novel way to study

complex concepts related to gene position (i.e. linear proximity), gene regulation, and gene

expression, “through the combination of topological and functional information into bipartite

networks.” Pet. Ex. 28 at 1 (Stylianos Mavropoulos Papoudas et al., Monitoring the Prolonged

Tnf Stimulation in Space and Time with Topological-Functional Networks, 18 Comput. &

Struct. Biotech. J. 220 (2020)). The study used RNA sequencing of “sustained [tumor necrosis

factor (“TNF”)] stimulation of mouse synovial fibroblasts” to “identify unexpected regulatory

changes taking place in the cells” after “prolonged exposure of fibroblasts to [TNF].” Id. at 1-3.

The authors do not suggest that this experiment, or the use of prolonged exposure of fibroblasts

to TNF was meant to simulate the effects of vaccination. See id. at 1-9. Instead, the goal of the

study was to determine whether the “bipartite networks” described provided “insight on the

functional modularity of gene expression profiles” and “genome organization.” Id. at 9.

34

Maria Foti, Introduction to Cytokine as Tissue Regulators in Health and Disease, in Cytokine

Effector Functions in Tissues 3 (Maria Foti & Massimo Locati eds., 2017).

35

Ryosuke Yamaguchi et al., HIF-1-Dependent IL-6 Activation in Articular Chondrocytes

Initiating Synovitis in Femoral Head Ischemic Osteonecrosis, 98 J. Bone & Joint Surgery 1122

(2016).

13

IL-6 in synovial fluid. Id. at 8. The study suggested a “link between the induction of femoral

head ischemia and the production of IL-6 from articular chondrocytes due to HIF-1α activation,

which stimulates an inflammatory response from synovial cells.” Id. However, Dr. Axelrod

does not explain how ischemia resulting in death and necrosis of the femoral head, leading to the

production of IL-6 activation, is comparable to vaccination. See Pet. Ex. 22 at 11. There is no

suggestion here that RA involves an ischemic mechanism which leads to bone death, thus

stimulating cytokine activation.

Moving to the flu vaccine, Dr. Axelrod cited Christian et al., 36 a study that compared

cytokine responses after vaccination in 28 pregnant and 28 non-pregnant women. Pet. Ex. 26 at

1. The study showed there were significant increases in cytokine IL-6, and an increase in TNF-

α, with peak responses at day one post-vaccination. Id. There were no differences in the

cytokine responses between pregnant and non-pregnant women. Id. From a clinical viewpoint,

the results were “consistent with prior data showing that inflammatory responses to [trivalent flu]

vaccination [were] mild and transient in pregnant women.” Id. at 6. The authors did not address

any association between the flu vaccination and induction of RA.

Although Dr. Axelrod cited the above papers in support of his proffered cytokine theory,

he did not offer any opinions based on these papers in his first report. See Pet. Ex. 22 at 11. For

example, he did not opine that the flu vaccine produces or activates cytokines such that they

cause or significantly contribute to the induction of RA. See id. Further, he did not state that he

held his opinions to a preponderant or more likely than not standard. See generally id. In his

second report, relevant to cytokines, Dr. Axelrod stated that “[w]ith regard to damage to the

synovia, it is possible that the elevated cytokine levels caused damage to the synovia.” Pet. Ex.

53 at 6 (citing Pet. Ex. 22 at 11). Regarding his opinions related to his cytokine theory, Dr.

Axelrod did not state that he held the opinions to a preponderant standard. See generally Pet.

Exs. 22, 53.

The second mechanism offered by Dr. Axelrod is molecular mimicry. Pet. Ex. 22 at 12-

16. Dr. Axelrod cited papers that discuss molecular mimicry, some of which are general in

nature and some that are more specific; however, none address the question of whether the flu

vaccine can cause RA via molecular mimicry. See id. He referenced Xia et al. 37 who “showed

that [flu] hemagglutinin [(“HA”) 38] could inhibit binding of type II collagen to the T-cell

receptor, suggesting a possible role of [flu] [HA] in the activation of autoreactive T-cells[] in

36

Lisa M. Christian et al., Serum Proinflammatory Cytokine Responses to Influenza Virus

Vaccine Among Women During Pregnancy Versus Non-Pregnancy, 70 Am. J. Reprod.

Immunol. 45 (2013).

37

L. Xia et al., Altered Influenza Virus Haemagglutinin Peptides Inhibit T Cell Responses to

Type II Collagen in Rheumatoid Arthritis, 64 Ann. Rheum. Dis. 1790 (2005).

38

HA is “an agglutinin, e.g., an antibody or lectin, that agglutinates erythrocytes.”

Hemagglutinin, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/

definition?id=21684 (last visited Mar. 12, 2026).

14

[RA].” Id. at 12 (citing Pet. Ex. 34). Xia et al. did not study the flu vaccine; they examined the

effect of altered flu virus HA with respect to T-cell receptors/T-cell responses to type II collagen

in RA. See Pet. Ex. 34. Dr. Axelrod did not explain how the study is comparable to vaccination.

See Pet. Ex. 22 at 12. Further, Dr. Axelrod characterized the conclusion he derived from Xia et

al. as “possible” and not likely or probable. Id.

Next, Dr. Axelrod suggested “there is an expectation that vaccine peptides are likely to

align with human peptides, including those that act as target autoantigens for [RA].” Pet. Ex. 22

at 12. However, Dr. Axelrod did not provide foundational literature which suggested that

vaccines in general, or the flu vaccine specifically, can induce RA via peptide homology.

In lieu of articles that discuss a role for vaccines in the pathogenesis of RA, Dr. Axelrod

generally referenced articles about molecular mimicry. Pet. Ex. 22 at 12-13. Johnson et al. 39

define autoimmune illnesses as rare conditions “in which immune responses to specific self-

antigens contribute the ongoing tissue damage.” Pet. Ex. 31 at 1. These are adaptive immune

responses, “usually directed against exogenous antigens—but its targets are autoantigens.” Id.

Although the foreign antigens may be structurally different from self-antigens, they may share

“significant similarity in focal regions,” which may allow for cross-reactive responses. Id. at 6.

This is a broad general statement about molecular mimicry that does not speak to vaccination or

vaccine-induced RA.

Next, Dr. Axelrod cited Kanduc et al. 40 for the proposition that “viruses (including [flu]

virus) share proteomes (peptides) with the human proteome.” Pet. Ex. 22 at 12 (citing Pet. Ex.

32). Kanduc et al. wrote molecular mimicry is a hypothesis, suggesting that when viruses (and

bacteria) share proteins with a host, “an immune response against the infectious agent may result

in formation of cross-reacting antibodies that bind the shared epitopes on the normal cell and

result in the auto-destruction of the cell.” Pet. Ex. 32 at 11. Dr. Axelrod similarly cited Trost et

al. 41 for the proposition that “bacteria share proteomes with the human proteome.” Pet. Ex. 22 at

12 (citing Pet. Ex. 33).

Dr. Axelrod cited Rojas et al., which discussed molecular mimicry and autoimmunity in

various autoimmune diseases. Pet. Ex. 22 at 12 (citing Pet. Ex. 63). Although the authors

discussed RA, they do not discuss vaccines in the context of RA or otherwise provide an opinion

about any association between vaccines, and particularly the flu vaccine, and RA. Dr. Axelrod

did not explain how the paper was relevant to RA. Dr. Axelrod similarly cited a review of

39

Tory P. Johnson et al., Mechanisms of Autoimmunity, in Clinical Immunology: Principles and

Practice 649 (Robert R. Rich et al. eds., 6th ed. 2022).

40

Darja Kanduc et al., Massive Peptide Sharing Between Viral and Human Proteomes, 29

Peptides 1755 (2008).

41

Brett Trost et al., Bacterial Peptides Are Intensively Present Throughout the Human Proteome,

1 Self/Nonself 71 (2010).

15

molecular mimicry from Martins et al., 42 which does not mention or discuss RA, nor did Dr.

Axelrod explain its relevance to RA. Id. (citing Pet. Ex. 35).

Dr. Axelrod cited other papers about T-cell function and recognition, antigen

presentation, and major histocompatibility complex (“MHC”) molecules 43 (including discussion

of the design and effectiveness of vaccines), the optimum length of peptides, and other related

subjects, but these papers did not discuss how the flu vaccine could cause RA by the mechanism

of molecular mimicry. See Pet. Ex. 36; 44 Pet. Ex. 37; 45 Pet. Ex. 38; 46 Pet. Ex. 39; 47 Pet. Ex.

40. 48

More specific to RA, Dr. Axelrod cited Yoshida et al., 49 stating that “the authors found

evidence to suggest that human Type II Collagen acts as an autoantigen” in RA patients. Pet. Ex.

22 at 14 (citing Pet. Ex. 41); see also Pet. Ex. 53 at 7. Yoshida et al. explained that RA is

“associated with citrullination, which is the conversion of arginine residues into citrulline

residues.” Pet. Ex. 41 at 1. Citrullination is important in protein degradation, “as molecular

interactions that are mediated by positively charged arginine residues are lost upon

citrullination.” Id. The study showed that type II collagen was citrullinated in joints affected by

RA, and that these patients had autoantibodies to citrullinated type II collagen. Id. at 1, 4.

42

Yuri Chaves Martins et al., Visiting Molecular Mimicry Once More: Pathogenicity, Virulence,

and Autoimmunity, 11 Microorganisms 1 (2023).

43

MHC is “the genes determining the major histocompatibility antigens, in all species a group of

closely linked multiallelic genes located in a small region on one chromosome.” Major

Histocompatibility Complex, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=66341 (last visited Mar. 12, 2026).

44

Abul K. Abbas et al., Cellular and Molecular Immunology 117-44 (9th ed. 2018).

45

Andrea J. Sant, Overview of T-Cell Recognition: Making Pathogens Visible to the Immune

System, in Clinical Immunology: Principles and Practice 93 (Robert R. Rich et al. eds., 5th ed.

2019).

46

J. Linsday Whitton et al., Molecular Analyses of a Five-Amino-Acid Cytotoxic T-Lymphocyte

(CTL) Epitope: An Immunodominant Region Which Induces Nonreciprocal CTL Cross-

Reactivity, 63 J. Virol. 4303 (1989).

47

Bernhard Hemmer et al., Minimal Peptide Length Requirements for CD4+ T Cell Clones—

Implications for Molecular Mimicry and T Cell Survival, 12 Int’l Immunol. 375 (2000).

48

Sune Frankild et al., Amino Acid Similarity Accounts for T Cell Cross-Reactivity and for

“Holes” in the T Cell Repertoire, 3 PLoS ONE e1831 (2008).

49

Mamoru Yoshida et al., Autoimmunity to Citrullinated Type II Collagen in Rheumatoid

Arthritis, 16 Mod. Rheumatol. 276 (2006).

16

“Immunocomplexes[50] composed of fragments of citrullinated type II collagen and

autoantibodies were formed and deposited in the inflamed articular synovium of RA patients.”

Id. at 4. Whether these immunocomplexes played a role in RA disease pathogenesis was not

determined. Id. at 4-5.

Employing the UniProtKB database, 51 Dr. Axelrod compared protein sequence alignment

between HA from two flu strains in the vaccine administered to Petitioner 52 with peptides from

human synovial membrane (Trefoil factor family peptide or TFF3) 53 and peptides from rabbit

synovial membranes (using “human equivalents”). 54 Pet. Ex. 22 at 14-16, apps. A1-A7; Pet.

Exs. 43-44. He identified seven examples of amino acid alignment between the flu B strain of

the flu vaccine and peptides from human equivalents (of peptides from the synovial membranes

of rabbits). Pet. Ex. 22 at 15-16, apps. A1-A7. The amino acid sequences varied in length (from

3 to 13 consecutive amino acids). Id. Based on his research, Dr. Axelrod concluded that the flu

50

Immunocomplexes, also known as antigen-antibody complexes, are “formed by the

noncovalent binding of an antibody and an antigen. Complexes of antibodies belonging to

certain immunoglobulin classes may activate complement. Antigen-antibody complexes are

mediators of type III immune responses (Arthus reactions, serum sickness, and immune complex

diseases).” Antigen-Antibody Complex, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=66292 (last visited Mar. 12, 2026).

51

“The UniProt Knowledgebase (UniProtKB) is the central hub for the collection of functional

information on proteins, with accurate, consistent[,] and rich annotation. In addition to capturing

the core data mandatory for each UniProtKB entry (mainly, the amino acid sequence, protein

name or description, taxonomic data[,] and citation information), as much annotation information

as possible is added.” UniProtKB, https://www.uniprot.org/help/uniprotkb (last modified Nov.

25, 2025).

52

Dr. Axelrod provided the following chart for reference.

Hemagglutinin from Influenza strain UniProtKB Entry ID

A/Brisbane/02/2018 (H1N1)pdm09-like

A/Kansas/14/2017 (H3N2)-like

B/Colorado/06/2017-like (Victoria lineage) A0A1X9RX59

B/Phuket/3073/2013-like (Yamagata lineage) A4D5Q0

Pet. Ex. 22 at 14. For more information on UniProtKB and entry identifiers, see UniProtKB,

https://www.uniprot.org/help/uniprotkb (last modified Nov. 25, 2025).

53

See Pet. Ex. 43 (Judith Popp et al., Human Synovia Contains Trefoil Factor Family (TFF)

Peptides 1–3 Although Synovial Membrane Only Produces TFF3: Implications in Osteoarthritis

and Rheumatoid Arthritis, 20 Int’l J Mol. Scis. 1 (2019)).

54

See Pet. Ex. 44 (Weilin Liu et al., Differential Proteomics of the Synovial Membrane Between

Bilateral and Unilateral Knee Osteoarthritis in Surgery-Induced Rabbit Models, 14 Mol. Med.

Reps. 2243 (2016)).

17

vaccine shared “similar consecutive amino acid sequences with synovial antigens.” Id. at 16.

Dr. Axelrod opined this data provided “scientific evidence to link the [flu] vaccination received

by [Petitioner] and an immune reaction to synovial autoantigens, including Type II Collagen that

is considered an autoantigen for [RA].” Pet. Ex. 53 at 4.

Regarding molecular mimicry, Dr. Axelrod did not state that he held his opinions to a

preponderant or more likely than not standard.

In his second report, Dr. Axelrod responded to Dr. Matloubian’s critique of his opinions.

Regarding Dr. Axelrod’s cytokine theory, Dr. Matloubian’s primary criticism was that the flu

vaccine here (inactivated and non-adjuvanted) does not cause “persistent or high level[s] of

cytokine production,” and therefore, it would be unlikely for it to cause joint damage. Resp. Ex.

A at 12. In response, Dr. Axelrod cited Christian et al., which he asserted showed that the flu

vaccine did cause elevated cytokine levels. Pet. Ex. 53 at 6 (citing Pet. Ex. 26). Dr. Axelrod

opined that “it is possible that the elevated cytokine levels cause[s] damage to the synovia.” Id.

Dr. Axelrod also offered rebuttal opinions to Dr. Matloubian’s criticisms of his molecular

mimicry theory. One criticism by Dr. Matloubian was that of the seven peptides proposed, “only

vimentin and collagen have been identified as targets of autoreactive T-cells in [RA].” Pet. Ex.

53 at 8; Resp. Ex. A at 15. Even so, Dr. Axelrod opined “[i]f attacked by the adaptive immune

response, damage with inflammation to the synovium would be an outcome.” Pet. Ex. 53 at 8.

Another concern by Dr. Matloubian about Dr. Axelrod’s sequence research was that

TFF3 has not been identified an antigen that causes disease in RA. Resp. Ex. A at 15. Further,

Dr. Axelrod failed to indicate the beginning and ending point of his proposed peptides. Dr.

Matloubian also took issue with Dr. Axelrod’s failure to account for how “peptides are generated

and presented to T cells,” which renders “comparing simple sequence homology

immunologically meaningless.” Id. While the undersigned does not summarize the details of the

experts’ discussions on the details of these immunological points, the following quote by Dr.

Axelrod is notable. Dr. Axelrod stated, “[p]erhaps the limited probability that similar sequences

will align with the central position of autoreactive T-cell receptors contributes to the safety of the

vaccines.” Pet. Ex. 53 at 10.

In response to Dr. Matloubian’s opinion that there was “no evidence of an association”

between the flu vaccine and RA, Dr. Axelrod did not identify case reports or other articles that

discussed any such association. Instead, he identified exhibits that he referenced in his first

report that discussed cytokines and molecular mimicry. Pet. Ex. 53 at 3 (citing Pet. Ex. 22 at 11

(relative to cytokines), 12-14 (relative to molecular mimicry)). Dr. Axelrod reiterated that he

provided evidence of the “molecular basis for associating the sequences of [HA]” based on his

research of similar amino acid sequences. Id.

18

In response to Dr. Matloubian’s opinion that infections have not been shown to induce

RA, Dr. Axelrod cited Mankia et al., 55 who reported an association between P. gingivalis

bacterial infection periodontal disease and RA. Pet. Ex. 53 at 5 (citing Pet. Ex. 54 at 1). Dr.

Axelrod did not explain, however, how P. gingivalis infection and periodontal disease and the

association between this condition and RA provides evidence in support of an association

between the flu vaccine and RA.

Next, regarding the studies cited by Dr. Matloubian supporting the safety profile of the

flu vaccine, Dr. Axelrod agreed that the inactivated flu vaccination “appears to be safe,” but

explained this finding does not “preclude an individual from developing [RA] as a result of [the]

[] vaccine.” Pet. Ex. 53 at 4. He discussed the limitations of epidemiology studies, bias, sample

size, and Type I and Type II errors, concluding that the “absence of evidence, [is] not evidence

of absence.” Id. (emphasis omitted).

Specifically related to the study by Ray et al., 56 Dr. Axelrod stated that the authors

“found that [flu] vaccination measurably increased the risk of developing [RA].” Pet. Ex. 53 at 6

(citing Pet. Ex. 61). However, this statement appears to be inaccurate. Ray et al. reported that

“[i]n [their] initial cohort analysis, [they] found a possible association between RA and [the] [flu]

vaccine in the previous 180 or 365 days, but the extended case-control analysis, bringing in more

data, did not demonstrate this increase.” Pet. Ex. 61 at 5.

Dr. Axelrod also quoted Ray et al. stating “[i]ndividual cases of RA and other

autoimmune disease occurring after vaccination have been reported for years.” Pet. Ex. 53 at 6

(quoting Pet. Ex. 61 at 4). The quote is accurate, but the references cited and examples

following the quote do not describe the flu vaccine and RA; instead, the references describe the

flu vaccine and Guillain-Barré Syndrome (“GBS”), the live virus rubella vaccine and arthritis,

hepatitis vaccination and RA, and hepatitis B vaccination and Sjogren’s syndrome. See Pet. Ex.

61 at 4-5. Ray et al. did not find or report that the flu vaccine was causally associated with RA.

Dr. Matloubian asserted that “RA-related autoimmunity and inflammation are present

long before [disease] onset,” referencing a 2019 review from Deane and Holers. 57 Resp. Ex. A

at 9 (citing Resp. Ex. A-6) (emphasis omitted). Dr. Axelrod disagreed, characterizing these

“immunological changes” as “susceptibility factors” that occur in individuals who “may or may

not develop [RA].” Pet. Ex. 53 at 4-5. Dr. Axelrod cited a 2021 paper by Deane and Holers that

stated most people who develop seropositive RA have elevated RA-related antibodies for a

55

Kulveer Mankia et al., Prevalence of Periodontal Disease and Periodontopathic Bacteria in

Anti-Cyclic Citrullinated Protein Antibody-Positive At-Risk Adults Without Arthritis, 2 JAMA

Network Open 1 (2019).

56

Paula Ray et al., Risk of Rheumatoid Arthritis Following Vaccination with Tetanus, Influenza

and Hepatitis B Vaccines Among Persons 15–59 Years of Age, 29 Vaccine 6592 (2011). This

study was also cited as Resp. Ex. A-9.

57

Kevin D. Deane & V. Michael Holers, The Natural History of Rheumatoid Arthritis, 41 Clin.

Ther. 1256 (2019).

19

period prior to the clinical manifestation of symptoms, suggesting not all people with RA-related

antibodies develop RA. Id. at 5 (citing Pet. Ex. 58). Here, it seems both experts agree, although

Dr. Axelrod referenced this “pre-RA” phase as a susceptibility, whereas Dr. Matloubian viewed

it as a pre-clinical phase of the illness.

Relative to molecular mimicry, Dr. Matloubian cited Rose, 58 who stated that although

there are examples of molecular mimicry triggering “a defined model of autoimmune disease in

experimental animals,” these occurrences are “still relatively rare in humans.” Pet. Ex. 53 at 7

(quoting Resp. Ex. A-19 at 1); see also Resp. Ex. A at 14. Examples of molecular mimicry in

humans include rheumatic fever and Streptococcus pyogenes, GBS and Campylobacter jejuni,

and possibly narcolepsy and the flu vaccine. Id. at 3. Dr. Axelrod does not take issue with Dr.

Rose’s conclusion that these are rare events or the fact that evidence of homology supporting

molecular mimicry is often lacking. See id. at 4.

Dr. Matloubian cited a paper authored by Malmström et al., who reported that T-cell

activation by an antigen from the flu virus was similarly activated in both normal patients and

RA patients (seropositive). Resp. Ex. A at 14-15; Pet. Ex. 53 at 7 (citing Resp. Ex. A-20 at 7).

This finding weighs against Dr. Axelrod’s theory of molecular mimicry, and in response, Dr.

Axelrod cited Xia et al. for the suggestion that there is a “possible” role of flu virus HA “in the

activation of autoreactive T-cells” in RA because Xia et al. showed flu HA could inhibit binding

of Type II collagen to the T-cell receptor. Pet. Ex. 53 at 7 (citing Pet. Ex. 34). Dr. Axelrod also

cited Yoshida et al., who “found evidence to suggested human Type II Collagen acts as an

autoantigen in [RA].” Id. (citing Pet. Ex. 41). Dr. Axelrod stated, “[t]hese studies suggest that

peptides derived from [flu] [HA] can activate autoreactive T-cells to participate in the

development of [RA].” Id.

ii. Althen Prong Two

Dr. Axelrod opined that Petitioner has RA, and thus, he had the “susceptibilities

required” to develop RA including “the presence of synovial autoreactive T-cells [in] his

peripheral immune system.” Pet. Ex. 22 at 16; see also Pet. Ex. 53 at 5. According to Dr.

Axelrod, Petitioner received the flu vaccine which contained flu HA that “share[d] similar

consecutive amino acid sequences with synovial antigens.” Pet. Ex. 22 at 16. “The [flu] [HA]

activated [Petitioner’s] autoreactive T-cells, allowing those cells to escape his tolerance

mechanisms and attack his synovial cells, resulting in synovitis, with the clinical picture of

[RA].” Id.

As it relates to molecular mimicry, Dr. Axelrod asserted that “Type II Collagen acts as an

autoantigen” in RA, and that both “citrullinated and non-citrullinated type antibodies” have been

found in “serum and synovium” of RA patients. Pet. Ex. 22 at 14. Thus, “[i]t is not

inconceivable that [Petitioner] has these antibodies in his synovial tissue, without being able to

detect them in his serum.” Id.

58

Noel R. Rose, Negative Selection, Epitope Mimicry and Autoimmunity, 49 Curr. Op.

Immunol. 51 (2017).

20

Regarding the cytokine theory, Dr. Axelrod opined that the flu vaccine increased

Petitioner’s cytokine levels, which “may have caused his pain symptoms in the hours and days”

following vaccination. Pet. Ex. 22 at 16. The increased cytokine levels caused “some damage to

his synovium, with release of synovial antigens, which activated his autoreactive T-cells to his

synovium,” resulting in synovitis and RA. Id. Although the sequences identified by Dr. Axelrod

(in his searches for homology between HA and human proteins) cannot be tested to determine

whether they would result in T-cell activation, Dr. Axelrod opined that Petitioner “did develop

[RA] following his November 11, 2019 [flu] vaccination. Therefore, he must have presented

[flu] [HA] peptides to autoreactive T-cells, if his [RA] was induced by the [flu] vaccination.” 59

Pet. Ex. 53 at 10.

Dr. Axelrod opined that, other than vaccination, Petitioner did not have an alternate cause

for his RA. Pet. Ex. 22 at 17. While Dr. Chimata documented on December 10, 2019, that

Petitioner had a sore throat about the time of vaccination (November 11, 2019), the more

contemporaneous records (December 3, 2019 and December 5, 2019) do not reference

complaints of a sore throat. Id.; Pet. Ex. 53 at 2. Records from December 3 and December 5 do

not document complaints of a sore throat or reveal a physical examination consistent with a sore

throat. Pet. Ex. 22 at 17. The records also do not show that Petitioner had inflammation,

lymphadenopathy, or receive diagnostic testing or treatment for a sore throat or infection. Id.

Thus, Dr. Axelrod concluded Petitioner did not have an alternative cause for his synovitis or RA.

Id.; Pet. Ex. 53 at 2, 12-15.

Dr. Axelrod disagreed with Dr. Matloubian’s opinion that Petitioner had a viral infection

which led to transient inflammatory arthritis. Pet. Ex. 53 at 2. Further, Dr. Axelrod stated there

was no evidence that Petitioner had an infection until November 2, 2020, almost one year after

vaccination, when he had streptococcal tonsillitis. Id.

Relevant to Althen prong two, Dr. Axelrod did not state that he held his opinions to a

preponderant standard. See Pet. Exs. 22, 53.

iii. Althen Prong Three

Dr. Axelrod opined that Petitioner developed RA “abruptly, without laboratory evidence

of inflammation prior to the onset of his clinical disorder.” Pet. Ex. 53 at 5, 15. Whatever

caused Petitioner’s RA “likely [occurred] in proximity to the time” that he first developed

symptoms of RA. Id. at 15. Dr. Axelrod opined that if Petitioner’s onset of RA was one or two

days after vaccination, it was consistent with “cytokine release following vaccination.” Id. If,

however, onset was four or eight days after vaccination, onset was “consistent with a secondary

adaptive immune response.” Id. He agreed that the notes regarding time intervals in Petitioner’s

records closer in time to vaccination are “consistent with a secondary adaptive immune

response” (molecular mimicry). Id. at 6.

59

Dr. Axelrod and Dr. Matloubian engaged in a significant colloquy about what is required for

molecular mimicry and T-cell activation. See Pet. Ex. 53 at 10-11; Resp. Ex. A at 14-21. A

summary of that discussion is omitted for the sake of brevity.

21

Petitioner had pain in his spine, shoulders, hips, knees and hands eight days after

vaccination, on November 19, 2019, according to Petitioner’s affidavit. Pet. Ex. 22 at 21 (citing

Pet. Ex. 1). Dr. Axelrod opined “[t]his time interval [was] a bit short for a primary adaptive

immune response,” but “consistent with a secondary adaptive immune response” to the flu

vaccine administered November 11, 2019. Id.

On December 5, 2019, Petitioner reported he had experienced widespread pain for the

past few weeks, which would place onset approximately November 15, four days post-

vaccination. Pet. Ex. 22 at 21. Dr. Axelrod opined that a time interval of four days is also

“consistent with a secondary adaptive immune response” to his flu vaccination. Id.

Related to the adaptive immune response and molecular mimicry, Dr. Axelrod referenced

several papers 60 showing that after a “booster” vaccination, 61 the secondary adaptive immune

response, characterized by increased antibody levels (of a “greater magnitude than the primary

adaptive immune response”), begins at two to four days post-vaccination, increasing through

eight days, and remaining elevated from 14 to 22 days. Pet. Ex. 22 at 18-20.

In the alternative, using Dr. Chimata’s note on December 10, 2019, Dr. Axelrod opined

that Petitioner had experienced pain for four weeks, which would place onset one or two days

after vaccination. Pet. Ex. 22 at 21. This time frame, according to Dr. Axelrod, “is too short for

a secondary adaptive immune response,” but consistent with an innate immune response and

“symptoms expected from the elevated cytokines.” Id. Dr. Axelrod concluded that Petitioner

developed an “innate immune response with elevated cytokines that caused his early symptoms

and activated his autoreactive T-cells (to the synovia), driving them out of the control of his

immune tolerance mechanisms, allowing him to cause immune damage to his synovia, with

resultant synovitis and a clinical picture of [RA].” Id. at 22.

60

See Pet. Ex. 36; Pet. Ex. 45 (John J. Miller et al, The Speed of the Secondary Immune

Response to Tetanus Toxoid with a Review of War Reports and Observations on Simultaneous

Injection of Toxoid and Antitoxin, 3 Pediatrics 64 (1949)); Pet. Ex. 46 (Asia Wyatt & Doron

Levy, Modeling the Effect of Memory in the Adaptive Immune Response, 82 Bull. Math. Biol.

124 (2020)).

61

A booster response, or a secondary immune response, refers to “the immune response

occurring on the second and subsequent exposures to an antigen; compared to a primary immune

response, the lag period is shorter, the peak antibody titer is higher and lasts longer, IgG

production predominates, the antibodies produced have a higher affinity for the antigen, and a

much smaller dose of the antigen is required to initiate the response.” Immune Response,

Secondary, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/

definition?id=103686 (last visited Mar. 12, 2026). Dr. Axelrod did not provide evidence that the

flu vaccine at issue here was a “booster vaccination.” He did not explain how or why his

discussion of a booster vaccination and/or secondary adaptive immune response was relevant

here.

22

Dr. Axelrod cited a paper about cytokines produced in the context of flu infection, not

vaccination. See Pet. Ex. 25. 62 Hayden et al. showed that when humans are infected with the flu

A virus, they release cytokines IL-6 and TNF-α (found in serum) in the first three days, which

“correlate[] directly with viral titers, temperature, mucus production, and symptoms scores”

during this timeframe. Id. at 1.

Dr. Axelrod also cited studies showing that cytokines IL-6 and TNF-α peak one day after

vaccination and up to seven days when there is a “shift from an acute inflammatory response to a

more generalized function of the immune system.” Pet. Ex. 22 at 18 (citing Pet. Exs. 26, 28)

(emphasis omitted). He also cited Yamaguchi et al. for the proposition that IL-6 induced other

proinflammatory cytokines (IL-1 β and TNF-α), “with increased proliferation of synovial cells at

24 and 48 hours.” Id. (citing Pet. Ex. 29). Based on these studies, Dr. Axelrod further opined

that it was “possible” that “elevated cytokine levels caused damage to the synovia.” Pet. Ex. 53

at 6 (citing Pet. Ex. 22 at 11).

In summary, Dr. Axelrod opined that the onset of Petitioner’s symptoms was consistent

with an innate response and a secondary adaptive immune response to the flu vaccination. Pet.

Ex. 22 at 22. Dr. Axelrod further opined that “[Petitioner] developed [RA] following his [flu]

vaccination of November 11, 2019. Therefore, whatever caused his [RA] was likely in

proximity to the time that he developed the first symptoms of [RA]” and “[t]he only new

environmental exposure prior to the onset of [RA] was the [flu] vaccination.” Pet. Ex. 53 at 15.

Regarding causation, Dr. Axelrod did not state in either of his expert reports that he held

his opinions to a preponderant evidence or “more likely than not” standard. See Pet. Exs. 22, 53.

2. Respondent’s Expert, Dr. Mehrdad Matloubian 63

a. Background and Qualifications

Dr. Matloubian is a “physician-scientist with basic science training in virology and

immunology and clinical training in adult rheumatology.” Resp. Ex. A at 1. He is board

certified in rheumatology and internal medicine. Resp. Ex. B at 1-2. He received his M.D. as

well as a Ph.D. in virology/immunology from University of California, Los Angeles. Resp. Ex.

A at 1; Resp. Ex. B at 1. Since 2001, he has taught at the University of California, San Francisco

where he is now a Professor. Resp. Ex. B at 2. Dr. Matloubian’s research for the past 20 years

has been focused on “innate and adaptive immune responses, including those of T and B cells, to

acute and chronic viral infections.” Resp. Ex. A at 1. “[His] areas of expertise include T and B

cell responses, especially to viruses as well as factors that regulate lymphocyte circulation and

trafficking.” Id. He has published numerous peer-reviewed articles in these areas. Id.; see Resp.

Ex. B at 10-17. “As an immunologist and board-certified rheumatologist who actively evaluates

62

Frederick G. Hayden et al., Local and Systemic Cytokine Responses During Experimental

Human Influenza A Virus Infection, 101 J. Clin. Invest. 643 (1998).

63

Dr. Matloubian submitted one expert report. Resp. Ex. A.

23

and treats patients with complex autoimmune diseases[,] . . . [Dr. Matloubian] [is] qualified to

address both diagnostic and immunological issues regarding these diseases.” Resp. Ex. A at 1.

b. Diagnosis

Before offering an opinion about diagnosis, Dr. Matloubian summarized Petitioner’s pre-

vaccination history. Resp. Ex. A at 1-2, 6. Before vaccination, based on available records from

Saudi Arabia, Petitioner took “multiple rounds” of antibiotics from 2016 through 2018. Id. at 2,

6. He also had abnormalities in his lungs seen on chest X-rays in 2017. Id.

Petitioner received the flu vaccine at issue on November 11, 2019. Resp. Ex. A at 2, 6.

He had documented swelling and tenderness in his thumbs and DIP joints of his index fingers

within three weeks of his flu vaccination, and steroids were prescribed. Id. at 6 (citing Pet. Ex.

19 at 270). Petitioner also had elevated inflammatory markers (ESR and CRP). Id. (citing Pet.

Ex. 19 at 272-77). Subsequently, Petitioner was seen by rheumatologist Dr. Chimata, who noted

joint tenderness in the hands and a swollen joint in the foot. Id. (citing Pet. Ex. 4 at 24). Dr.

Chimata diagnosed Petitioner with seronegative RA and prescribed treatment with methotrexate

followed by Arava, resulting in a favorable result. Id.

Dr. Matloubian questioned Petitioner’s diagnosis of seronegative RA. Resp. Ex. A at 6-

9. When seen by Dr. Nolan on December 3, 2019, Petitioner’s physical examination did not

reveal swollen joints. Id. at 7 (citing Pet. Ex. 3 at 8). Two days later, on December 5, Petitioner

was seen by Dr. Hodges who noted that Petitioner had swelling and tenderness in the small joints

of his hands. Id. (citing Pet. Ex. 19 at 270). Petitioner had elevated inflammatory markers, but

these were “nonspecific.” Id. Dr. Matloubian explained that because the lab results were non-

specific, the results “do not distinguish between inflammation due to a recent infection or an

autoimmune inflammatory process.” Id. On December 10, 2019, while Petitioner was taking

steroids, Petitioner was seen by Dr. Chimata who documented “only one swollen small joint of

the foot” and a small knee effusion. Id. (citing Pet. Ex. 4 at 24). Dr. Matloubian also noted

these findings were non-specific, though he agreed they “could be consistent with an

inflammatory arthritis, such as RA.” Id.

In addition to findings that were non-specific, Dr. Matloubian believed that Petitioner’s

presentation was “atypical” of RA. Resp. Ex. A at 7. Petitioner reported severe muscle pain,

which Dr. Matloubian opined is not typical in RA since RA primarily affects joints and not

muscles. Id. Another unusual feature of Petitioner’s presentation was that his pain began in his

neck, shoulders, and hips, before it moved to his hands, knees, and feet. Id. According to Dr.

Matloubian, most patients report symptoms in the small joints before larger joints. Id. (citing

Resp. Ex. A-3 at 2, 4, 9). 64 Next, Dr. Matloubian noted that when seen by Dr. Hodges on

December 5, 2019, Petitioner had tenderness in the DIP joints of the index fingers. Id. at 8. Dr.

Matloubian opined this is not characteristic of RA, since it “rarely, if ever, involves the [DIP]

joints.” Id. (citing Resp. Ex. A-3 at 4-5).

64

James R. O’Dell et al., Rheumatoid Arthritis, in Current Diagnosis & Treatment in

Rheumatology (John Imboden et al. eds., 3d ed. 2013).

24

Due to Petitioner’s “atypical presentation,” and because he had an antecedent sore throat,

Dr. Matloubian suggested Petitioner “possibly had a virus associated transient arthritis that was

labeled as seronegative RA.” Resp. Ex. A at 8. Dr. Matloubian opined that Petitioner responded

well to Arava and did well when he discontinued Arava, suggesting his condition was transient.

Id. Moreover, Petitioner was prescribed 10 mg per day, and Dr. Matloubian opined that the

“typical dose” for RA is 20 mg per day. Id. at 23. As to whether Petitioner was able to

discontinue Arava, Dr. Matloubian noted he only reviewed Petitioner’s medical records through

June 2021 and had not reviewed updated records, and thus, he acknowledged his opinions were

limited in time to events occurring up until June 2021. 65 Id. at 8. He issued a caveat and noted

that if updated records showed that Petitioner developed a recurrence of symptoms after

discontinuing immunosuppressive theory, this would support a diagnosis of chronic

inflammatory arthritis (RA). Id.

Dr. Matloubian did not dispute Dr. Axelrod’s opinion that Petitioner satisfied the

ACR/EULAR 2010 criteria for the diagnosis of RA, “especially since he was observed to have at

least one swollen joint on physical examination.” Resp. Ex. A at 9. However, Dr. Matloubian

opined that the diagnosis of seronegative RA is “challenging” and “requires careful longitudinal

observation for confirmation.” Id. While he believed it was “possible” that Petitioner was

correctly diagnosed, Petitioner’s atypical presentation combined with the lack of recurrence of

symptoms when Arava was discontinued, “suggest[ed] a more likely transient inflammatory

arthritis.” Id.

c. Causation

i. Athen Prong One

Dr. Matloubian disagreed that the flu vaccine is “associated with the development [] of

RA.” Resp. Ex. A at 10. He explained that the causes of RA are not known; however,

“established and evolving research” suggests there is a “pre-RA” phase and that “RA-related

autoimmunity and inflammation are present long before” onset of symptoms. Id. at 9 (quoting

Resp. Ex. A-6 at 2) (emphasis omitted). Thus, there is a “breakdown of tolerance and []

autoimmunity” years before swollen joints develop. Id. (emphasis omitted).

In support, Dr. Matloubian cited studies showing that “RA-related autoantibodies are

detectable . . . 3-5 years before” symptoms are “clinically detectable.” Resp. Ex. A at 9 (quoting

Resp. Ex. A-6 at 2) (emphasis omitted); see also Pet. Ex. 31 at 1 (“[S]ignificant recent data from

longitudinal studies have demonstrated that the onset of autoimmune responses and the

development of clinical symptoms are separated in time.”). Deane and Holers wrote that “[i]t is

now well established that RA develops in a series of phases.” Resp. Ex. A-6 at 1. The first

phase is characterized by genetic and/or environmental risk factors, “in the absence of detectable

systemic autoimmunity” such as autoantibodies or inflammatory markers. Id. The second phase,

65

No additional medical records were filed documenting treatment related to RA after June

2021. Records from Houston Methodist Oncology Group after June 2021 were filed, but do not

speak to the issue of whether Petitioner continued to take Arava or have a recurrence of

symptoms if he discontinued Arava. See generally Pet. Ex. 21.

25

or propagation phase, is notable for “autoimmunity, inflammation, and symptoms.” Id. This

leads to “clinically detectable inflammatory arthritis . . . classified as RA.” Id. Studies have

shown that ‘”RA-related autoantibodies are detectable in the circulation a mean of 3-5 years”

before symptoms of inflammatory arthritis occur. Id. at 2. Based on this current knowledge, Dr.

Matloubian opined “it is [] highly likely that factors that trigger and propagate RA-related

autoimmunity [and] drive the transition from pre-RA to [RA] are acting years before diagnosis.”

Resp. Ex. A at 10 (emphasis omitted). Smoking has been identified as a major risk factor,

“which is thought to act years before transition to clinical RA.” Id.

Further, Dr. Matloubian stated that acute infections have not been shown to induce RA.

Resp. Ex. A at 10. He acknowledged that there are references to acute infections in the

literature, but opined there is no conclusive evidence that they trigger RA. Id. Dr. Matloubian

further opined that based on currently available literature, the flu virus has not been shown to

cause RA. Id. (citing Resp. Ex. A-4 (listing viruses that cause arthritis and not listing the flu

virus); 66 Resp. Ex. A-8 (same)). 67 For these reasons, “RA is not a post-infectious disease.” Id.

After opining that infections are not thought to cause RA, Dr. Matloubian opined there is

no association between vaccines and RA, specifically the flu vaccine and RA, and discussed

studies in support. Resp. Ex. A at 10-11. Ray et al. conducted a large study of one million

Kaiser Permanente Northern California patients and found no association between hepatitis B,

tetanus, and flu vaccinations and RA. Pet. Ex. 61 at 1, 4. The study employed a retrospective

chart review with cohort and case-control analysis (of ages 15 to 59) from 1997 to 1999. Id. at 1.

A “possible association” between the flu vaccination and RA was seen in the range of 180 and

365 days after vaccination in the cohort analysis, but in the larger case-control analysis, this

association was not seen. Id.

Fomin et al., 68 a small study with case controls, studied the efficacy of the flu vaccine

given to patients with RA being treated with disease modifying drugs. Resp. Ex. A-10 at 1.

Vaccination did not cause significant worsening of symptoms or adversely affect inflammatory

markers. Id. at 4.

66

Terry L. Moore & Reema Syed, Viruses That Cause Arthritis, UpToDate,

https://www.uptodate.com/contents/viruses-that-cause-arthritis?search=viral+arthritis&topic

Ref=5614&source=see_link (last updated Nov. 27, 2018).

67

Terry L. Moore, Viral Arthritis: Approach to Evaluation and Management, UpToDate,

https://www.uptodate.com/contents/viral-arthritis-approach-to-evaluation-and-management?

search=viral+arthritis&topicRef=5584&source=see_link (last updated Feb. 11, 2019).

68

I. Fomin et al., Vaccination Against Influenza in Rheumatoid Arthritis: The Effect of Disease

Modifying Drugs, Including TNFα Blockers, 65 Ann. Rheum. Dis. 191 (2006).

26

Bengtsson et al. 69 conducted a larger study of 1,998 Swedish RA patients with matched

controls (2,252) and found no increased risk of RA after vaccinations, including the flu, tetanus,

diphtheria, and hepatitis vaccinations. Resp. Ex. A-11 at 1-2. The study group included patients

with and without ACPAs. Id. Vaccinations did not increase the risk of RA in a control group or

in patients with a history of smoking who are at higher risk of developing RA. Id. at 2.

And Westra et al. 70 showed that vaccination is effective and safe in patients with

autoimmune inflammatory rheumatic diseases to prevent vaccine preventable diseases, even in

patients being treated with immunomodulatory drugs. Resp. Ex. A-14 at 8.

Based on these studies and others, the ACR in 2015 issued guidelines for patients with

RA who were beginning or receiving disease modifying treatment or biologic agents,

recommending use of killed vaccines (like the flu vaccine) and live attenuated vaccines (herpes

zoster vaccine). Resp. Ex. A-15 at 17 fig.8, 18. 71

In summary, based on multiple studies, Dr. Matloubian concluded that “no association

has been found” between vaccinations, including the flu vaccination, and RA. Resp. Ex. A at 11.

Next, Dr. Matloubian addressed Dr. Axelrod’s theories based on cytokines and molecular

mimicry. Starting with the cytokine theory, especially IL-6 and TNF-α, Dr. Matloubian opined

that the literature does not support such a theory. Resp. Ex. A at 12. Christian et al. showed that

while there were post-vaccination elevations of cytokines IL-6 and TNF-α, the peak occurred

one day after vaccination and was transient. Id. (citing Pet. Ex. 26 at 5). No safety issues were

associated with the increased cytokines. See id. (citing Pet. Ex. 26 at 6). Thus, Dr. Matloubian

opined the findings by Christian et al. do not support the idea that an inactivated non-adjuvanted

flu vaccine causes levels of cytokines that lead to joint damage. Id.

Dr. Matloubian also commented on Papoudas et al., who studied TNF-α effects on mouse

synovial cells and showed that it changed expression of proteins in these cells. Resp. Ex. A at 12

(citing Pet. Ex. 28 at 2). However, Dr. Matloubian explained the study did not show that low or

transient levels of TNF-α can cause joint injury. Id.

Dr. Matloubian disagreed that Yamaguchi et al. supported Petitioner’s cytokine theory.

Resp. Ex. A at 13. Yamaguchi et al. studied the role of IL-6 in synovial fluid in children with

ischemic osteonecrosis of the femoral head. Pet. Ex. 29 at 1, 8. Hip MRIs revealed the presence

of synovitis and additional studies showed elevated IL-6 in synovial fluid. Id. at 8. The study

69

Camilla Bengtsson et al., Common Vaccinations Among Adults Do Not Increase the Risk of

Developing Rheumatoid Arthritis: Results from the Swedish EIRA Study, 69 Ann. Rheum. Dis.

1831 (2010).

70

Johanna Westra et al., Vaccination of Patients with Autoimmune Inflammatory Rheumatic

Diseases, 11 Nat. Rev. Rheumatol. 135 (2015).

71

Jasvinder A. Singh et al., 2015 American College of Rheumatology Guideline for the

Treatment of Rheumatoid Arthritis, 68 Arthritis Care & Rsch. 1 (2016).

27

suggested a “link between the induction of femoral head ischemia and the production of IL-6

from articular chondrocytes.” Id. Dr. Matloubian opined that the study does not support vaccine

causation due to cytokine effects but instead shows that surgically induced injury that causes

joint damage can lead to inflammation that involves the production of IL-6. Resp. Ex. A at 13.

Hayden et al. studied cytokine responses to flu A virus infection and showed that IL-6

peaked at two days and returned to baseline between four to eight days after infection. Resp. Ex.

A at 12 (citing Pet. Ex. 25 at 4). TNF-α peaked three days after infection and returned to

baseline between days four to eight. Id. (citing Pet. Ex. 25 at 4). If Petitioner’s cytokine theory

was likely, Dr. Matloubian opined that RA would be commonly associated with flu infections,

but it is not. Id.

While Dr. Matloubian agreed that IL-6 and other proinflammatory cytokines may be

elevated during infections, after surgery, and in patients with certain autoimmune illnesses, these

instances or illnesses “differ in their pathogenic mechanism.” Resp. Ex. A at 13. Further, he

opined that elevated IL-6 levels “seem[] to be a consequence of multiple disease processes,” and

“not the triggering cause.” Id.

Moreover, Dr. Matloubian explained that if Dr. Axelrod’s cytokine hypothesis—that

vaccinations (including the flu vaccine) increase IL-6 leading to disease or worsening of

symptoms—was well founded, then ACR and others in the medical community would not

recommend vaccinations (including the flu vaccine) to patients with RA and other autoimmune

diseases. Resp. Ex. A at 13. For support, Dr. Matloubian cited Westra et al., who showed that

vaccination is effective and safe in patients with autoimmune inflammatory rheumatic diseases to

prevent vaccine preventable diseases, even in patients being treatment with immunomodulatory

drugs. Resp. Ex. A-14 at 8. Dr. Matloubian also cited to 2015 ACR guidelines recommending

vaccinations, including inactivated killed vaccines (flu) and live attenuated vaccines (herpes

zoster), to RA patients following review of numerous studies. Resp. Ex. A-15 at 17 fig.8, 18.

Regarding Dr. Axelrod’s molecular mimicry theory, Dr. Matloubian summarized

Petitioner’s theory: RA was caused by activation of flu specific T cells, which through the

mechanism of molecular mimicry, “recognized joint associated self-antigens” and induced

seronegative RA. Resp. Ex. A at 14 (citing Pet. Ex. 22 at 16, 22). More specifically, Dr.

Axelrod suggested that the flu vaccine “share[d] similar consecutive amino acid sequences with

synovial antigens. The [flu vaccine] [HA] activated [] autoreactive T cells, allowing those cells

to escape [] tolerance mechanisms and attack [] synovial cells,” causing synovitis and resulting

in RA. Id. (citing Pet. Ex. 22 at 16). Dr. Matloubian disagreed with this theory.

First, although natural infections have been shown to cause autoimmune illness via

molecular mimicry, the natural flu virus infection has not been demonstrated to cause RA. Resp.

Ex. A at 14. Since there is no cause-and-effect link between the flu infection and RA, Dr.

Matloubian argued it is not probable (“exceedingly improbable”) that antigens from the natural

infection contained in the flu vaccine could cause RA via molecular mimicry. Id. (emphasis

omitted). He explained that flu antigens are not thought to be associated with RA. Id. In fact,

this is why research studies about autoreactive T cells in RA patients use antigens derived from

the flu virus as a control. Id. (citing Resp. Ex. A-20 at 7 (noting studies have shown “reactivity

28

to an unrelated antigen (from [flu] virus) was similar between healthy controls and patients with

RA”)).

Second, Dr. Matloubian noted he is not aware of any reliable evidence in medical

literature or from his experience caring for RA patients, suggesting that RA occurs after flu

infections or flu vaccination. Resp. Ex. A at 10, 14. As described above, based on his review of

the relevant studies, Dr. Matloubian concluded that “multiple controlled studies have shown that

immunizations do not lead to development of RA . . . [or] lead to exacerbation of symptoms in

those who already suffer from this disease.” Id. at 11.

Moving to Dr. Axelrod’s sequence homology research, Dr. Matloubian raised several

concerns. Of the peptide sequences identified, Dr. Matloubian stated that “only vimentin and

collagen have been identified as targets of autoreactive T cells in RA.” Resp. Ex. A at 15. There

was no evidence provided by Dr. Axelrod to show that the other proteins identified are

“biologically relevant to the pathogenesis of RA.” Id.

Next, Dr. Matloubian opined that simply having homologous protein sequences between

pathogen and host is not sufficient to achieve molecular mimicry. Resp. Ex. A at 15 (citing Pet.

Ex. 35 at 5). Without information about “how peptides are generated and presented to T cells,” it

is not meaningful to simply compare sequence homology. 72 Id. Therefore, showing that the flu

vaccine shares short sequences of amino acids with the synovium “does not constitute evidence

for molecular mimicry.” Id. at 16, 18-20.

Further, Dr. Matloubian takes issue with Dr. Axelrod’s suggestion that molecular

mimicry can occur with similarity as opposed to complete identity. Resp. Ex. A at 18.

According to Dr. Matloubian, even one amino acid difference in a peptide sequence can

significantly affect the ability of the peptide to activate T cells. Id. Thus, he disagreed that

similar but not identical sequences support molecular mimicry for T cells. 73 Id. at 18-19.

Moreover, the critical and identical amino acids must be “at a specific position within a peptide.”

Id. at 19-20.

72

For Dr. Matloubian’s discussion of how peptides are presented to T cells and what is required

for molecular mimicry to occur, see Resp. Ex. A at 15-22.

73

For support of this aspect of Dr. Matloubian’s opinion, see Resp. Ex. A-23 (Mark A. Daniels

et al., Thymic Selection Threshold Defined by Compartmentalization of Ras/MAPK Signalling,

444 Nature 724 (2006)); Resp. Ex. A-24 (Amitabh Gaur et al., Amelioration of Relapsing

Experimental Autoimmune Encephalomyelitis with Altered Myelin Basic Protein Peptides

Involves Different Cellular Mechanisms, 74 J. Neuroimmunol. 149 (1997)); Resp. Ex. A-25

(Nathan Karin et al., Reversal of Experimental Autoimmune Encephalomyelitis by a Soluble

Peptide Variant of a Myelin Basic Protein Epitope: T Cell Receptor Antagonism and Reduction

of Interferon γ and Tumor Necrosis Factor α Production, 180 J. Exp. Med. 2227 (1994)); Resp.

Ex. A-26 (Vijay K. Kuchroo et al., A Single TCR Antagonist Peptide Inhibits Experimental

Allergic Encephalomyelitis Mediated by a Diverse T Cell Repertoire, 153 J. Immunol. 3326

(1994)).

29

Dr. Axelrod cited Xia et al., stating they showed “a possible role of [flu] [HA] in the

activation of autoreactive T-cells[] in RA.” Resp. Ex. A at 21 (quoting Pet. Ex. 22 at 12, 14)

(citing Pet. Ex. 34); see also Pet. Ex. 53 at 7. Dr. Matloubian opined Dr. Axelrod’s interpretation

of Xia et al. as a “misinterpretation of the findings” for several reasons. Resp. Ex. A at 21. First,

the study did not suggest molecular mimicry between flu HA and collagen peptides. Id. at 22.

Second, “[t]he residues of a peptide that bind to MHC molecules are distinct from those that are

recognized by T cells.” Id. (quoting Pet. Ex. 36 at 25). Dr. Matloubian explained that “just

because two peptides bind to the same MHC/HLA molecule, does not mean that they are going

to be recognized by the same T cell” or constitute a molecular mimic of each other. Id.

According to Dr. Matloubian, Xia et al. “took advantage of this fact and altered the [flu] HA

peptide so that it [could] bind to HLA-DR1/4 but not be recognized by T cells.” Id. The altered

peptide ligand 74 binds to “a specific MHC/HLA molecule with high affinity,” thus preventing the

binding by a pathogenic self-peptide, like collagen, to prevent T cells that recognize the

autoantigens from being activated. Id. at 22, 23, fig. 6.

Dr. Matloubian summarized that

Dr. Axelrod opine[d] that Petitioner “developed RA due to vaccine induced

cytokine damage to joints leading to activation of autoreactive T cells as well as

through molecular mimicry between [flu] HA and components of the joint.

However, natural infection with [flu] virus induces higher and more prolonged

levels of cytokines . . . than vaccination, yet, it has not been established to cause

RA. Since [flu] vaccines contain the same antigens as the wild-type [flu] virus, it

is unlikely that [the flu] vaccination would induce RA through molecular mimicry

when the [flu] virus itself does not. Moreover, . . . peptide sequence homologies

and even extensive identities do not reliably demonstrate molecular mimicry even

under a more likely than not standard.

Resp. Ex. A at 25.

ii. Althen Prong Two

Dr. Matloubian opined that Petitioner’s inflammatory arthritis diagnosed as seronegative

RA was not caused by his flu vaccination. Resp. Ex. A at 25. He further opined that “[t]he

cause of RA is not known and [he] [did] not know what caused [P]etitioner’s inflammatory

arthritis.” Id. at 23.

While Dr. Matloubian does not know the cause of Petitioner’s RA, he discussed a

possible alternate cause for his illness: a viral infection that led to a “transient virus associated

74

A ligand is “a molecule that binds to another molecule, used especially to refer to a small

molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a

hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to

an enzyme.” Ligand, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition?id=28261 (last visited Mar. 12, 2026).

30

inflammatory arthritis” instead of seronegative RA. Resp. Ex. A at 23. This opinion, however,

was not stated as more likely than not, but as a “possibility.” Id.

Dr. Matloubian referenced medical records documenting that Petitioner had a sore throat

prior to his vaccination. Resp. Ex. A at 22. Although he discussed the possibility of a viral

infection, Dr. Matloubian was careful to explain that Petitioner’s RA was not caused by

infection. See id. at 22-24. However, Dr. Matloubian described a growing body of evidence

suggesting that the gut microbiome 75 may be involved in the development of RA. Id. at 24.

Antibiotics can disrupt the “equilibrium of the gut microbiome, which can then indirectly affect

the immune system.” Id. Petitioner’s medical records show that he was treated with “multiple

courses of antibiotics,” presumably for infections prior to the onset of his RA. Id. And

“alteration of the gut microbiome by repeated antibiotic usage” may affect self-tolerance in

susceptible people. Id. Resulting imbalance of “intestinal flora composition of patients with

preclinical and diagnosed RA indicate that the imbalance of intestinal flora may have an

important impact on the induction and persistence of RA.” Id. (quoting Resp. Ex. A-30 at 2). 76

Regardless, Dr. Matloubian opined there is no reliable evidence to suggest that either the flu

vaccine or an acute flu infection can cause RA. Id.

Dr. Matloubian concluded that Petitioner’s illness “more likely than not was not a

consequence of his [flu vaccine].” Resp. Ex. A at 25.

iii. Althen Prong Three

Dr. Matloubian opined that “RA develops for several years before symptoms manifest.”

Resp. Ex. A at 25. Therefore, he opined that, more likely than not, Petitioner developed RA

before his flu vaccination on November 11, 2019. Id.

Regarding clinical symptom manifestation, Dr. Matloubian cited Petitioner’s affidavit

and excerpts from the medical records which provide inconsistent references to symptom onset.

Resp. Ex. A at 24-25. Beginning with his affidavit, Petitioner averred he developed muscle and

joint pain approximately eight days after his flu vaccination. Id. at 24 (citing Pet. Ex. 1 at 1).

Then, the medical records show Petitioner called Dr. Nolan requesting a prescription for

Motrin on November 25, 2019, approximately 14 days post-vaccination. Resp. Ex. A at 24

(citing Pet. Ex. 15 at 6).

75

Dr. Matloubian defined the microbiome as “the collection of all microbes, especially bacteria

that constantly live on our external and internal body surfaces that are open to the environment.”

Resp. Ex. A at 24.

76

Yanhui Peng et al., Associations Between Rheumatoid Arthritis and Intestinal Flora, with

Special Emphasis on RA Pathologic Mechanisms to Treatment Strategies, 188 Microb. Pathog. 1

(2024).

31

On December 5, 2019, Dr. Hodges took a history that noted Petitioner had joint pain for

the “past few weeks,” which would place onset approximately November 19, or eight days post-

vaccination. Resp. Ex. A at 24 (quoting Pet. Ex. 19 at 266).

However, on December 10, Dr. Chimata’s history referenced symptoms for the “last 4

weeks” and “for the past 1-2 months.” Resp. Ex. A at 24 (quoting Pet. Ex. 4 at 23). This would

place onset in a range from approximately October 10, 2019 (two month) to November 12, 2019

(four weeks). Id. This range begins pre-vaccination and ends one day after vaccination. Id.

In summary, Dr. Matloubian opined that Petitioner’s onset is not clear. Resp. Ex. A at

25. However, based on the current understanding of the illness, “more likely than not,”

Petitioner’s RA onset predated his flu vaccination. Id.

III. DISCUSSION

A. Standards for Adjudication

The Vaccine Act was established to compensate vaccine-related injuries and deaths. §

10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system as

a simple, fair and expeditious means for compensating vaccine-related injured persons. The

Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty

and generosity.’” Rooks v. Sec’y of Health & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting

H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The

preponderance standard requires a petitioner to demonstrate that it is more likely than not that the

vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315,

1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health

& Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). Petitioner need not make a specific type of

evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological

markers or genetic predisposition, or general acceptance in the scientific or medical communities

to establish a logical sequence of cause and effect.” Capizzano v. Sec’y of Health & Hum.

Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead, Petitioner may satisfy his burden by

presenting circumstantial evidence and reliable medical opinions. Id. at 1325-26.

In particular, Petitioner must prove that the vaccine was “not only [the] but-for cause of

the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321

(quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999));

see also Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). The

received vaccine, however, need not be the predominant cause of the injury. Shyface, 165 F.3d

at 1351. A petitioner who satisfies this burden is entitled to compensation unless Respondent

can prove, by a preponderance of the evidence, that the vaccinee’s injury is “due to factors

unrelated to the administration of the vaccine.” § 13(a)(1)(B). However, if a petitioner fails to

establish a prima facie case, the burden does not shift. Bradley v. Sec’y of Health & Hum.

Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

32

“Regardless of whether the burden ever shifts to the [R]espondent, the special master

may consider the evidence presented by the [R]espondent in determining whether the [P]etitioner

has established a prima facie case.” Flores v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 157,

162-63 (2014); see also Stone v. Sec’y of Health & Hum. Servs., 676 F.3d 1373, 1379 (Fed. Cir.

2012) (“[E]vidence of other possible sources of injury can be relevant not only to the ‘factors

unrelated’ defense, but also to whether a prima facie showing has been made that the vaccine

was a substantial factor in causing the injury in question.”); de Bazan v. Sec’y of Health & Hum.

Servs., 539 F.3d 1347, 1353 (Fed. Cir. 2008) (“The government, like any defendant, is permitted

to offer evidence to demonstrate the inadequacy of the [P]etitioner’s evidence on a requisite

element of the [P]etitioner’s case-in-chief.”); Pafford, 451 F.3d at 1358-59 (“[T]he presence of

multiple potential causative agents makes it difficult to attribute ‘but for’ causation to the

vaccination. . . . [T]he Special Master properly introduced the presence of the other unrelated

contemporaneous events as just as likely to have been the triggering event as the vaccinations.”).

B. 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). The special master is required to consider “all [] relevant

medical and scientific evidence contained in the record,” including “any diagnosis, conclusion,

medical judgment, or autopsy or coroner’s report which is contained in the record regarding the

nature, causation, and aggravation of the petitioner’s illness, disability, injury, condition, or

death,” as well as “the results of any diagnostic or evaluative test which are contained in the

record and the summaries and conclusions.” § 13(b)(1)(A).

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) (rejecting

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 (2011) (“[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.” (quoting Murphy v. Sec’y of

Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam, 968 F.2d 1226 (Fed. Cir.

1992))), recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d mem., 503 F. App’x 952

(Fed. Cir. 2013).

However, there are situations in which compelling oral testimony may be more

persuasive than written records, such as where records are deemed to be incomplete or

inaccurate. Campbell v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike

any norm based upon common sense and experience, this rule should not be treated as an

absolute and must yield where the factual predicates for its application are weak or lacking.”);

Lowrie v. Sec’y of Health & Hum. Servs., No. 03-1585V, 2005 WL 6117475, at *19 (Fed. Cl.

Spec. Mstr. Dec. 12, 2005) (“Written records which are, themselves, inconsistent, should be

33

accorded less deference than those which are internally consistent.” (quoting Murphy, 23 Cl. Ct.

at 733)). Ultimately, a determination regarding a witness’s credibility is needed when

determining the weight that such testimony should be afforded. Andreu v. Sec’y of Health &

Hum. Servs., 569 F.3d 1367, 1379 (Fed. Cir. 2009); Bradley, 991 F.2d at 1575.

Despite the weight afforded to medical records, special masters are not rigidly bound by

those records in determining onset of a petitioner’s symptoms. Valenzuela v. Sec’y of Health &

Hum. Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see

also Eng v. Sec’y of Health & Hum. Servs., No. 90-1754V, 1994 WL 67704, at *3 (Fed. Cl.

Spec. Mstr. Feb. 18, 1994) (noting Section 13(b)(2) “must be construed so as to give effect also

to § 13(b)(1) which directs the special master or court to consider the medical records (reports,

diagnosis, conclusions, medical judgment, test reports, etc.), but does not require the special

master or court to be bound by them”).

C. Causation

To receive compensation through the Program, Petitioner must prove either (1) that he

suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a

vaccine that he received, or (2) that he suffered an injury that was actually caused by a

vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano, 440 F.3d at 1319-20. Petitioner must

show 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 (quoting Shyface, 165 F.3d at 1352-53).

Because Petitioner does not allege he suffered a Table Injury, he must prove a vaccine he

received caused his injury. To do so, Petitioner must establish, by preponderant evidence: “(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.” Althen, 418 F.3d at 1278.

The causation theory must relate to the injury alleged. Petitioner must provide a sound

and reliable medical or scientific explanation that pertains specifically to this case, although the

explanation need only be “legally probable, not medically or scientifically certain.” Knudsen v.

Sec’y of Health & Hum. Servs., 35 F.3d. 543, 548-49 (Fed. Cir. 1994). Petitioner cannot

establish entitlement to compensation based solely on his assertions; rather, a vaccine claim must

be supported either by medical records or by the opinion of a medical doctor. § 13(a)(1). In

determining whether a petitioner is entitled to compensation, the special master shall consider all

material in the record, including “any . . . conclusion, [or] medical judgment . . . which is

contained in the record regarding . . . causation.” § 13(b)(1)(A). The undersigned must weigh

the submitted evidence and the testimony of the parties’ proffered experts and rule in Petitioner’s

favor when the evidence weighs in his favor. See Moberly, 592 F.3d at 1325-26 (“Finders of

fact are entitled—indeed, expected—to make determinations as to the reliability of the evidence

presented to them and, if appropriate, as to the credibility of the persons presenting that

evidence.”); Althen, 418 F.3d at 1280 (noting that “close calls” are resolved in Petitioner’s

favor).

34

Testimony that merely expresses the possibility—not the probability—is insufficient, by

itself, to substantiate a claim that such an injury occurred. See Waterman v. Sec’y of Health &

Hum. Servs., 123 Fed. Cl. 564, 573-74 (2015) (denying Petitioner’s motion for review and

noting that a possible causal link was not sufficient to meet the preponderance standard). The

Federal Circuit has made clear that the mere possibility of a link between a vaccination and a

petitioner’s injury is not sufficient to satisfy the preponderance standard. Moberly, 592 F.3d at

1322 (emphasizing that “proof of a ‘plausible’ or ‘possible’ causal link between the vaccine and

the injury” does not equate to proof of causation by a preponderance of the evidence); Boatmon

v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019). While certainty is

by no means required, a possible mechanism does not rise to the level of preponderance.

Moberly, 592 F.3d at 1322; see also de Bazan, 539 F.3d at 1351.

IV. ANALYSIS

A. Diagnosis

As Federal Circuit precedent establishes, in certain cases it is appropriate to determine the

nature of an injury before engaging in the Althen analysis. Broekelschen v. Sec’y of Health &

Hum. Servs., 618 F.3d 1339, 1346 (Fed. Cir. 2010). Since “each prong of the Althen test is

decided relative to the injury [,]” determining facts relating to the claimed injury can be

significant. Id. Here, the parties disagree as to diagnosis. The undersigned finds that

preponderant evidence supports Petitioner’s diagnosis of seronegative RA. There are several

reasons for this finding.

First, Petitioner’s treating rheumatologist made a diagnosis of seronegative RA.

Petitioner saw his rheumatologist, Dr. Chimata, for an initial evaluation in December 2019. Dr.

Chimata noted that Petitioner’s CRP and ESR were abnormal. Physical examination revealed

wrist tenderness and tenderness of the MCP and PIP joints of the fingers without involvement of

the DIP joints. Petitioner had a small knee effusion. He also had tenderness and swelling of the

MTP joints of both of his feet. Testing for RA-related antibodies was ordered. At a follow-up

visit in January 2020, Dr. Chimata diagnosed Petitioner with seronegative RA. Dr. Chimata

continued to see Petitioner at six months intervals, and the diagnosis of seronegative RA

remained consistent. The latest relevant records show that in June 2021, Petitioner continued to

see Dr. Chimata for his RA and continued to take Arava daily. See Pet. Ex. 19 at 21, 24.

Here, the undersigned gives weight to the statements of Petitioner’s treating physician as

she is “in the best position” to determine Petitioner’s injury. See Andreu, 569 F.3d at 1367;

Capizzano, 440 F.3d at 1326; Cucuras, 993 F.2d at 1528 (noting contemporaneous medical

records, “in general, warrant consideration as trustworthy evidence”).

Second, Dr. Axelrod was persuasive in showing why Petitioner’s diagnosis of

seronegative RA was appropriate under the relevant criteria. Applying Dr. Chimata’s physical

examination findings and Petitioner’s lab results to the 2010 ACR/EULAR criteria, Dr. Axelrod

calculated a score of seven, which was based on swelling of at least one joint, involvement of

more than 10 joints, elevated CRP and ESR, symptoms lasting longer than six weeks, and no

other disease implicated, and he concluded that Petitioner met the requirements for RA.

35

Furthermore, Dr. Matloubian did not dispute Dr. Axelrod’s opinion that Petitioner satisfied the

ACR/EULAR 2010 criteria for the diagnosis of RA. See Resp. Ex. A at 9.

Using the Gera and Muley classification criteria for seronegative RA and applying the

physical examination findings and labs for Petitioner also shows that Petitioner’s diagnosis of

seronegative RA was appropriate due to documented swelling of five or more joints, elevated

CRP and ESR, and absence of infection, psoriasis, or other disqualifying conditions.

Further, although Dr. Matloubian questioned the diagnosis of seronegative RA due to

Petitioner’s nonspecific findings and atypical presentation, he agreed that Dr. Chimata’s initial

physical examination findings could be consistent with RA.

Moreover, Dr. Matloubian’s opinion suggesting that Petitioner had a transitory

inflammatory arthritis instead of RA was based on a caveat. Dr. Matloubian’s opinion was based

on the assumption that after June 2021, Petitioner did not continue to require Arava for treatment

of his symptoms. Dr. Matloubian did not review records after that date, and no relevant records

were filed that reflect care after that date. Thus, while there is a question about whether

Petitioner continued to take medication for his RA, this question does not negate the fact that

Petitioner required medication for his illness beginning in December 2019, and that he continued

to take the medication diagnosis for his RA through June 2021.

For the above reasons, the undersigned finds Petitioner has proven by preponderant

evidence that his appropriate diagnosis was seronegative RA.

B. Causation

1. Althen Prong One

Under Althen prong o, Petitioner must set forth a medical theory explaining how the

received vaccine could have caused the sustained injury. Andreu, 569 F.3d at 1375; Pafford, 451

F.3d at 1355-56. Petitioner’s theory of causation need not be medically or scientifically certain,

but it must be informed by a “sound and reliable” medical or scientific explanation. Boatmon,

941 F.3d at 1359; see also Knudsen, 35 F.3d at 548; Veryzer v. Sec’y of Health & Hum. Servs.,

98 Fed. Cl. 214, 223 (2011) (noting that special masters are bound by both § 13(b)(1) and

Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”). If

Petitioner relies upon a medical opinion to support his theory, the basis for the opinion and the

reliability of that basis must be considered in the determination of how much weight to afford the

offered opinion. See Broekelschen, 618 F.3d at 1347 (“The special master’s decision often times

is based on the credibility of the experts and the relative persuasiveness of their competing

theories.”); Perreira v. Sec’y of Health & Hum. Servs., 33 F.3d 1375, 1377 n.6 (Fed. Cir. 1994)

(stating that an “expert opinion is no better than the soundness of the reasons supporting it”

(citing Fehrs v. United States, 620 F.2d 255, 265 (Ct. Cl. 1980))).

The undersigned finds Petitioner failed to provide preponderant evidence of a sound and

reliable theory to explain how the flu vaccination can cause RA.

36

First, the undersigned finds there is not preponderant evidence of a causal association

between the flu vaccine and RA. Petitioner did not file a case report, a case series study, or other

medical literature or evidence showing that the flu vaccine can cause RA. Studies filed and

referenced by Respondent also did not show an association between the flu vaccine and RA. For

example, Ray et al. conducted a study involving medical chart review of approximately one

million patients with RA from 1997 to 1999 and found a “possible association” between flu

vaccination and RA with onset periods between six months and one year (180 days to 365 days)

in their cohort analysis but no association in their larger case-control analysis. Bengtsson et al.,

in a large study of 1,998 Swedish RA patients with matched controls (2,252), found no increased

risk of RA after vaccinations, including the flu vaccination. Fomin et al. conducted a small study

on the efficacy of the flu vaccine in RA patients and noted no significant worsening of symptoms

or adversely affect inflammatory markers were seen. Similarly, Westra et al. showed

vaccinations are effective and safe in patients with autoimmune inflammatory rheumatic

diseases.

Although a petitioner need not make a specific type of evidential showing (i.e.,

epidemiologic studies) to satisfy her burden, special masters shall still consider and weigh the

evidence in the record, including the epidemiological studies filed. See § 13(b)(1) (indicating the

special master shall consider all materials in the record); Capizzano, 440 F.3d at 1325-26; Grant

v. Sec’y of Health & Hum. Servs., 956 F.2d 1144, 1149 (Fed. Cir. 1992) (finding

“epidemiological studies are probative medical evidence relevant to causation” and

“considerable weight [is] due to epidemiological studies in the absence of direct evidence of

actual causation”). And after weighing the submitted evidence, the undersigned finds the

evidence does not preponderate in Petitioner’s favor. See Moberly, 592 F.3d at 1325-26

(“Finders of fact are entitled—indeed, expected—to make determinations as to the reliability of

the evidence presented to them and, if appropriate, as to the credibility of the persons presenting

that evidence.”). The undersigned finds the totality of the medical literature evidence presented

demonstrates no association between the flu vaccine and the development of RA.

Second, Petitioner’s expert did not offer his opinions using the preponderant evidence

standard. That is, Dr. Axelrod did not offer his causation opinions to a more likely than not

standard. The few times that he quantified his opinion, he used words suggesting possibility, not

more likely than not. See Pet. Ex. 22 at 12, 14 (referencing Xia et al. and stating they “showed

that [flu] [HA] could inhibit binding of type II collagen to the T-cell receptor, suggesting a

possible role of [flu] [HA] in the activation of autoreactive T-cells[] in [RA]”); Pet. Ex. 22 at 14

(“It is not inconceivable that [Petitioner] has these antibodies in his synovial tissue, without

being able to detect them in his serum.”); Pet. Ex. 53 at 6 (regarding “damage to the synovia, it is

possible that the elevated cytokine levels caused damage”); Resp. Ex. 53 at 10 (“Perhaps the

limited probability that similar sequences will align with the central position of autoreactive T-

cell receptors contributes to the safety of the vaccines.”). Opinions based on possibilities are

insufficient to prove causation. See Waterman, 123 Fed. Cl. 564, 573-74; Moberly, 592 F.3d at

1322; de Bazan, 539 F.3d at 1351.

Lastly, the undersigned’s finding that Petitioner has failed to provide preponderant

evidence of causation is consistent with case law regarding vaccination (including but not limited

to the flu vaccine) and RA. See, e.g., Hock v. Sec’y of Health & Hum. Servs., No. 17-168V,

37

2020 WL 6392770, at *23-25 (Fed. Cl. Spec. Mstr. Sept. 30, 2020) (discussing numerous

reasoned Program decisions that have dismissed petitions alleging the flu vaccine can cause RA);

Aultman v. Sec’y of Health & Hum. Servs., No. 21-1802V, 2025 WL 2401983, at *22 (Fed. Cl.

Spec. Mstr. July 11, 2025) (listing reasoned decisions that have not found any covered vaccine

can cause RA); Maxwell v. Sec’y of Health & Hum. Servs., No. 17-1367V, 2025 WL 1291642,

at *29-30 (Fed. Cl. Spec. Mstr. Mar. 26, 2025) (discussing reasoned decisions that have rejected

petitioners’ theories that a vaccine can cause RA).

In Hock, the Chief Special Master found the petitioner’s theory was not “sufficiently

reliable” to show that the flu vaccine can cause RA. Hock, 2020 WL 6392770, at *1. There,

petitioner’s expert proposed a three-phase theory: an initial innate response with rapid secretion

of cytokines, followed by “bystander activation,” and ending with molecular mimicry. Id. at *5-

7. The special master in Moran rejected the petitioner’s theory that the flu vaccine can cause RA

via molecular mimicry, finding it was not a sound and reliable theory. Moran v. Sec’y of Health

& Hum. Servs., No. 16-538V, 2021 WL 4853544, at *22-30 (Fed. Cl. Spec. Mstr. Oct. 4, 2021).

And the special master in Maxwell found the petitioner did not provide preponderant evidence to

support his theory that the flu vaccine can cause an abnormal innate immune response in the

joints. Maxwell, 2025 WL 1291642, at *23-27.

Recently, the undersigned issued a dismissal decision in a flu/RA case. Powell v. Sec’y

of Health & Hum. Servs., No. 20-1726V, 2025 WL 3443590, at *31-34 (Fed. Cl. Spec. Mstr.

Oct. 8, 2025). Petitioner’s expert in Powell described six immunological concepts by which the

flu vaccine can cause RA. Id. The undersigned found that none of the mechanisms reached the

level of preponderant evidence required, and thus, due to the lack of a sound and reliable theory

under Althen prong one, among other reasons, Petitioner’s case was dismissed. Id.

The undersigned acknowledges there is one case where a petitioner was found entitled to

compensation in a flu vaccine/RA case; however, the undersigned finds this case is not

instructive because it applies a different standard (plausibility) and the facts and circumstances

are distinct from this present case. See Campbell v. Sec’y of Health & Hum. Servs., 97 Fed. Cl.

650 (2011).

Although decisions of other special masters are not binding, the undersigned finds the

above cases instructive and follows the reasoning of her colleagues. See Boatmon, 941 F.3d at

1358; Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998), aff’d, 191 F.3d

1344 (Fed. Cir. 1999).

Overall, the undersigned finds that here, Petitioner’s proffered concepts do not constitute

sound and reliable causal theories. Thus, the undersigned finds Petitioner has failed to provide

preponderant evidence with respect to the first Althen prong.

2. Althen Prong Two

Under Althen Prong Two, Petitioner must prove by a preponderance of the evidence that

there is a “logical sequence of cause and effect showing that the vaccination was the reason for

the injury.” Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). “Petitioner must

38

show that the vaccine was the ‘but for’ cause of the harm . . . or in other words, that the vaccine

was the ‘reason for the injury.’” Pafford, 451 F.3d at 1356 (internal citations omitted).

In evaluating whether this prong is satisfied, the opinions and views of the vaccinee’s

treating physicians are entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d

at 1326 (“[M]edical records and medical opinion testimony are favored in vaccine cases, as

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.’” (quoting Althen,

418 F.3d at 1280). Medical records are generally viewed as trustworthy evidence, since they are

created contemporaneously with the treatment of the vaccinee. Cucuras, 993 F.2d at 1528.

Petitioner need not make a specific type of evidentiary showing, i.e., “epidemiologic studies,

rechallenge, the presence of pathological markers or genetic predisposition, or general

acceptance in the scientific or medical communities to establish a logical sequence of cause and

effect.” Capizzano, 440 F.3d at 1325. Instead, Petitioner may satisfy his burden by presenting

circumstantial evidence and reliable medical opinions. Id. at 1325-26.

Since Petitioner failed to prove Althen prong one, it follows that he cannot prove Althen

prong two. However, even if Petitioner had proven Althen prong one, the undersigned finds an

additional reason why Petitioner has failed to provide preponderant evidence that there is a

logical sequence of cause and effect showing Petitioner’s flu vaccine caused his RA.

The undersigned bases her finding on the lack of support by Petitioner’s treating

physicians. Petitioner’s treating physicians did not offer opinions in his medical records

associating his RA with his flu vaccination. In cases with such evidence, it can be considered in

an analysis of Althen prong two. See Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d at 1326

(“[M]edical records and medical opinion testimony are favored in vaccine cases, as 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.’” (quoting Althen, 418 F.3d

at 1280)).

There is one reference where Dr. Chimata noted in the history that Petitioner had

received a flu vaccine before he presented with symptoms of RA. However, this notation

reflects merely a temporal association. Dr. Chimata did not offer any opinion to suggest vaccine

causation. Isaac v. Sec’y of Health & Hum. Servs., No. 08-601V, 2012 WL 3609993, at *26

(Fed. Cl. Spec. Mstr. July 30, 2012) (“A treating physician’s recognition of a temporal

relationship does not advance the analysis of causation.”).

Regarding alternative causes, the undersigned acknowledges that Petitioner is not

required to eliminate other potential causes in order to be entitled to compensation. See Walther

v. Sec’y of Health & Hum. Servs., 485 F.3d 1146, 1149-52 (Fed. Cir. 2007) (finding petitioner

does not bear the burden of eliminating alternative independent potential causes). However, it is

reasonable to consider “evidence of other possible sources of injury” in determining “whether a

prima facie showing has been made that the vaccine was a substantial factor in causing the injury

in question.” Stone, 676 F.3d at 1379; see also Winkler v. Sec’y of Health & Hum. Servs., 88

F.4th 958, 963 (Fed. Cir. 2023) (“Such contemplation of a potential causative agent when

evaluating whether or not a petitioner has established a prima facie case is in accordance with the

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law.”); Flores, 115 Fed. Cl. at 162-63 (“[T]he special master may consider the evidence

presented by the [R]espondent in determining whether the [P]etitioner has established a prima

facie case.”). Here, the record indicates two other possible causes: (1) medical record

documentation of a sore throat prior to his illness and (2) Petitioner’s history of antibiotic use, as

described by Dr. Matloubian. However, the undersigned finds Dr. Matloubian did not opine that

he held either of these opinions to a preponderant evidence standard. Thus, the undersigned does

not find evidence of an alternative cause for Petitioner’s RA.

Regardless, for the reasons stated above, the undersigned finds that Petitioner failed to

satisfy his burden under Althen prong two.

3. Althen Prong Three

Althen prong three requires Petitioner to establish a “proximate temporal relationship”

between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been

defined as a “medically acceptable temporal relationship.” Id. The Petitioner must offer

“preponderant proof that the onset of symptoms occurred within a time frame for which, given

the medical understanding of the disorder’s etiology, it is medically acceptable to infer

causation-in-fact.” de Bazan, 539 F.3d at 1352. The explanation for what is a medically

acceptable time frame must also coincide with the theory of how the relevant vaccine can cause

the injury alleged (under Althen Prong One). Id.; Koehn v. Sec’y of Health & Hum. Servs., 773

F.3d 1239, 1243 (Fed. Cir. 2014); Shapiro, 101 Fed. Cl. at 542; see also Pafford, 451 F.3d at

1358. A temporal relationship between a vaccine and an injury, standing alone, does not

constitute preponderant evidence of vaccine causation. See, e.g., Veryzer, 100 Fed. Cl. at 356

(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”).

Since Petitioner failed to prove Althen prong one, it follows that he cannot prove Althen

prong three. In addition, there are independent reasons why the undersigned finds Petitioner

failed to prove Althen prong three.

Petitioner offered two theories of causation, each having a different medically acceptable

time frame within which onset would be expected to occur. In support of his cytokine theory,

Dr. Axelrod cited Hayden et al., who showed that when humans are infected with the flu A virus,

they release cytokines IL-6 and TNF-α in the first three days. He also cited studies showing that

cytokines IL-6 and TNF-α peak a day after vaccination and up to seven days, although

Yamaguchi et al. noted increased proinflammatory cytokines (IL-1 β and TNF-α) within 24 to 48

hours.

Both experts note there are inconsistencies in the record regarding onset of Petitioner’s

symptoms. Petitioner’s affidavit placed onset eight days after vaccination. The medical records

show that Petitioner requested a prescription for Motrin approximately 14 days after vaccination.

Other medical records indicate Petitioner had widespread pain approximately November 15, four

days after vaccination. And Dr. Chimata’s history referenced onset began four weeks prior or

one to two months prior, which would place onset between October 10 and November 12, 2019,

which ranges pre-vaccination to one day after vaccination.

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Dr. Axelrod opined that onset of either four days or eight days is consistent with a

secondary adaptive immune response, but this opinion is premised on research related to booster

vaccinations. There is no foundational evidence that the flu shot administered to Petitioner was a

booster vaccine. Therefore, the undersigned does not find this opinion to be supported by the

evidence.

In the alternative, based on Dr. Chimata’s note on December 10, 2019, Dr. Axelrod

opined that Petitioner had experienced pain for four weeks, which would place onset a day or

two after vaccination. He opined this time frame was consistent with an innate immune response

and “symptoms expected from the elevated cytokines.” Pet. Ex. 22 at 21. However, the

undersigned did not find that Petitioner proved his Althen prong one theories by preponderant

evidence, thus, this opinion, or any other opinion offered by Dr. Axelrod as to Althen prong one

is insufficient to support Althen prong three.

Therefore, the undersigned finds that Petitioner failed to provide preponderant evidence

of Althen prong three.

V. CONCLUSION

The undersigned extends her sympathy to Petitioner for the pain and suffering that he has

experienced due to his illness. The undersigned’s Decision, however, cannot be decided based

upon sympathy, but rather on the evidence and law.

For the reasons discussed above, the undersigned finds that Petitioner has failed to

establish by preponderant evidence that his flu vaccine caused his RA. Therefore, Petitioner is

not entitled to compensation, and the petition must be dismissed.

In the absence of a timely filed motion for review pursuant to Vaccine Rule 23, the Clerk

of Court SHALL ENTER JUDGMENT in accordance with this Decision.

IT IS SO ORDERED.

s/Nora Beth Dorsey

Nora Beth Dorsey

Special Master

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