VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_17-vv-01770
Package ID: USCOURTS-cofc-1_17-vv-01770
Petitioner: Alexzander Rose
Filed: 2017-11-13
Decided: 2025-03-20
Vaccine: HPV
Vaccination date: 2015-03-30
Condition: alopecia areata
Outcome: denied
Award amount USD: 

AI-assisted case summary:
On November 13, 2017, Denise Sheffield-Rose and Mark Rose filed a petition for compensation on behalf of their son, Alexzander Rose, alleging that the human papillomavirus (HPV) vaccine administered on March 30, 2015, caused him to develop alopecia areata (AA). Alexzander Rose was 13 years old at the time of vaccination. His parents first noticed hair loss around mid-to-late April 2015, approximately 22-32 days after the vaccination, and he was subsequently diagnosed with alopecia areata and later alopecia universalis. Petitioner's expert, M. Eric Gershwin, M.D., proposed a theory of molecular mimicry, suggesting that the HPV vaccine triggered cytotoxic T cells that cross-reacted with hair follicle antigens, leading to AA. Respondent's experts, Arnold I. Levinson, M.D., Maryanne Makredes Senna, M.D., and Emanual Maverakis, M.D., countered that there was no reliable scientific evidence linking the HPV vaccine to AA. They highlighted numerous large-scale studies showing no association between HPV vaccination and autoimmune diseases, including AA, and argued that the aluminum-adjuvanted HPV vaccine primarily elicits antibody responses, not the specific cytotoxic T cells implicated in AA pathogenesis. They also pointed to Petitioner's personal risk factors, such as a history of atopy and potential stressors, as more likely contributors to his condition. Special Master Herbrina D.S. Young found that Petitioner failed to establish a prima facie case under the three-pronged Althen test. The court found that the medical literature did not persuasively support the theory that the HPV vaccine causes cytotoxic T cell production leading to AA, nor was there sufficient evidence of a logical sequence of cause and effect specific to Alexzander's case beyond temporal proximity. The onset of symptoms also did not fit the proposed 14-day window for a T-cell response. Consequently, the petition was denied. Petitioner was represented by Mark Theodore Sadaka of the Law Offices of Sadaka Associates, LLC, and Respondent was represented by Meghan Murphy of the U.S. Department of Justice.

Theory of causation field:
Third HPV/Gardasil vaccine on March 30, 2015, age about 13.4, followed 22-32 days later by alopecia areata progressing to alopecia universalis. DENIED. Petitioners Denise Sheffield-Rose and Mark Rose relied on Dr. M. Eric Gershwin's molecular mimicry/cytotoxic T-cell theory. Respondent's Dr. Arnold Levinson, Dr. Maryanne Senna, and Dr. Emmanuel Maverakis cited large studies finding no HPV-autoimmune association, disputed the T-cell mechanism, and pointed to personal risk factors. Special Master Herbrina Sanders Young dismissed the petition March 20, 2025.

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_17-vv-01770-1
Date issued/filed: 2025-04-25
Pages: 27
Docket text: PUBLIC DECISION (Originally filed: 3/20/2025) regarding 96 DECISION of Special Master. Signed by Special Master Herbrina D S Young. (krt) Service on parties made.
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Case 1:17-vv-01770-UNJ Document 98 Filed 04/25/25 Page 1 of 27
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: March 20, 2025
* * * * * * * * * * * * * * *
ALEXZANDER ROSE, * No. 17-1770V
*
Petitioner, * Special Master Young
*
v. *
*
SECRETARY OF HEALTH *
AND HUMAN SERVICES, *
*
Respondent. *
* * * * * * * * * * * * * * *
Mark Theodore Sadaka, Law Offices of Sadaka Associates, LLC, Englewood, NJ, for Petitioner.
Meghan Murphy, U.S. Department of Justice, Washington, DC, for Respondent.
ENTITLEMENT DECISION1
On November 13, 2017, Denise Sheffield-Rose and Mark Rose filed a petition for
compensation in the National Vaccine Injury Compensation Program (“the Program”)2 on behalf
of their then-minor son Alexzander Rose (“Petitioner”).3 Pet., ECF No. 1. Petitioner’s parents
alleged the human papillomavirus (“HPV”) vaccine Petitioner received on March 30, 2015, caused
him to suffer from alopecia areata (“AA”). Id. After carefully analyzing and weighing all the
evidence and testimony presented in this case in accordance with the applicable legal standards,4
I find that Petitioner has failed to provide preponderant evidence that the HPV vaccine he received
1 Because this Decision contains a reasoned explanation for the action taken in this case, it must be made
publicly accessible and will be posted on the United States Court of Federal Claims’ website, and/or at
https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government Act
of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic Government
Services). This means the Decision will be available to anyone with access to the internet. In accordance
with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact medical or other information,
the disclosure of which would constitute an unwarranted invasion of privacy. If, upon review, I agree that
the identified material fits within this definition, I will redact such material from public access.
2 National Childhood Vaccine Injury Act of 1986, Pub L. No. 99-660, 100 Stat. 3755 (“the Vaccine Act” or
“Act”). Hereinafter, for ease of citation, all “§” references to the Vaccine Act will be to the pertinent
subparagraph of 42 U.S.C. § 300aa (2018).
3 On January 24, 2025, the case caption was amended to reflect Petitioner’s adult status. ECF No. 95.
4 While I have reviewed all of the information filed in this case, only those filings and records that are most
relevant to the decision will be discussed. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322, 1328
(Fed. Cir. 2016) (“We generally presume that a special master considered the relevant record evidence even
though he does not explicitly reference such evidence in his decision.”) (citation omitted); see also Paterek
v. Sec’y of Health & Hum. Servs., 527 F. App’x 875, 884 (Fed. Cir. 2013) (“Finding certain information not
relevant does not lead to—and likely undermines—the conclusion that it was not considered.”).
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Case 1:17-vv-01770-UNJ Document 98 Filed 04/25/25 Page 2 of 27
on March 30, 2015, caused him to develop alopecia. Accordingly, Petitioner is not entitled to
compensation.
I. Procedural History5
On November 13, 2017, Mark Rose and Denise Sheffield-Rose filed the petition. Pet.
Petitioners filed medical records on November 14, 2017. Pet’r’s Exs. 1–11, ECF Nos. 5–6.
Petitioners filed two affidavits and a statement of completion on January 11, 2018. Pet’r’s Exs.
12–13, ECF Nos. 14–15.
On April 19, 2018, Respondent filed his Rule 4(c) Report, recommending that
compensation be denied. Resp’t’s Report, ECF No. 19. Petitioners submitted additional medical
records on May 24, 2018, and June 11, 2018. Pet’r’s Ex. 14, ECF No. 21; Pet’r’s Ex. 15, ECF No.
22. On August 14, 2018, Petitioners filed an expert report from M. Eric Gershwin, M.D., M.A.C.P.,
M.A.C.R. as well as his curriculum vitae (“CV”) and accompanying medical literature. Pet’r’s Ex.
16, ECF No. 29; Pet’r’s Exs. 27–97, ECF Nos. 31–37; Pet’r’s Ex. 98, ECF No. 38. Petitioners filed
additional medical literature on August 15, 2018. Pet’r’s Exs. 17–26, ECF No. 41.
Respondent filed expert reports and CVs from Arnold I. Levinson, M.D., and Maryanne
Makredes Senna, M.D., on May 8, 2019. Resp’t’s Exs. A–D, ECF No. 47. On March 9, 2020,
Respondent filed a supplemental expert report from Dr. Levinson and the accompanying medical
literature. Resp’t’s Ex. E, ECF No. 63; Resp’t’s Ex. C, Tabs 1–61, ECF Nos. 57–62. Petitioners
filed a responsive expert report from Dr. Gershwin on March 27, 2020. Pet’r’s Ex. 99, ECF No.
64. Petitioners submitted additional medical literature on March 30, 2020. Pet’r’s Exs. 100–105,
ECF No. 65.
On April 30, 2020, Respondent filed a second supplemental expert report from Dr.
Levinson. Resp’t’s Ex. F, ECF No. 66. Petitioners filed a responsive supplemental expert report
from Dr. Gershwin, along with accompanying medical literature, on September 14, 2020. Pet’r’s
Ex. 106, ECF No. 68; Pet’r’s Exs. 107–115, ECF No. 69. Respondent filed additional medical
literature on October 20, 2020. Resp’t’s Ex. A, Tabs 1–14, ECF Nos. 70–71. Respondent filed a
third responsive supplemental expert report from Dr. Levinson on December 11, 2020. Resp’t’s
Ex. G, ECF No. 75. Petitioners filed a final supplemental expert report from Dr. Gershwin and
medical literature on June 25, 2021. Pet’r’s Ex. 116, ECF No. 77; Pet’r’s Exs. 117–123, ECF No.
78. Respondent filed an expert report from Emanual Maverakis, M.D., on March 27, 2023. Resp’t’s
Ex. H, ECF No. 86. On February 5, 2024, Petitioners filed a motion for ruling on the record. Pet’r’s
Mot., ECF No. 92. Respondent filed his response on March 4, 2024; Petitioners replied on March
18, 2024. Resp’t’s Response, ECF No. 93; Pet’r’s Reply, ECF No. 94. Petitioner reached the age
of majority on November 15, 2019, and the caption was amended on January 24, 2025. ECF No.
95. This matter is ripe for consideration.
II. Factual Background
5 Although Alexzander Rose is the captioned Petitioner as of January 24, 2025, prior to that date, his parents
served as Petitioners on his behalf and were responsible for all filings. Therefore, throughout the procedural
history section of this decision, Mark Rose and Denise Sheffield-Rose will be referred to as Petitioners to
indicate that they completed the record while the captioned petitioner, Alexzander Rose, was still a minor.
Alexzander Rose is the designated Petitioner in all other sections of this decision.
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A. Medical Records
Petitioner was born on November 15, 2001. Pet’r’s Ex. 3 at 1; ECF No. 5–3. On August
28, 2014, Petitioner was seen at Pediatric Health Care Alliance (“PHCA”) for his annual health
maintenance examination. Id. 3 at 7–9. He received a Tdap booster and his first HPV (Gardasil)
and meningococcal vaccinations during this visit. Id. at 5. Petitioner returned to PHCA on
November 3, 2014, and March 30, 2015, to receive his second and third HPV vaccinations. Id. at
38, 1.
Almost three months later, on June 12, 2015, Petitioner presented to Florida Acupuncture
Solutions with a chief complaint of hair loss and allergies. Pet’r’s Ex. 1 at 20, ECF No. 5.
According to the visit notes, Ms. Sheffield-Rose noticed several bald spots on Petitioner’s scalp
after a haircut two weeks prior, but she had not noticed any hair loss after previous haircuts. Id.
There was no history of stress or physical or emotional trauma, and the cause of Petitioner’s hair
loss was unclear. Id. Assessment notes indicated alopecia and a plan to administer a B12 injection.
Id. Lab tests performed on June 16, 2015, for thyroid stimulating hormone (“TSH”) levels,
thyroglobulin antibodies, and thyroid peroxidase antibodies were unremarkable. Pet’r’s Ex. 4 at
10, ECF No. 4.6 Petitioner returned to Florida Acupuncture Solutions on June 29, 2015, July 3,
2015, July 14, and July 20, 2015, complaining of hair loss and allergies. Pet’r’s Ex. 1 at 16–19,
22. Each visit noted alopecia under the assessment section. Id.
On July 15, 2015, Petitioner saw dermatologist Philip Barton, M.D., at Ocala Dermatology
for AA on the scalp. Pet’r’s Ex. 5 at 3, ECF No. 5. The history of present illness section noted that
Petitioner “complained of hair loss that [was] multifactorial and moderate in severity.” Id.
Additional section notes indicated that Petitioner was using Clobetasol and Rogaine and had been
given a Kenalog7 injection four weeks prior. Id. Petitioner reported some hair regrowth to Dr.
Barton. Id. On examination, Petitioner had “discrete, round, smooth to slightly shiny, alopecic
patches” on the scalp. Id. Dr. Barton injected one lesion with Kenalog. Id. Petitioner was advised
to contact Dr. Barton’s office if his alopecia did not improve or if it worsened despite treatment.
Id. On August 12, 2015, Petitioner visited with Ocala Dermatology to follow up on his AA. Id. at
1. Dr. Barton administered another Kenalog injection. Id.
On September 10, 2015, Petitioner presented to All Pediatrics complaining of AA that
started in May 2015. Pet’r’s Ex. 4 at 5–6. Visit notes showed that Petitioner reported receiving
scalp steroid shots at New York City Dermatology and was given steroid lotions.8 Id. at 6.
6 On June 22, 2015, Petitioner presented to Murray Hill Dermatology. Pet’r’s Ex. 6 at 1, ECF No. 5–6. Visit
notes were illegible; however, Respondent’s brief stated that Petitioner “was assessed with alopecia areata
(“AA”) with hair loss on the scalp, but good hair in the eyebrows, eyelid, axilla, and pubic area.” Resp’t’s
Response at 4 (citing Pet’r’s Ex. 6 at 3).
7 Kenalog is a “trademark for preparations of triamcinolone acetonide.” Dorland’s Illustrated Medical
Dictionary (33rd ed. 2020) [hereinafter “Dorland’s”]. Triamcinolone acetonide “is applied topically to the
skin or oral mucosa as an antiinflammatory and administered by inhalation for the chronic treatment of
asthma, intranasally in the treatment of allergic rhinitis and other inflammatory nasal conditions, and by
intra-articular, intradermal, intralesional, intramuscular, intrabursal, or tendon sheath injection as an
antiinflammatory and immunosuppressant in a wide variety of disorders.” Id.
8 Petitioner did not submit records from the New York City dermatology visit.
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Assessment notes listed the diagnosis as “alopecia totalis.”9 Id. Petitioner was encouraged to
follow up with dermatology for alopecia treatments. Id. Additional notes also showed that
Petitioner had sought a referral to “USF” for further evaluation and treatment.10 Id.
Office notes from a February 8, 2016, visit to Pediatric Health Care Alliance referenced
Petitioner’s mother’s statement that he received treatment at “NYU”11 for alopecia, and that all
testing was normal. Pet’r’s Ex. 3 at 36. He was offered a referral for further treatment of his
alopecia. Id.
B. Affidavits
In her affidavit filed on January 11, 2018, Ms. Sheffield-Rose stated that prior to
developing alopecia, Petitioner “did not suffer from any chronic medical condition.” Pet’r’s Ex.
13 at ¶ 4, ECF No. 14-2. Ms. Sheffield-Rose recounted Petitioner’s March 30, 2015 vaccination
and recalled that she began noticing an unusual amount of hair in Petitioner’s bathroom sink in
mid to late April 2015. Id. at ¶¶ 5, 7. She noted that her sister visited on May 3, and June 9, 2015.
Id. at ¶ 10. During the June visit, her sister commented that when she came in May, she noticed
“the initial small bald spot, but did not mention anything to us.” Id. Ms. Sheffield-Rose stated that
she also “noticed a small bald spot on the top of [Petitioner’s] head on or about May 4, 2015.” Id.
at ¶ 7. On May 18, 2015, Ms. Sheffield-Rose recounted that she “noticed another dime-sized bald
spot on the top of [Petitioner’s] head towards the back.” Id.
Ms. Sheffield-Rose took Petitioner to Great Clips on May 31, 2015, where she noticed
three quarter-sized bald spots toward the back of his head after his haircut. Id. at ¶ 9. She asked
the hairdresser what happened, and the hairdresser “indicated that she did not know.” Id. At that
time, Ms. Sheffield-Rose believed that the hairdresser somehow made a mistake with a razor and
“figured the hair would grow back soon.” Id.
According to the affidavit, on June 29, 2015, Petitioner “began taking vitamins, airborne,
emergen-C packs, and began applying Fluocinonide in his hair at night. He also used Clobetasol
Propionate and Rogaine, recommended by Dr. Barton and the specialist at NYU.” Id. at ¶ 13.
Ms. Sheffield-Rose described how Petitioner began to lose his body hair, and noted that by
November 2015, he did not have hair on any part of his body. Id. at ¶ 17. Ms. Sheffield-Rose also
noticed Petitioner’s declining academic performance and behavioral changes. Id. at ¶ 19. Ms.
Sheffield-Rose explained that Petitioner became “frustrated, non-social, and kept to himself.” Id.
She stated that Petitioner ultimately changed schools in 2016. Id. at ¶ 20.
III. Experts
A. Expert Qualifications
9 Total alopecia, or alopecia totalis, is “complete loss of hair from the entire scalp, resulting from
progression of alopecia areata.” Dorland’s.at 53.
10 Neither Petitioner nor the medical records further clarified “USF,” and no medical records from “USF”
were filed. It is unclear if Petitioner was seen at USF or by any other dermatologist.
11 Neither Petitioner nor the medical records further clarified “NYU,” and no medical records from “NYU”
were filed.
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1. Petitioner’s Expert, M. Eric Gershwin, M.D.
Dr. Gershwin received his medical degree from Stanford University in 1971. Pet’r’s Ex.
98 at 1, ECF No. 38. He completed his internship and residency at Tufts-New England Medical
Center in Boston, Massachusetts, before working as a clinical associate in immunology at the
National Institutes of Health in Bethesda, Maryland. Id. at 2. He joined the University of California
Davis School of Medicine faculty in 1975 as an assistant professor of rheumatology and allergy.
Id. He has been a full-time professor since 1981 and was the chief of the medical school’s division
of rheumatology/allergy and clinical immunology for 38 years. Id. Dr. Gershwin is board certified
by the American Board of Internal Medicine with a subspecialty in rheumatology and by the
American Board of Allergy and Clinical Immunology. Id. Dr. Gershwin has received numerous
honors, is a member of multiple professional societies, and has served as an editor of various
journals. Id. at 3–8. He is an author or editor of 72 books or monographs and more than 1,000
other publications. Id. at 9–135.
2. Respondent’s Expert, Dr. Arnold I. Levinson, M.D.
Dr. Levinson is an Emeritus Professor of Medicine and Neurology at the University of
Pennsylvania, Perelman School of Medicine. Resp’t’s Ex. A at 1, ECF No. 47-1. He also holds the
following positions: Chief of the Allergy and Immunology Section, Director of the Fellowship
Training Program in Allergy and Immunology, Director of the Penn Center of Clinical
Immunology, and Associate Dean for Research. Id. Dr. Levinson is board certified in internal
medicine allergy and clinical immunology. Id. He is regarded as an expert in allergic and
immunologic diseases. Id. For over 35 years, he maintained a clinical practice, evaluating and
treating patients with a broad range of immune-mediated diseases, including autoimmune,
hypersensitivity, and immunodeficiency disorders. Id. He also treated patients who experienced
adverse reactions to drugs and vaccines. Id. Dr. Levinson has conducted research funded by the
National Institutes of Health, the Veterans Administration, and several private foundations dealing
with various aspects of autoimmunity, hypersensitivity, and immunodeficiency. Id.
3. Respondent’s Expert, Maryanne Makredes Senna, M.D.
Dr. Senna is an Assistant Professor of Dermatology at Harvard Medical School and an
attending board-certified dermatologist at Massachusetts General Hospital (“MGH”) in Boston.
Resp’t’s Ex. C at 1, ECF No. 47-3. She has clinical and research expertise in hair loss disorders,
including AA. Id. She co-directs the MGH Hair Loss Clinic, where she sees 50+ new alopecia
patient consults per month and receives national and international patient referrals. Id. At MGH,
she directs the Hair Academic Innovative Research Unit, dedicated to hair loss disorders. Id. The
unit conducts multiple ongoing clinical trials and epidemiologic studies for AA. Id. Her clinical
trial research has been primarily focused on inflammatory hair loss disorders such as AA and
lichen planopilaris. Id. at 2. Dr. Senna has published peer-reviewed articles on AA pathogenesis,
associated conditions, and treatments, in addition to authoring a paper on how to properly diagnose
hair loss conditions in pediatric patients. Id. at 1–2. She has also lectured and presented her
alopecia research at national and international meetings, as listed in her curriculum vitae. Id.
4. Respondent’s Expert, Emmanual Maverakis, M.D.
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Dr. Maverakis is a member of the American Association of Immunologists. Resp’t’s Ex.
H at 1, ECF No. 86-1. He holds medical board certifications in dermatology and clinical
informatics. Id. He is a tenured full-time professor at the University of California, Davis, where he
holds a variety of additional titles, including the Director of Autoimmunity and Director of
Immune Monitoring. Id. He was a Howard Hughes Medical Institute fellow at the La Jolla Institute
for Immunology, where he received additional training in immunology. Id. There, he studied
molecular mimicry, epitope spreading, and T-cell antigen processing. Id. He has published 190
peer-reviewed, PubMed-indexed manuscripts. Id. at 2 As a clinician, he specializes in treating
patients with rare diseases, including rare skin cancers and rare immune-mediated diseases. Id. He
has been awarded visiting professorships/lectureships by a variety of institutions. Id.
B. Expert Reports
1. Petitioner’s Expert, Dr. Gershwin
In his first expert report, Dr. Gershwin provided a general overview of alopecia. He
explained that “[AA] consists of one or more circular bald patches around the scalp,” while
“[a]lopecia totalis includes complete loss of hair on the scalp and is the most extreme form of
[AA].” Pet’r’s Ex. 16 at 1, ECF No. 29. He noted that AA and alopecia totalis are “considered
inflammatory and non-scarring” and that AA occurs in about 1.7% of people at some point during
their lifetime. Id. at 1–2. Additionally, he claimed that “alopecia universalis is diagnosed with
100% loss of both scalp and body hair.” Id. at 2. Dr. Gershwin further explained that alopecia is
so dynamic that patches of hair loss “may be seen in other areas of the body such as elbow, arms,
and thigh.” Id. He continued that “the disease may involve facial hair, including eyelashes,
eyebrows, and the beard area.” Id. Dr. Gershwin also noted that alopecia is a systemic disease that
can affect the nails and eyes in addition to the hair follicles. Id.
Dr. Gershwin then explained that “[t]he genetic basis of alopecia is strongly supported by
its observed heritability in first degree relatives, twin studies[,] and genetic linkage analysis of
alopecia families.” Id. He noted that 10% to 42% of alopecia patients have a first-degree relative
who is also affected. Id. Among these cases, “7% of patients have at least one parent with alopecia,
3% have at least one sibling with the disease, and a minority of 2% have a child who suffers from
alopecia.” Id. Citing Martinez-Mir et al.,12 Dr. Gershwin asserted that “[a] genome wide search
for linkage of 20 families with alopecia consisting of 102 affected and 118 unaffected individuals
demonstrated the association of [human leukocyte antigens (“HLA”)][13] with alopecia.” Id. (citing
Pet’r’s Ex. 21, ECF No. 41-5). Dr. Gershwin identified multiple HLA class I and II alleles “that
potentially contribute to the diagnosis of alopecia,” and noted DQ3, DR11, and DQ7 are associated
with the more severe iterations of the disease: alopecia totalis and universalis. Id. There were
several other associations, which Dr. Gershwin discussed, of certain alleles found more commonly
in individuals from specific geographical locations and ethnic backgrounds and in alopecia
12 Amalia Martinez-Mir et al., Genomewide Scan for Linkage Reveals Evidence of Several Susceptibility
Loci for Alopecia Areata, 80 AM. J. HUM. GENETICS 316 (2007).
13 HLA are “histocompatibility antigens governed by genes of the HLA complex (the human major
histocompatibility complex), a region on the short arm of chromosome [six] containing several genetic loci,
each having multiple alleles.” Dorland’s at 103.
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Case 1:17-vv-01770-UNJ Document 98 Filed 04/25/25 Page 7 of 27
patients. Id. Citing Petukhova et al.,14 Dr. Gershwin stated that in a genome-wide association study
of 1,054 alopecia cases and 3,278 controls, it was “reported that eight genomic regions, including
loci encoding genes in both innate and adaptive immunity [were] associated with alopecia.” Id.
(citing Pet’r’s Ex. 26, ECF No. 41-10). He explained that the effectiveness of immunosuppressive
agents in treating alopecia indicated that it is autoimmune and that HLA “has been reported to play
a major role in the etiology of autoimmunity.” Id. at 3 (citing Pet’r’s Ex. 53, ECF No, 33-7;15
Pet’r’s Ex. 54, ECF No. 33-8).16 As “confirmation of this specific hypothesis,” Dr. Gershwin notes
“the increased expression of specific HLAs in alopecia patients such as HLA-DR, HLA-A, HLA-
B, and HLA-C, which are rarely seen in healthy individuals[, ] as well as the identification of a
number of genetic risk factors within various innate and adaptive immunity gene loci [ ].” Id.
(citing Pet’r’s Ex. 55, ECF No. 33-917 Pet’r’s Ex. 56, ECF No. 33-10;18 Pet’r’s Ex. 26). Indeed,
“[t]he most widely affected hypothesis for the effector mechanism of alopecia is the destruction of
the [hair follicle], an immune privilege site.” Id.
Dr. Gershwin explained that in addition to a genetic component, the autoimmune nature of
alopecia is “strongly supported by clinical observations that patients with AA are often diagnosed
with one or more other autoimmune disorders, including vitiligo, lupus erythematosus, myasthenia
gravis, scleroderma, ulcerative colitis, Type I diabetes, thyroiditis, celiac disease, and rheumatoid
arthritis.” Id. (citing Pet’r’s Ex. 47, ECF No. 33-1;19 Pet’r’s Ex. 51, ECF No. 33-5).20 Additionally,
stress hormones “are known to affect alopecia,” and “exposure to ultraviolet light, natural and
chemical bodily offenses, physical injury, and emotional distress” have been linked to alopecia.
Id. (citing Pet’r’s Ex. 35, ECF No. 31-9).21 More generally, “[c]linical and experimental studies
[have] show[n] that environmental insults such as emotional/physical stressors, hormones and
infections contribute to autoimmunity,” and autoimmune disease. Id. (citing Pet’r’s Ex. 31, ECF
No. 31-5;22 Pet’r’s Ex. 32, ECF No. 31-6;23 Pet’r’s Ex. 33, ECF No. 31-7;24 Pet’r’s Ex. 34, ECF
14 Lynn Petukhova et al., Genome-Wide Association Study in Alopecia Areata Implicates Both Innate and
Adaptive Immunity, 466 NATURE 113 (2010).
15 Nili Avidan et al., Genetic Basis of Myasthenia Gravis - a Comprehensive Review, 52 J. AUTOIMMUNITY
146 (2014).
16 Alia Hasham et al., Genetic Analysis of Interferon Induced Thyroiditis (IIT): Evidence for a Key Role for
MHC and Apoptosis Related Genes and Pathways, 44 J. AUTOIMMUNITY 61 (2013).
17 D. Martin Carter & Brian V. Jegasothy BV, Alopecia Areata and Down syndrome, 112 ARCHIVES
DERMATOLOGY 1397 (1976).
18 Amos Gilhar et al., Lymphocytes, Neuropeptides, and Genes Involved in Alopecia Areata, 117 J.
CLINICAL INVESTIGATION 2019 (2007).
19 William V.R. Shellow, Profile of Alopecia Areata: A Questionnaire Analysis of Patient and Family, 31
INT’L J. DERMATOLOGY 186 (1992).
20 S. Sipetić et al., Family History and Risk of Type 1 Diabetes Mellitus, 39 ACTA DIABETOLOGICA 111
(2002).
21 Taisuke Ito, Recent Advances in the Pathogenesis of Autoimmune Hair Loss Disease Alopecia Areata,
2013 CLINICAL DEVELOPMENTAL IMMUNOLOGY 1 (2013).
22 Carlo Perricone et al., Autoimmune/Inflammatory Syndrome Induced by Adjuvants (ASIA) 2013:
Unveiling the Pathogenic, Clinical and Diagnostic Aspects, 47 J. AUTOIMMUNITY 1 (2013).
23 Shiv Pillai, Rethinking Mechanisms of Autoimmune Pathogenesis, 45 J. AUTOIMMUNITY 97 (2013).
24 Carlo Selmi et al., Mechanisms of Environmental Influence on Human Autoimmunity: A National Institute
of Environmental Health Sciences Expert Panel Workshop, 39 J. AUTOIMMUNITY 272 (2012).
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No. 31-8).25 Dr. Gershwin stated that viruses, such as “hepatitis B, hepatitis C, Epstein-Barr, and
swine flu [] have also been suggested to trigger alopecia [].” Id. (citing Pet’r’s Ex. 43, ECF No.
32-7;26 Pet’r’s Ex. 44, ECF No. 32-8;27 Pet’r’s Ex. 45, ECF No. 32-9;28 Pet’r’s Ex. 46, ECF No.
32-10;29 Pet’r’s Ex. 47). He stated that, “[t]heories have also been put forward regarding seasonal
associations, with evidence of increased disease relapses between the months of February and
March.” Id. He further explained that “[t]his may also be a result of the high multitudes of viruses
in early spring, supporting the hypothesis that alopecia may be an effect of certain viral infections.”
Id.
Dr. Gershwin asserted that individuals without alopecia maintain immune privilege within
the hair follicle “in multiple ways, such as omitting [major histocompatibility complex
(“MHC”)][30] class I in the proximal outer root sheath [, while] patients identified with alopecia
have a strong association with those same MHC class I alleles.” Id. at 3–4. He explained that in
alopecia patients, “[a]utoreactive cytotoxic T cells[31] target melanogenesis-associated peptides [in
hair follicles] that produce melanin pigment.” Id. at 4 (citing Pet’r’s Ex. 57, ECF No. 34-1;32
Pet’r’s Ex. 58, ECF No. 34-2).33 According to Dr. Gershwin, this process results in “the sparing
of unpigmented hairs, and regrowth of initially white or gray hairs following the onset of alopecia.”
Id. (citing Pet’r’s Ex. 23, ECF No. 41-7).34
Dr. Gershwin also asserted that cytokines35 and natural killer (“NK”) cells36 have been
implicated in the breakdown of immune privilege in alopecia. Id. at 3–4. For example, NKG2D
25 Karen H. Costenbader et al., Genes, Epigenetic Regulation and Environmental Factors: Which is the
Most Relevant in Developing Autoimmune Diseases, 11 AUTOIMMUNITY REVS. 604 (2011).
26 Nesrine Gamal et al., Alopecia Universalis After Discontinuation of Pegylated Interferon and Ribavirin
Combination Therapy for Hepatitis C: A Case Report, 13 ANNALS HEPATOLOGY 293 (2014).
27 David A. Geier & Mark R. Geier, A Case-Control Study of Serious Autoimmune Adverse Events
Following Hepatitis B Immunization, 38 AUTOIMMUNITY 295 (2005).
28 Taisuke Ito, Advances in the Management of Alopecia Areata, 39 J. OF DERMATOLOGY, (2012).
29 Thomas A. Rodriguez et al., Onset of Alopecia Areata after Epstein-Barr Virus Infectious Mononucleosis,
59 J. AM. ACAD. DERMATOLOGY 11 (2008).
30 MHC are “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.” Dorland’s at 391.
31 Cytotoxic T cells are “differentiated T lymphocytes that can recognize and lyse target cells bearing
specific antigens recognized by their antigen receptors.” Dorland’s at 1070. Cytotoxic T cells are a type of
CD8 T cell, which is a T cell that “carr[ies] the CD8 antigen[.]” Id. at 311.
32 Ralf Paus et al., Is Alopecia Areata an Autoimmune-Response Against Melanogenesis-Related Proteins,
Exposed by Abnormal MHC Class I Expression in the Anagen Hair Bulb, 66 YALE J. BIOLOGY MED. 541
(1994).
33 Amos Gilhar et al., Melanocyte-Associated T Cell Epitopes can Function as Autoantigens for Transfer of
Alopecia Areata to Human Scalp Explants on Prkdc(scid) Mice, 117 J. INVESTIGATIVE DERMATOLOGY 1357
(2001).
34Abdullateef A. Alzolibani, Epidemiologic and Genetic Characteristics of Alopecia Areata (Part 1), 20
ACTA DERMATOVENEROLOGICA ALPINA, PANNONICA, ET ADRIATICA 191 (2011).
35 Cytokine is “a generic term for nonantibody proteins released by one cell population (e.g., primed T
lymphocytes) on contact with a specific antigen, which act as intercellular mediators, as in the generation
of an immune response.” Dorland’s at 460.
36 NK cells are “cells capable of mediating cytotoxic reactions without prior sensitization against the target.”
Dorland’s at 316.
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NK cells “attack by recognizing certain glycoproteins, CMV UL16 proteins, and MHC class I
related proteins MlCA/MICB.” Id. (citing Pet’r’s Ex. 74, ECF No. 35-8).37 Further, “[i]n alopecia
patients, the outer root sheath presents MICA proteins, leading NKG2D + NK cells to target the
HF.” Id. (citing Pet’r’s Ex. 60, ECF No. 34-4).38 He explained that the process causes “[t]he
breaking of tolerance in HF and subsequent change in cytokine/chemokine profiles lead[ing] to
infiltration of lymphocytes.” Id. (citing Pet’r’s Ex. 26; Pet’r’s Ex. 35).
Dr. Gershwin further asserted that specific “[c]hemokines [that] are involved with the
development of autoimmune interactions[,]are more prominent in alopecia patients than healthy
individuals.” Id. (citing Pet’r’s Ex. 63, ECF No. 34-7;39 Pet’r’s Ex. 64, ECF No. 34-8;40 Pet’r’s
Ex. 65, ECF No. 34-9;41 Pet’r’s Ex. 66, ECF No. 34-10;42 Pet’r’s Ex. 67, ECF No. 35-1).43 To
support this contention, Dr. Gershwin cited the C3H/HeJ spontaneous mouse model of alopecia,
“which manifests the clinical pathological features of human alopecia, including infiltration of
CD8 + NKG2D + T cells [from] around the epithelial layers of [hair follicles].” Id. at 4 (citing
Pet’r’s Ex. 75, ECF No. 35-9;44 Pet’r’s Ex. 76, ECF No. 35-10).45 All of these different
components, he asserted, defined “[t]he mechanism that leads to alopecia[,] includ[ing ] genetic
susceptibility and the generation of cytotoxic CD8 T cells.” Id. at 5. He noted that “[i]mportantly,
the signals required to generate CD8 T cells beyond the initial exposure are not required for
proliferation[,] and indeed there is likely to be early immunological programming of such
cytotoxic T cell expansion[].” Id. (citing Pet’r’s Ex. 77, ECF No. 36-1;46 Pet’r’s Ex. 78, ECF No.
36-2;47 Pet’r’s Ex. 79, ECF No. 36-3;48 Pet’r’s Ex. 80, ECF No. 36-4;49 Pet’r’s Ex. 81, ECF No.
37 Stefan Bauer et al., Activation of NK Cells and T cells by NKG2D, a Receptor for Stress-Inducible MICA,
285 SCI. 727 (1999).
38 Taisuke Ito et al., Maintenance of Hair Follicle Immune Privilege is Linked to Prevention of NK Cell
Attack, 128 J. INVESTIGATIVE DERMATOLOGY 1196 (2008).
39 Alessandro Antonelli et al., Chemokine (C-X-C motif) Ligand (CXCL)10 in Autoimmune Diseases, 13
AUTOIMMUNITY REVS. 272 (2014).
40 Chiara Cordiglieri et al., Innate Immunity in Myasthenia Gravis Thymus: Pathogenic Effects of Toll-Like
Receptor 4 Signaling on Autoimmunity, 52 J. AUTOIMMUNITY 74 (2014).
41 Perrine Cufi et al., Central Role of Interferon-Beta in Thymic Events Leading to Myasthenia Gravis, 52
J. AUTOIMMUNITY 44 (2014).
42 Eun Young Lee et al., The Interaction Between CXCL10 and Cytokines in Chronic Inflammatory Arthritis,
12 AUTOIMMUNITY REVS. 554 (2013).
43 Sandrine Benoit et al., Selective Expression of Chemokine Monokine Induced by Interferon-Gamma in
Alopecia Areata, 121 J. INVESTIGATIVE DERMATOLOGY 933 (2003).
44 John P. Sundberg et al., Alopecia Areata in Aging C3H/HeJ Mice, 102 J. INVESTIGATIVE DERMATOLOGY
847 (1994).
45 Luzhou Xing et al., Alopecia Areata is Driven by Cytotoxic T Lymphocytes and is Reversed by JAK
Inhibition, 20 NATURE MED. 1043 (2014).
46 Hannah Rabenstein et al., Differential Kinetics of Antigen Dependency of CD4+ and CD8+ T Cells, 192
J. IMMUNOLOGY 3507 (2014).
47 Julius C. R. Hafalla et al., Short-Term Antigen Presentation and Single Clonal Burst Limit the Magnitude
of the CD8+ T Cell Responses to Malaria Liver Stages, 99 PROC. NAT’L ACAD. SCIS. U.S. 1819 (2002).
48 Susan M. Kaech & Rafi Ahmed, Memory CD8+ T Cell Differentiation: Initial Antigen Encounter Triggers
a Developmental Program in Naïve Cells, 2 NATURE IMMUNOLOGY 415 (2001).
49 Roberto Mercado et al., Early Programming of T Cell Populations Responding to Bacterial Infection,
165 J. IMMUNOLOGY 6833 (2000).
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36-5;50 Pet’r’s Ex. 82, ECF No. 36-6;51 Pet’r’s Ex. 83, ECF No. 36-7;52 Pet’r’s Ex. 84, ECF No.
36-8;53 Pet’r’s Ex. 85, ECF No. 36-9;54 Pet’r’s Ex. 86, ECF No. 36-10).55 He further noted that
“[o]nset within 14 days would certainly be consistent with generation of a CD8 response.” Id.
Summarizing his medical theory, Dr. Gershwin wrote that Petitioner “developed alopecia
because of his unique genetic susceptibility.” Id. He claimed that Petitioner “received a vaccine
that produced cytotoxic T cells that were directed at his hair follicles and [] cross react[ed] with an
epitope or region of the Gardasil vaccine.” Id. Dr. Gershwin supported this contention by
mentioning that “[t]he kinetics and the production of such cytotoxic T cells is consistent and
biologically plausible with the literature on the production of such cytotoxic T cells.” Id. He
explained that the mechanism is similar to the mouse model and “is due to molecular mimicry.”
Id.
In order to link the Gardasil HPV vaccine to the autoimmune attack on Petitioner’s hair
follicles, Dr. Gershwin cited Wise et al.56 Id. (citing Pet’r’s Ex. 88 at 3, ECF No. 37-2). He wrote
that the data from Wise et al. “suggest[s] that HPV is the most likely initiating immunogen herein.”
Id. The authors noted their “speculat[ion] that cell growth cycles might be pathologically
modulated by vaccine-induced antibodies.” Pet’r’s Ex. 88 at 3. The article “suggest[ed] antigenic
similarities between vaccines and hair follicles, at least in susceptible patients, that should be
investigated.” Id. Alternatively, the authors conceded that “[u]nexpected hair loss could
occasionally follow vaccine exposure by chance alone since vaccine exposures are extremely
common, and unexplained hair loss ([AA] or other syndromes) is not rare.” Id. Furthermore, they
claimed that “possible biases in case ascertainment” was identified due to the gender and
occupation of the study group. Id. Thus, the authors concluded that “individuals may be more
likely to suspect recent immunization when they develop hair loss, and they are familiar with the
importance of reporting adverse events.” Id.
Next, Dr. Gershwin made some additional points noting that the variation in the human
immune system is largely driven by non-heritable influences. Pet’r’s Ex. 16 at 5–6. He further
50 Marianne J.B. van Stipdonk et al., Dynamic Programming of CD8+ T Lymphocyte Responses, 4 NATURE
IMMUNOLOGY 361 (2003).
51 Matthew A. Williams & Michael J. Bevan, Shortening the Infectious Period Does Not Alter Expansion
of CD8 T Cells but Diminishes Their Capacity to Differentiate into Memory Cells, 173 J. IMMUNOLOGY
6694 (2004).
52 Phillip Wong & Eric G. Pamer, Disparate in Vitro and in Vivo Requirements for IL-2 During Antigen-
Independent CD8 T Cell Expansion, 172 J. IMMUNOLOGY 2171 (2004).
53 Gabriel R. Starbeck-Miller et al., IL-12 and Type I Interferon Prolong the Division of Activated CD8 T
Cells by Maintaining High-Affinity IL-2 Signaling in Vivo, 211 J. EXPERIMENTAL MED. 105 (2014).
54 Michael J. Bevan & Pamela J. Fink, The CD8 Response on Autopilot, 2 NATURE IMMUNOLOGY 381
(2001).
55 David Masopust et al., The Role of Programming in Memory T-Cell Development, 16 CURRENT OP.
IMMUNOLOGY 217 (2004).
56 Robert P. Wise et al., Hair Loss After Routine Immunizations, 278 JAMA 1176 (1997). Wise et al.
discussed 60 reports of hair loss following various vaccinations, but primarily hepatitis B vaccinations,
identified through the Vaccine Adverse Event Reporting System (“VAERS”). After reviewing the 60 case
reports, the authors noted that “immunizations warrant consideration among potential causes of hair loss.
Id. at 3.
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stated that “[r]ecent advances in technology now allow much more comprehensive surveys to be
conducted across the many different components of the immune system.” Id. at 6. He reasoned
that “the immune system of healthy individuals is very much shaped by the environment and most
likely by the many different microbes that an individual encounters in their lifetime.” Id. He then
concluded that “the immune response cannot always be predicted and that in fact rare events can
be explained by stochastic events that have occurred in an individual’s lifetime.” Id. In any
particular case, “for diseases as uncommon as [AA], one cannot rely on epidemiology because the
power calculations are insufficient to provide the necessary data to draw statistical conclusions.”
Id.
In a responsive report, Dr. Gershwin explained that he could not identify the specific
component of the Gardasil vaccine that triggered the cytotoxic T cell response. See generally
Pet’r’s. Ex. 99, ECF No. 64. He asserted that “identification and definition of epitopes is
extraordinarily complex and requires data that is not available and could not be achieved without
a major research effort.” Id. at 1 (emphasis in original). Dr. Gershwin referred to the Colmenares
et al.57 article to note “the imbalance of CD8 T cells following Gardasil vaccine[.]” Id. at 2 (citing
Pet’r’s Ex. 105, ECF No. 65-6). He then quoted the authors’ observations,
Interestingly, [the authors] observed that while the proportion of CD8+
lymphocytes that expressed ILT2 decreased after immunization, there was an
increase in the density (MFI) of this receptor in these cells. Although the underlying
mechanism for this apparent paradoxical effect remains to be determined, [their]
data suggest[ed] that in the fraction of CD8+ cells that remain ILT2 positive after
quadrivalent HPV (type 6/11/16/18) vaccine immunization, the enhanced density
of this receptor may exert an increased regulatory effect[.]
Id. (quoting Pet’r’s Ex. 105 at 7).
In a supplemental report, Dr. Gershwin asserted that Gardasil contains two components
that could affect the production of CD8+ T cells. Pet’r’s Ex. 106 at 1–2, ECF No. 68. He
acknowledged literature that notes the addition of an aluminum adjuvant to Gardasil “is limited by
weak stimulation of cell-mediated immunity, [and] this can be enhanced by the addition of other
immunomodulatory molecules.” Id. at 1 (quoting Pet’r’s Ex. 107 at 1, ECF No. 69-1).58 Hogenesch
endeavored to “increase our understanding of the mechanisms involved in adsorption of antigens
onto aluminum adjuvants and the effect of adsorption on the stability of antigens and the immune
response.” Pet’r’s Ex. 107 at 9. The article abstract noted that aluminum adjuvants “support[ed]
activation of CD8 T cells, but these cells d[id] not undergo terminal differentiation to cytotoxic T
cells.” Id. at 1. The author further noted that “[a]luminum adjuvants primarily enhance antibody
production and have little effect on the cell-mediated arm of the immune response.” Id. at 2.
Dr. Gershwin stated that the Gardasil vaccine contained polysorbate 80, which is “added
to vaccines as an emulsifier to spread the antigenic components of the vaccine and facilitate the
57 V. Colmenares et al., Human Papillomavirus Immunization is Associated with Increased Expression of
Different Innate Immune Regulatory Receptors, 19 CLINICAL VACCINE IMMUNOLOGY 1005 (2012).
58 Harm Hogenesch, Mechanism of Immunopotentiation and Safety of Aluminum Adjuvants, 3 FRONTIERS
IMMUNOLOGY 1 (2013).
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production of cell-mediated immunity.” Pet’r’s Ex. 106 at 1. He cites Macleod et al.,59 to assert
that “[t]his point [was] studied specifically with respect to CD8 cells in literature that describes
the mechanism” Id. (Pet’r’s Ex. 108, ECF No. 69-2). Dr. Gershwin explained that “[t]he use of
other materials in vaccines, when alum is included, to facilitate cell-mediated immunity has been
known for decades.” Id. at 2 (citing Pet’r’s Ex. 112, ECF No. 69-6).60 He opined that “there is
literature that does document T cell immune responses, measured as inflammatory cytokine
production, of peripheral blood cells in young women immunized with HPV.” Id. at 2 (citing
Pet’r’s Ex. 111, ECF No. 69-5).61 The literature cited by Dr. Gershwin is the Toh et al. study,
whose authors sought “to document the elevated cellular immune responses in girls who were
previously vaccinated with at least [one] dose of [quadrivariate HPV] when compared with
unvaccinated girls, [six] years following the last dose.” Pet’r’s Ex. 111 at 8.
Additionally, he reiterated that “the mechanism herein is molecular mimicry at the T cell
level [and restated that Petitioner] would not have developed alopecia if he did not uniquely have
an antigen in his hair follicles that was cross-reactive with a component of the HPV vaccine.”
Pet’r’s Ex. 106 at 2. He further stated that Petitioner did not have “an abnormal initial immune
response to the Gardasil, rather that the pathology is due to molecular mimicry via the cross
reactive antigen.” Id. He opined that Petitioner’s “self-antigen is always present and is the basis
for the continued production of cytotoxic CD8 T cells and subsequent alopecia.” Id. In support of
this argument, Dr. Gershwin cited Kaech et al., which showed that naïve CD8+ T cells differentiate
in effector and memory cells following antigenic stimulation. Pet’r’s Ex. 113 at 1. The article
described how CD8+ T cells become activated and differentiate into effector cytotoxic T
lymphocytes, following exposure to an antigen such as an infection or vaccine. Id. The authors
“propose[d] that the most effective T cell vaccines will be those that produce the optimal burst of
antigen expression and recruit the greatest number of antigen-specific CD8+ T cells into the
response.” Id. at 7. Two additional articles, Cho et al.62 and Veiga-Fernandes et al.,63 further
discussed the effect that antigen stimulation has on naïve CD8+ cells. See Pet’r’s Ex. 114, ECF
No. 69-8; Pet’r’s Ex. 115, ECF No. 69-9). Dr. Gershwin reiterated that he could not provide the
sequence or identification of hair follicle antigen but asserted that molecular mimicry is well
accepted and the identification of such antigenic determinants would require a major research
effort. Pet’r’s Ex. 106 at 2.
59 Megan K.L. MacLeod et al., Vaccine adjuvants aluminum and monophosphoryl lipid A provide distinct
signals to generate protective cytotoxic memory CD8 T cells, 108 PROCS. NAT’L ACAD. SCIS. U.S. 7914
(2011).
60 Noelene E. Byars & Anthony C. Allison, Adjuvant Formulation for Use in Vaccines to Elicit Both Cell-
Mediated and Humoral Immunity, 5 VACCINE 223 (1987).
61 Zheng Quan Toh et al., Cellular Immune Responses 6 Years Following 1, 2, or 3 Doses of Quadrivalent
HPV Vaccine in Fijian Girls and Subsequent Responses to a Dose of Bivalent HPV Vaccine, 5 OPEN F.
INFECTIOUS DISEASES 1 (2018).
62 Bryan K. Cho et al., Functional Differences Between Memory and Naive CD8 T Cells, 96 PROC. NAT’L
ACAD. SCI. U.S. 2976 (1999).
63 Henrique Veiga-Fernandes et al., Response of Naïve and Memory CD8+ T Cells to Antigen Stimulation in
Vivo, 1 NATURE IMMUNOLOGY 47 (2000).
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In Dr. Gershwin’s final submitted report, he briefly reiterated “the importance (and
difficulty) of epitope production.” Pet’r’s Ex. 116 at 1 (citing Pet’r’s Ex. 119, ECF No. 78-3;64
Pet’r’s Ex. 120, ECF No. 78-4;65 Pet’r’s Ex. 121, ECF No. 78-5).66 He cited literature in support
of this assertion as well as “recent literature of an increased incidence of [AA] after HPV
infection.” Id. (citing Pet’r’s Ex. 118, ECF No. 78-2).67 Tu et al. summarized an “investigat[ion
of] the correlation between a history of [HPV] infection and [AA] risk.” Pet’r’s Ex. 118 at 1. The
authors identified “30,001 patients with newly diagnosed HPV infection between 2000 and 2012.”
Id. Patients who did not have HPV, “were randomly selected as the comparison cohort. HPV
infection cohort were matched to comparison individuals at a 1:1 ratio by age, gender and index
year.” Id. The authors ultimately concluded that “[a] history of HPV infection is associated with
the development of subsequent [AA] in Taiwanese subjects.” Id.
2. Respondent’s Expert, Dr. Levinson
Dr. Levinson concurred with Petitioner’s “initial diagnosis of [AA] and later diagnosis of
alopecia universalis.” Resp’t’s Ex. A at 3; ECF No. 47-1. However, he disagreed with the
“assignment of causality” to the vaccine Petitioner received on March 30, 2015, or any prior
Gardasil vaccination that Petitioner received. Id.
According to Dr. Levinson, “local injection site reactions including pain, erythema and
swelling were more common after vaccine than placebo but systemic adverse effects including
development of systemic disease and presumed autoimmune disease were not.” Id. at 3.
Dr. Levinson cited a study by Chao et al.,68 which evaluated 189,629 women of all ages
who received at least one dose of the vaccine and another group of women who did not receive the
vaccine to compare the incidence of autoimmune disease among the two groups. Id. (citing
Resp’t’s Ex. C, Tab 58, at 2, ECF No. 62-8). Ultimately, this study showed “no clear evidence of
safety signal for [autoimmune] conditions following vaccination with HPV4[.]” Resp’t’s Ex. C,
Tab 58, at 9. Dr. Levinson also cited Arnheim-Dahlström et al.69 from 2013 which evaluated
997,585 girls aged 10-17 years, 296,826 of whom had received quadrivalent HPV vaccine. Id. at
4 (citing Resp’t’s Ex. C, Tab 56, ECF No. 62-6). Within this study, the investigators “identified
no safety signals with respect to autoimmune, neurological, and venous thromboembolic events
after the HPV vaccine had been administered.” Resp’t’s Ex. C, Tab 56, at 5. Dr. Levinson cited
64 Mette Voldby Larsen et al., An Integrative Approach to CTL Epitope Prediction: A Combined Algorithm
Integrating MHC Class I Binding, TAP Transport Efficiency, and Proteasomal Cleavage Predictions, 35
EUR. J. IMMUNOLOGY 2295 (2005).
65 Claus Lundegaard et al., State of the Art and Challenges in Sequence Based T-Cell Epitope Prediction, 6
IMMUNOME RSCH. 1 (2010).
66 Ruth E. Soria-Guerra et al., An Overview of Bioinformatics Tools for Epitope Prediction: Implications on
Vaccine Development, 53 J. BIOMEDICAL INFORMATICS 405 (2015).
67 Ting-Yu Tu et al., Human Papillomavirus Symptomatic Infection Associated with Increased Risk of New-
Onset Alopecia Areata: A Nationwide Population-Based Cohort Study, 119 J. AUTOIMMUNITY (2021).
68 C. Chao et al., Surveillance of Autoimmune Conditions Following Routine use of Quadrivalent Human
Papillomavirus Vaccine, 271 J. INTERNAL MED. 193 (2011).
69 Lisen Arnheim-Dahlström, Autoimmune, Neurological, and Venous Thromboembolic Adverse Events
After Immunisation of Adolescent Girls with Quadrivalent Human Papillomavirus Vaccine in Denmark and
Sweden: Cohort Study, 347 BMJ (2013).
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three additional studies that found no evidence of an increased risk for autoimmune disorders
following HPV vaccinations in large populations of girls. Resp’t’s Ex. A at 3–4; see Resp’t’s Ex.
A, Tab 4, ECF No. 70-4;70 Resp’t’s Ex A, Tab 5, ECF No. 70-5;71 Resp’t’s Ex. A, Tab 6, ECF No.
70-6;72 Resp’t’s Ex. A, Tab 7, ECF No. 70-7.73
Describing alopecia spectral disorders as “products of autoimmune mechanisms that injure
hair follicles,” Dr. Levinson again agreed with Dr. Gershwin that “[e]pidemiologic studies clearly
demonstrate an underlying genetic basis to these disorders as well as a number of environmental
and emotional/physical stress factors.” Id. at 4. He noted that “cytotoxic CD8+ T cells and NK
cells are thought to target autoantigens expressed on hair follicles.” Id. Further, he stated that
“[d]ata also suggest that CD4+ T cells and a myriad of soluble factors, e.g., cytokines and
chemokines, contribute to injury of the hair follicle.” Id.
Dr. Levinson’s disagreement with Dr. Gershwin lies in the “giant leap of faith” necessary
to invoke molecular mimicry in connecting the HPV vaccine to the development of alopecia. Id.
at 5. Dr. Levinson explained that Dr. Gershwin “failed to identify any semblance of molecular
mimicry between molecular motifs expressed on the hair follicle and the viral antigens that are
found in the Gardasil vaccine.” Id. According to Dr. Levinson, accepting Dr. Gershwin’s opinion
would “legitimize the claim that literally any exogenous antigen, be it a vaccine component, an
infectious agent, etc., can cause just about any autoimmune disease by the process of molecular
mimicry despite there being no demonstrable evidence for said molecular mimicry between the
putative exogenous agent and the relevant target self-antigen.” Id.
Dr. Levinson then stated that “there is no reliable epidemiological evidence that supports
the proposition that the Gardasil vaccine causes [AA].” Id. Dr. Levinson stated that Dr. Gershwin
mischaracterized the Wise et al. findings. Id. (citing Pet’r’s Ex. 88 at 3). According to Dr.
Levinson, “[t]here was no mention of whether the alopecia was characterized by clinical features
of [AA], and the onset of alopecia occurred at variable times after vaccination.” Id. He asserted
that “most of these incidents occurred within [one] month of immunization with a variety of
vaccines, and some occurred within one day of vaccination.” Id. Additionally, Dr. Levinson noted
that “patients ranged in age from neonates to 84 years-old. [Furthermore, s]everal of the patients
experienced complete regrowth of hair after an episode of alopecia.” Id. at 5–6. Notably, Dr.
Levinson stated “that none of the subjects had received Gardasil, or for that matter any HPV
vaccine” Id. at 6. Dr. Levinson then identified a case study of the development of AA after Gardasil
vaccination involved a “[two-]year-old Japanese boy who developed alopecia areata/totalis one
week and [three] days after receiving a third dose of Japanese encephalomyelitis vaccine and third
dose of influenza vaccine, respectively.” Id. (citing Resp’t’s Ex. A, Tab 14, ECF No. 71-7).74
70 L. Grimaldi-Bensouda et al., Autoimmune Disorders and Quadrivalent Human Papillomavirus
Vaccination of Young Female Subjects, 275 J. INTERNAL MED. 398 (2014).
71 Sara Miranda et al., Human Papillomavirus Vaccination and Risk of Autoimmune Diseases: A Large
Cohort Study of over 2 Million Young Girls in France, 35 VACCINE 4761 (2017).
72 Lamiae Grimaldi-Bensouda et al., Risk of Autoimmune Diseases and Human Papilloma Virus (HPV)
Vaccines: Six Years of Case-Referent Surveillance, 79 J. AUTOIMMUNITY 84 (2017).
73 Erin Y. Liu et al., Quadrivalent Human Papillomavirus Vaccination in Girls and the Risk of Autoimmune
Disorders: The Ontario Grade 8 HPV Vaccine Cohort Study, 190 CANADIAN MED. ASS’N J. 648 (2018).
74 Chien-Ho Chu et al., Alopecia Areata After Vaccination: Recurrence with Rechallenge, 33 PEDIATRIC
DERMATOLOGY 218 (2016).
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Dr. Levinson clarified his objection to Dr. Gershwin’s causality theory in his supplemental
report. Resp’t’s Ex. E, ECF No. 63-1. He explained that Dr. Gershwin’s opinion has “no evidence
of molecular mimicry between viral antigens in the Gardasil vaccine and self antigens expressed
on hair follicles.” Id. at 1. He further stated that there is no “scientific literature that supports the
contention that any type of molecular mimicry accounts for the autoimmune destruction of hair
cells in AA” Id.
Dr. Levinson responded to Dr. Gershwin’s claim that “cytotoxic CD8+ T cells were key
contributors to the destruction of hair follicles.” Id. at 2–3. He criticized this view as flawed, stating
that it is unlikely Gardasil would have triggered the development of any cytotoxic CD8+ T cells
Id. at 3.
Furthermore, Dr. Levinson explained that “Gardasil, like so many commercial vaccines
administered in the U.S., contains an adjuvant, namely an aluminum compound that potentiates
the induced specific immune response.” Id. And, he noted, “the principle immune response elicited
by an aluminum compound-adjuvanted vaccine is essentially an antibody response.” Id. (citing
Resp’t’s Ex. E, Tab 5, ECF No. 63-6). He continued, “vaccines adjuvanted with aluminum salts,
are very effective generating potent antibody responses but are ineffective generating protective
cell-mediated immune responses, especially cytotoxic T cell responses.” Id. (citing Resp’t’s Ex.
E, Tab 5). Dr. Levinson noted that “[t]his limitation is the overriding impetus for developing
vaccines formulated with novel adjuvants that elicit more protective broad-based immune
responses, including cytotoxic T cell response, when administered in humans.” Id. Thus, he
concluded that it was “extremely unlikely that Gardasil induced the development of cytotoxic
CD8+ T cells, let alone ones that are specific for any epitopes that are putatively shared by Gardasil
viral antigens and self-antigens expressed on hair follicles.” Id.
Dr. Levinson also noted that he “was unable to find a single case report that linked the
wild-type infection with HPV to the development of AA.” Id. Dr. Levinson explained that although
identification of T cell epitopes and molecular mimicry is a complex subject, “it is certainly
possible to identify autoimmune diseases in which mimicry of exogenous antigens by self antigens
is pathogenic.” Resp’t’s Ex. F at 2, ECF No. 66-1. He further stated that the difficulty of generating
data to support an expert’s causality opinion is immaterial because it would “undermine the merits
of the claim being made.” Id. Dr. Levinson then went on to note that he does not consider the
absence of epidemiologic evidence when constructing his opinion during vaccine injury cases. Id.
Instead, he relied on the totality of the experiential data in formulating his opinion. Id. Dr. Levinson
then stated that he is more compelled to question a vaccine’s causality when there are only a few
published case reports that possibly link a particular vaccine to a disease. Id.
Clarifying his statement that it was unlikely that Gardasil would have induced any type of
cytotoxic T cells, Dr. Levinson noted that he was “referring to cytotoxic CD8+ T cells that were
in this case alleged to actively destroy hair follicles.” Id. at 3. He further stated, “that such an
outcome following Gardasil vaccination would be extremely unlikely even if molecular mimicry
was operative, since this alum-adjuvanted vaccine, like all other alum-adjuvanted vaccines, do not
induce the emergence of functional CD8+ T cells, i.e., cells that kill their targets in response to
specific vaccine antigens.” Id. He stated that Dr. Gershwin’s reliance on the Colmenares et al.
publication was flawed. Id. (citing Pet’r’s Ex. 99 at 2). He noted that the authors “analyzed the
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expression and function of Immunoglobulin-like transcript 2 (ILT2) as well as the expression of
other NK cell receptors, which seem to participate in the innate immune response against different
viruses.” Id. at 3 (citing Pet’r’s Ex. 105). Dr. Levinson acknowledged the imbalance identified by
Dr. Gershwin but also pointed out that, in summarizing their results, the authors stated, “it is also
possible that [the induction of ILT2 expression by quadrivalent HPV] is mediated by cytokines
released by T cells.” Id. (quoting Pet’r’s Ex. 105 at 7). He argued that, in context, the study only
showed that the authors observed a change in the expression of ILT2 on CD8+ T cells following
vaccination. Id. Thus, he asserted that this did not provide any “demonstra[tion] that the Gardasil
vaccination caused the development of any type of functional CD8+ cytotoxic T cells.” Id. They
concluded “that “HPV immunization is associated with significant changes in the expression and
function of different innate immune receptors, including ILT2, which may participate in the
protective effect of HPV vaccines.” Id. (quoting Pet’r’s Ex. 105 at 1). Dr. Levinson opined that
“this paper clearly did not demonstrate that Gardasil vaccination caused the development of any
type of functional CD8+ cytotoxic T cells” and that “no evidence has been presented to critique
his theory.” Id.
In a supplemental report, Dr. Levinson addressed Dr. Gershwin’s idea about polysorbate
80 and how it elicits a stronger immune response. Resp’t’s Ex. G, ECF No. 75-1. He opined that
Dr. Gershwin’s discussion of this issue is irrelevant and fails to prove that Gardasil facilitates
active CD8+ cytotoxic T cells. Id. at 1–2. Dr. Levinson then pointed to a previously cited study,
Macleod et al., to argue that it reinforced his “assertion that vaccines adjuvanted only with an
aluminum salt do not induce the development of antigen-specific functionally active cytotoxic
CD8+ T cells.” Id. at 2 (citing Pet’r’s Ex. 108). However, he explained, “when a vaccine containing
alum is ‘fortified’ with certain other immunomodulators like MPLA, the vaccine gains the capacity
to induce the cytotoxic CD8+ T cells.” Id. He goes on to state that Dr. Gershwin failed to mention
that “polysorbate 80 and any of the other ingredients in the Gardasil vaccine do not possess such
alum-fortifying adjuvant action.” Id. Dr. Levinson reiterated that no literature supports Dr.
Gershwin’s statements, and asserted that instead, Dr. Gershwin has “conflated T cell-induced
cytokine responses with T cell-induced cytotoxic T cell responses.” Id.
3. Respondent’s Expert, Dr. Senna
Dr. Senna’s expert report began with a summary of Petitioner’s medical history, his clinical
presentation, and ultimate alopecia diagnosis. Resp’t’s Ex. C at 2–6, ECF No. 47-3 She then
defined AA and described it as “an autoimmune disorder characterized by patches of non-scarring
hair loss that can affect the scalp and/or the body.” Id. at 6. Dr. Senna explained that her process
of evaluating AA patients includes reviewing a patient’s “extended history of the hair loss and
other past medical history, family history, medications, and potential exacerbating factors.” Id. at
10. She then looks for “clues that are supported by medical evidence that more than likely affect
an individual’s disease course, response to treatment, and overall prognosis.” Id. Dr. Senna stated
that she applied the same process to Petitioner’s case and concluded that the HPV vaccine did not
play a role in causation. Id.
Dr. Senna noted that AA affects up to 3% of the general population. Id. Like many
autoimmune disorders, AA commonly presents and peaks during adolescence and early childhood.
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Id. (citing Resp’t’s Ex. C, Tab 54, ECF No. 62-4).75 Dr. Senna explained that this is the time when
individuals receive the HPV vaccine series, which would lead one to “attribute the development
of autoimmune conditions to the vaccine.” Id. at 10–11. However, “large epidemiologic studies
have not detected any such associations.” Id. at 11 (citing Resp’t’s Ex. C, Tab 55, ECF No. 62-
5;76 Resp’t’s Ex. C, Tab 56, ECF No. 62-6;77 Resp’t’s Ex. C Tab 57, ECF No. 62-7;78 Resp’t’s Ex.
C, Tab 58, ECF No. 62-8;79 Resp’t’s Ex. C, Tab 59, ECF No. 62-9).80 Dr. Senna cited a paper from
Genovese et al.81, detailing “[a] large meta-analysis on six studies on bivalent and quadrivalent
HPV vaccines that in 243,289 patients who received the HPV vaccines [revealed] no correlation
between autoimmune disorders and HPV vaccination.” Id. (citing Resp’t’s Ex. C, Tab 50, ECF
No. 61-10). Further, Skufca et al.82 studied “134,615 11- to 15-year-olds vaccinated with the HPV
vaccine [which] showed that vaccination was not associated with a higher risk of any adverse
outcome during the entire [three] year follow-up.” Id. (citing Resp’t’s Ex. C, Tab 51, ECF No. 62-
1). Dr. Senna noted that a review of VAERS revealed 60,461,220 females and males who received
HPV vaccines between 2009 and 2015 in the United States. Id. In these submitted cases, “dizziness
and syncope were the most commonly reported nonserious [adverse events] in both males and
females.” Id. Dr. Senna further noted that this study showed “no reports of [AA] or other forms of
hair loss.” Id. Dr. Senna asserted that, in fact, “[t]here is no evidence that HPV vaccination causes
[AA] or other autoimmune diseases.” Id. at 11.
In Petitioner’s case, Dr. Senna stated that Petitioner “had a number of baseline poor
prognostic risk factors, including a history of atopy (allergic rhinitis, seasonal allergies),
development at a young age (age 13).” Id. at 12. In Dr. Senna’s expert opinion, “any one of the
above [three] factors on its own would portend a poorer AA prognosis for a patient, making it
more likely than not that the patient would be resistant to treatment, have a progressive course,
and develop severe [AA] over time.” Id. at 12–13.
Dr. Senna noted an that, “[e]xogenous stress[,] has been implicated as a trigger for AA
exacerbations.” Id. at 13 (citing Resp’t’s Ex. C, Tab 35, ECF No. 60-5;83 Resp’t’s Ex. C, Tab 36,
75 S. Macleod & R.E. Appleton, Neurological Disorders Presenting Mainly in Adolescence, 92 ARCHIVES
DISEASE CHILDHOOD 170 (2007).
76 Julianne Gee et al., Monitoring the Safety of Quadrivalent Human Papillomavirus Vaccine: Findings
from the Vaccine Safety Datalink, 29 VACCINE 8279 (2011).
77 Lisen Arnheim-Dahlström, Autoimmune, Neurological, and Venous Thromboembolic Adverse Events
After Immunisation of Adolescent Girls with Quadrivalent Human Papillomavirus Vaccine in Denmark and
Sweden: Cohort Study, 347 BMJ 1 (2013).
78 Allison L. Naleway et al., Absence of Venous Thromboembolism Risk Following Quadrivalent Human
Papillomavirus Vaccination, Vaccine Safety Datalink, 34 VACCINE 167 (2016).
79 C. Chao et al., Surveillance of Autoimmune Conditions Following Routine use of Quadrivalent Human
Papillomavirus Vaccine, 271 J. INTERNAL MED. 193 (2011).
80 Nikolai Madrid Scheller et al., Quadrivalent HPV Vaccination and Risk of Multiple Sclerosis and Other
Demyelinating Diseases of the Central Nervous System, 313 JAMA 54 (2015).
81 C. Genovese et al., HPV Vaccine and Autoimmune Diseases: Systematic Review and Meta-Analysis of
the Literature, 59 J. PREVENTIVE MED. HYGIENE 194 (2018).
82 Jozica Skufca et al., The Association of Adverse Events with Bivalent Human Papilloma Virus
Vaccination: A Nationwide Register-Based Cohort Study in Finland, 36 VACCINE 5926 (2018).
83 Soraya Azzawi et al., Immune Privilege Collapse and Alopecia Development: Is Stress a Factor, 4 SKIN
APPENDAGE DISORDERS 236 (2018).
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ECF No. 60-6;84 Resp’t’s Ex. C, Tab 37, ECF No. 60-7).85 Dr. Senna cited a 2017 World Congress
of Hair Research article86 that tracked “77 [AA] patients seen over a 10-month period [and] found
that 63% of patients cited a stressor as an inciting factor for AA disease exacerbation.” Id. (citing
Resp’t’s Ex. C, Tab 42, ECF No. 61-2). She continued, “[s]tressors included personal
illness/infection, death of a loved one, and work or relationship stress. The duration between the
timing of the stressor and the onset or exacerbation in AA was [two to three] months.” Id. In the
present case, Dr. Senna identified family circumstances as Petitioner’s potential stressor, including
“his maternal grandmother[‘s] bladder cancer [diagnosis] at a time that his mother was teaching
and in graduate school.” Id. at 14. She further stated that “[a]lthough [Petitioner] is clearly a
resilient young man, it is not infrequent that stressors like this contribute to hair follicle immune
collapse in genetically predisposed patients, even in the most stoic pediatric patients.” Id.
Finally, Dr. Senna stated that Petitioner’s “AA treatment regimen was conservative at best
and lacked an evidence-based approach.” Id. She described how Petitioner sought treatment for
his AA with acupuncture, herbal supplements, and a vitamin B12 injection; however, “[n]one of
these treatment modalities have been shown to be beneficial to reversing the inflammation in
[AA].” Id. Dr. Senna argued that the “best therapeutic interventions for this condition were not
implemented early enough and likely contributed to the progression of his [AA] from patchy
involvement to more severe involvement.” Id. at 15–16.
4. Respondent’s Expert, Dr. Maverakis
Dr. Maverakis agreed with Dr. Senna’s assessment that, given the vast number of children
that are vaccinated in the United States versus the incidence rate of AA, “by chance alone, we
expect there to be thousands of AA cases occurring in children after vaccination, or any other
random predetermined event.” Resp’t’s Ex. H at 4, ECF No. 86-1 . He also agreed with Petitioner’s
diagnosis of severe AA; however, he noted that “[t]here is no strong reason to believe that
[Petitioner’s] AA developed because he was vaccinated.” Id. Dr. Maverakis then discussed the
Wise et al. article, which he described as “not specific for AA, as all causes of hair loss were
included.” Id. (citing Resp’t’s Ex. H, Tab 12, ECF No. 86-13). Furthermore, Dr. Maverakis
distinguished the argument made in that paper from the current case, noting the transient hair loss
discussed, “is unlike the current case.” Id.
There was also an agreement between Drs. Maverakis and Dr. Senna that “the ability of
[the HPV vaccine] to induce autoimmunity has been specifically and extensively studied.” Id. at
5. Dr. Maverakis opined that “studies have uniformly demonstrated that there is no association
between autoimmune diseases and HPV vaccination.” Id. Of note to Dr. Maverakis, is the
Gronlund et al.87 study wherein “a cohort of patients with one form of autoimmunity were
84 F. Rajabi et al., Alopecia Areata: A Review of Disease Pathogenesis, 179 BRIT. J. DERMATOLOGY 1033.
85 R. Paus, Exploring the “Brain-Skin Connection”: Leads and Lessons from the Hair Follicle, 64 CURRENT
RSCH. TRANSLATIONAL MED. 207 (2016).
86 Ralf Paus et al., Neuroendocrinology of the Hair Follicle: Principles and Clinical Perspectives, 20
TRENDS MOLECULAR MED. 559 (2014).
87 O. Grönlund et al., Incidence of New-Onset Autoimmune Disease in Girls and Women with Pre-Existing
Autoimmune Disease After Quadrivalent Human Papillomavirus Vaccination: A Cohort Study, 280 J.
INTERNAL MED. 618 (2016).
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monitored for the development of a second form of autoimmunity after receiving the HPV
vaccination.” Id. (citing Resp’t’s Ex. H, Tab 19, ECF No. 86-20). According to Dr. Maverakis, the
increased susceptibility of autoimmune disease patients to additional autoimmune conditions
allowed for the monitoring of such patients, both vaccinated and unvaccinated, to track the
“development of a new form of autoimmunity [and] determine if a particular exposure, e.g. HPV
vaccination, increases the risk of autoimmunity.” Id. The Gronlund et al. study, which he discussed
at length, “not only failed to identify a positive association between the HPV vaccination and
autoimmunity, but it showed that patients who had received the HPV vaccination were less likely
to develop additional forms of autoimmunity.” Id. (citing Resp’t’s Ex. H, Tab 19). Dr. Maverakis
asserted that “we can confidently conclude that HPV vaccination does not predispose individuals
with autoimmunity to develop new onset autoimmunity.” Id. He conceded that the studies he relied
on do not specifically mention AA, however, he noted that “several AA-related autoimmune
diseases were indeed included.” Id.
Dr. Maverakis noted that “[t]he pathogenic immune response in AA has been extensively
studied[,] and NKG2D+ CD8+ T cells appear to be the main drivers” of the disease. Id. at 6. Dr.
Maverakis reiterated Dr. Levinson’s point that “in the majority of vaccinated individuals, vaccine-
specific CD8+ T cell responses are not detectable.” Id. (citing Resp’t’s Ex. H, Tab 23, ECF No.
86-24;88 Resp’t’s Ex. H, Tab 24, ECF No. 86-25).89 Specifically, “[w]hen CD8+ T cell responses
to the Gardasil vaccine were specifically studied, CD8 responses were below reliable detection.”
Id. (citing Resp’t’s Ex. H, Tab 24). He concluded that because the HPV vaccine does not activate
the relevant immune cells for AA pathology, “there is no reliable immunological link between the
pathophysiology of AA and the immune response induced by HPV vaccination.” Id.
In response to some of the points Dr. Gershwin made, Dr. Maverakis included a
Comment/Reply section at the end of his report. The replies were restatements of arguments
previously made by Respondent’s other experts and opinions Dr. Maverakis expressed at earlier
points in his report. He then reiterated that Petitioner’s causation theory is inconsistent with AA
pathogenesis, and Petitioner’s medical history, including atopy, is evidence of his susceptibility to
AA without relation to his HPV vaccination. See id. 6–9.
IV. Applicable Legal Standards
I am resolving Petitioner’s claim on the filed record. The Vaccine Act and Rules not only
contemplate but encourage special masters to decide petitions on the papers where, in the exercise
of their discretion, they conclude that doing so will properly and fairly resolve the case. See 42
U.S.C. § 12(d)(2)(D); Vaccine Rule 8(d). The decision to rule on the record in lieu of a hearing has
been affirmed on appeal. Kreizenbeck v. Sec’y of Health & Hum. Servs., 945 F.3d 1362, 1366 (Fed.
Cir. 2020); see also Hooker v. Sec’y of Health & Hum. Servs., No. 02-472V, 2016 WL 3456435, at
*21 n.19 (Fed. Cl. Spec. Mstr. May 19, 2016) (citing numerous cases where special masters
decided cases on the papers in lieu of hearing and those decisions were upheld). I am simply not
required to hold a hearing in every matter, no matter the preferences of the parties. Hovey v. Sec’y
of Health & Hum. Servs., 38 Fed. Cl. 397, 402–03 (1997) (determining that the special master
88 Gounwa Awad et al., Robust Hepatitis B Vaccine-Reactive T Cell Responses in Failed Humoral Immunity,
21 MOLECULAR THERAPY: METHODS CLINICAL DEV. 288 (2021).
89 Douglas M. Herrin et al., Comparison of Adaptive and Innate Immune Responses Induced by Licensed
Vaccines for Human Papillomavirus, 10 HUM. VACCINES & IMMUNOTHERAPEUTICS 3446 (2014).
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acted within his discretion in denying an evidentiary hearing); Burns v. Sec’y of Health & Hum.
Servs., 3 F.3d 415, 417 (Fed. Cir. 1993); Murphy v. Sec’y of Health & Hum. Servs., No. 90-882V,
1991 WL 71500, at *2 (Fed. Cl. Spec. Mstr. Apr. 19, 1991).
To receive compensation under the Vaccine Act, a petitioner must demonstrate either that:
(1) the petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently
developing a listed injury within the time frame prescribed by the Vaccine Injury Table set forth at
42 U.S.C. § 300aa-14, as modified by 42 C.F.R. § 100.3; or (2) that the petitioner suffered an “off-
Table injury,” one not listed on the Table, as a result of receiving a covered vaccine. See 42 U.S.C.
§§ 300aa-11(c)(1)(C); Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed. Cir.
2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1319–20 (Fed. Cir. 2006).
Petitioner does not allege a Table injury in this case; thus, he must prove that his injury was caused-
in-fact by a Table vaccine.
To establish causation-in-fact, a petitioner must demonstrate by a preponderance of the
evidence that the vaccine was the cause of the injury. 42 U.S.C. § 300aa-13(a)(1)(A). A petitioner
is required to prove that the vaccine was “not only a but-for cause of the injury but also a substantial
factor in bringing about the injury.” Moberly, 592 F.3d at 1321–22 (quoting Shyface v. Sec’y of
Health & Hum. Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)).
In the seminal case of Althen v. Sec’y of Health & Hum. Servs., the Federal Circuit set forth
a three-pronged test used to determine whether a petitioner has established a causal link between
a vaccine and the claimed injury. See 418 F.3d 1274, 1278–79 (Fed. Cir. 2005). The Althen test
requires petitioners to set forth: “(1) a medical theory causally connecting the vaccination and the
injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for
the injury; and (3) a showing of a proximate temporal relationship between vaccination and injury.”
Id. at 1278. To establish entitlement to compensation under the Program, a petitioner is required
to establish each of the three prongs of Althen by a preponderance of the evidence. Id. “[C]lose
calls regarding causation are resolved in favor of injured claimants.” Id. at 1280. Further, evidence
used to satisfy one prong of the test may overlap to satisfy another prong. Capizzano, 440 F.3d at
1326.
A petitioner who satisfies all three prongs of the Althen test has established a prima facie
showing of causation. Hammitt v. Sec’y of Health & Hum. Servs., 98 Fed. Cl. 719, 726 (2011). A
petitioner who demonstrates by a preponderance of the evidence that he suffered an injury caused
by vaccination is entitled to compensation unless the respondent can demonstrate by a
preponderance of the evidence that the injury was caused by factors unrelated to the vaccination.
See Althen, 418 F.3d at 1278; Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 547 (Fed.
Cir. 1994). In such a case, the government must not merely prove the existence of an alternative
cause, but that such an alternative actually caused the injury. Knudsen, 35 F.3d at 549.
Consequently, when and if the petitioner establishes a prima facie case, the burden then shifts to
the government to prove that an alternative cause, unrelated to the administration of the vaccine,
was the “sole substantial factor” in causing the alleged injury. See de Bazan v. Sec’y of Health &
Hum. Servs., 539 F.3d 1347, 1354 (Fed. Cir. 2008); see also Hammitt, 98 Fed. Cl. at 726
(explaining that the respondent’s burden is to show that the “factor unrelated” was the “sole
substantial factor” in causing the injury). Additionally, a factor unrelated “may not include ‘any
idiopathic, unexplained, unknown, hypothetical, or undocumentable cause, factor, injury, illness
or condition.’” 42 U.S.C. § 300aa-13(a)(2); see also Doe v. Sec’y of Health & Hum. Servs., 601
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F.3d 1349 (Fed. Cir. 2010) (stating that an idiopathic diagnosis cannot be a “factor unrelated,” as
it is idiopathic).
V. Discussion
A. Althen Prong One
Under the first prong of Althen, a petitioner must offer a scientific or medical theory that
answers in the affirmative the question: “can the vaccine[] at issue cause the type of injury
alleged?” See Pafford v. Sec’y of Health & Hum. Servs., No. 01-0165V, 2004 WL 1717359, at *4
(Fed. Cl. Spec. Mstr. July 16, 2004), mot. for rev. denied, 64 Fed. Cl. 19 (2005), aff’d, 451 F.3d
1352 (Fed. Cir. 2006). A petitioner’s theory must be based on a “sound and reliable medical or
scientific explanation.” Knudsen, 35 F.3d at 548. Such a theory must only be “legally probable,
not medically or scientifically certain.” Id. at 548–49. Petitioners are not required to identify
“specific biological mechanisms” to establish causation, nor are they required to present
“epidemiologic studies, rechallenge[] the presence of pathological markers or genetic disposition,
or general acceptance in the scientific or medical communities.” Capizzano, 440 F.3d at 1325
(quoting Althen, 418 F.3d at 1280). Scientific and “objective confirmation” of the medical theory
with additional medical documentation is unnecessary. Althen, 418 F.3d at 1278–81; see also
Moberly, 592 F.3d at 1322. However, as the Federal Circuit has made clear, “simply identifying a
‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of proof.” LaLonde
v. Sec’y of Health & Hum. Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014) (citing Moberly, 592 F.3d
at 1322). Indeed, the Federal Circuit has “consistently rejected theories that the vaccine only ‘likely
caused’ the injury and reiterated that a ‘plausible’ or ‘possible’ causal theory does not satisfy the
standard.” Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, (Fed. Cir. 2019) (citing
Moberly, 592 F.3d at 1322 and LaLonde, 746 F.3d at 1339). Rather, “[a] petitioner must provide
a reputable medical or scientific explanation that pertains specifically to the petitioner’s case.”
Moberly, 592 F.3d at 1322. In general, “the statutory standard of preponderance of the evidence
requires a petitioner to demonstrate that the vaccine more likely than not caused the condition
alleged.” LaLonde, 746 F.3d at 1339.
Presently, Petitioner does not establish that it is more likely than not that the HPV vaccine
can cause AA. His theory that molecular mimicry between viral antigens in Gardasil and self-
antigens expressed on the hair follicle led to the development of AA is not supported by sufficient
reliable evidence. In his expert report, Dr. Gershwin opined that “[t]he mechanism that leads to
alopecia includes [] genetic susceptibility and the generation of cytotoxic CD8 T cells.” Pet’r’s Ex.
16 at 5. Specifically, he asserted that the vaccine “produced cytotoxic T cells that were directed at
[Petitioner’s] hair follicles and which cross react with an epitope or region of the Gardasil vaccine.”
Id. This iteration of molecular mimicry begins with the HPV vaccine and ends with AA. For this
sequence to compose a successful theory, all these pieces must work together, even if it is not quite
understood how. Petitioner did not present reliable evidence of the assumed intermediate step: the
HPV vaccine’s role in the production of CD8+ T cells. This is where the theory fails.
While Petitioner does not need to rely on medical literature specifically to support his
theory, he must still provide some form of preponderant evidence that his proposed mechanism
can or does occur. Dr. Gershwin filed four different expert reports with accompanying medical
literature but did not identify persuasive support for his contention that the Gardasil vaccine
induces the production of cytotoxic T cells.
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Dr. Gershwin cited an article from Colmenares et al. to assert that this literature “notes the
imbalance of CD8 T cells following Gardasil vaccine.” Pet’r’s Ex. 99 at 2. The imbalance that the
authors observed was a decrease in certain CD8+ lymphocytes, but an increase “in the density
(MFI) of [the ILT2] receptor in these cells.” Pet’r’s Ex. 105 at 7. The article does not discuss how
this imbalance is related to AA pathology or autoimmune disease in general. In fact, the authors
viewed their findings as indications “that HPV immunization is associated with significant changes
in the expression and function of immune innate and regulatory receptors, phenomena that may
contribute to the protective effect of this vaccine.” Id. The article did not address Dr. Gershwin’s
contention that HPV vaccination leads to the production of CD8+ cytotoxic cells.
Dr. Gershwin acknowledged the de minimis effect that the addition of an aluminum
adjuvant has on cellular mediated immunity. However, he asserted that the addition of polysorbate
80 to Gardasil enables the vaccine to elicit not only stronger cellular immunity but also the
production of cytotoxic CD8+ T cells. See Pet’r’s Ex. 106 at 1–2. Dr. Levinson disputed Dr.
Gershwin’s opinion and asserted that “the principle immune response elicited by an aluminum
compound-[adjuvanted] vaccine is essentially an antibody response.” Resp’t’s Ex. E at 3. Dr.
Levinson further stated that “vaccines [adjuvanted] with aluminum salts, are very effective
generating potent antibody responses but are ineffective generating protective cell-mediated
immune responses, especially cytotoxic T cell responses.” Id. Dr. Maverakis similarly noted that
“[t]raditional vaccines predominantly activate CD4 T cells and B cells. CD8 T cells are not strongly
activated by traditional vaccines.” Resp’t’s Ex. H at 7. Respondent’s argument is more persuasive.
Dr. Gershwin’s response that Dr. Levinson’s argument is not supported by “a single paper that
states that CD8 responses do not occur or are not possible,” highlights the same problem for his
argument. Pet’r’s Ex. 116 at 1. There is no medical literature that provides persuasive support for
Dr. Gershwin’s contention that the Gardasil vaccine results in the production of cytotoxic T cells.
Respondent does not have the burden of proof unless and until Petitioner presents a prima facie
case. In this case, Petitioner did not meet this burden.
Dr. Gershwin further pointed to the Macleod et al. publication and asserted that there exists
an immunomodulatory molecule in Gardasil that enables this vaccine with the capacity to induce
functionally active CD8+ T cells in an immunized host. See Pet’r’s Ex. 106 at 1 (citing Pet’r’s Ex.
108). However, this publication investigated the immunomodulatory agent, MPLA, and did not
connect immunomodulatory agents within the Gardasil vaccine to the development of cytotoxic T
cells. The article specifically discussed influenza vaccinations, and the authors stated, “effective
cytotoxic T-cell differentiation occurred only in the presence of [aluminum and] an additional
adjuvant, [MPLA].” Pet’r’s Ex. 108 at 1. Dr. Gershwin referred to this article to show that certain
agents, when added to a vaccine, can promote cytotoxic T cells. He further stated that “[t]he use
of other materials in vaccines, when alum is included, to facilitate cell-mediated immunity has
been known for decades,” but ultimately failed to point to MPLA or another immunomodulatory
agent within the Gardasil vaccine that produces cytotoxic T cells. Pet’r’s Ex. 106 at 2 (citing Pet’r’s
Ex. 112).
In one of his supplemental reports, Dr. Gershwin clarified his opinion that Petitioner
“would not have developed alopecia if he did not uniquely have an antigen in his hair follicles that
was cross-reactive with a component of the HPV vaccine.” Id. Thus, he claimed, this self-antigen
that was always present was the basis for the “continued production of cytotoxic CD8 T cells and
subsequent alopecia.” Id. Dr. Gershwin asserted that this self antigen is a necessary condition for
the development of AA following HPV vaccination; however, he does not provide preponderant
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evidence of the presence of a unique antigen that is distinct from the generally accepted genetic
predisposition that some individuals have to autoimmune disease. Furthermore, the studies that Dr.
Gershwin cited did not mention AA at all. In fact, there was no connection made between exposure
to any vaccination and the development of an autoimmune disease due to the production of CD8+
T cells.
In Farag and Cordova, Dr. Gershwin was also the petitioners’ expert asserting a causal
relationship between the HPV vaccine and AA. Farag v. Sec’y of Health & Hum. Servs., No. 17-
714V, 2023 WL 7203034 (Fed. Cl. Spec. Mstr. Sept. 29, 2023); Cordova v. Sec’y of Health & Hum.
Servs., No. 17-1282V, 2021 WL 3285367 (Fed. Cl. Spec. Mstr. June 21, 2021). Similar to this case,
in Farag, the petitioner did not file “a single article indicating that the HPV vaccine can or does
produce cytotoxic T cells.” 2023 WL 7203034, at *20. I concluded that the petitioner failed to
present preponderant evidence that the HPV vaccine could cause AA via the upregulation of
cytotoxic T cells. Id. In Cordova, the petitioner presented “a few small-scale studies aimed at
evaluating the immunogenicity of the HPV vaccine, noting that they suggest some increased T cell
upregulation after receipt of the vaccine.” 2021 WL 3285367, at *17. Nonetheless, the Chief
Special Master ultimately found that the articles did not show an increase in T cells that was “(a)
[]likely causal of AA, or (b) even involve[] the specific kind of cytotoxic T cells that drive AA.”
Id. Petitioner was unsuccessful in this case as well. Although special masters are not bound by
self-authored prior decisions or the decisions of other special masters, these cases can be helpful
in the evaluation of evidence that has been previously introduced and considered in the Program.
Dr. Levinson asserted that “there is no evidence in the extant scientific literature that
supports the contention that any type of molecular mimicry accounts for the autoimmune
destruction of hair cells in AA.” Resp’t’s Ex. E at 1. In her expert report, Dr. Senna explained that
there was no evidence that the HPV vaccine caused AA or autoimmune disease. See Resp’t’s. Ex.
C at 11. Her report relied on data analysis, where “[a] large meta-analysis on six studies on bivalent
and quadrivalent HPV vaccines showed that in 243,289 patients who received the HPV vaccines
there was no correlation between autoimmune disorders and HPV vaccination.” Id.; see Resp’t’s
Exhibit C, Tab 50. Further, she cited VAERS to state that no reports of AA or other forms of hair
loss were reported in females and males who received HPV vaccination between 2009 through
2015. Id. (citing Resp’t’s Ex. C, Tab 52, ECF No. 62-2).90 In Dr. Maverakis’ report, he noted that
“[t]here is no evidence that HPV vaccination causes, or significantly aggravates, preexisting
autoimmunity. In fact, when at risk individuals were studied, HPV vaccination was associated with
a reduced risk of autoimmunity, i.e., HPV vaccination was protective for autoimmunity.” Resp’t’s
Ex. H at 9. He then pointed to the Gronlund et al. study, which “not only failed to identify a positive
association between HPV vaccination and autoimmunity, but it showed that patients who had
received the HPV vaccination were less likely to develop additional forms of autoimmunity.” Id.
at 5 (citing Resp’t’s Ex. H, Tab, 19). Due to the rare occurrence rate of many of the injuries that
are examined in the Vaccine Program, it is often difficult, if not impossible, to find relevant studies
to prove or disprove vaccine causation. Consequently, this type of evidence is not required to bring
a successful claim. However, to the extent that studies do exist, they can be used to support or
rebut a theory that a petitioner presents. In the present case, the vaccination is widespread, and the
disease incident rate is over one percent of the population. Respondent’s experts have persuasively
90 Jorge E. Arana et al., Post-Licensure Safety Monitoring of Quadrivalent Human Papillomavirus
Vaccine in the Vaccine Adverse Event Reporting System (VAERS), 2009-2015, 36 VACCINE 1781 (2018).
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used studies that fail to show a correlation as supporting evidence that the proposed mechanism is
faulty. Dr. Gershwin is not required to identify large scale studies or conclusive literature.
However, he failed to persuasively rebut the arguments and support provided by Respondent’s
experts. Petitioner must do more than demonstrate a ‘plausible’ or ‘possible’ causal link between
the vaccination and the injury. W.C. v. Sec’y of Health & Hum. Servs., 704 F.3d at 1356 (Fed. Cir.
2013).
Dr. Gershwin presented the Tu et al. article to show “increased incidence of [AA] after
HPV infection.” Pet’r’s Ex. 116 at 1 (citing Pet’r’s Ex. 118). His reliance on this article does not
provide preponderant support for his proposition because the article “reviewed patient medical
records spanning a period of approximately twelve years, and they did not indicate when the
patients in the HPV group developed AA relative to the onset of their HPV symptoms or the date
they were infected with HPV.” Farag, 2023 WL 7203034 at *22. Further, the results are limited in
application because the underlying data is derived from a mono-country evaluation, which may
not be applicable to non-Asian ethnic groups, and the authors did not incorporate data regarding
HPV vaccination.
Lastly, even if the HPV vaccine could induce a pathologic cytotoxic T cell response,
Petitioner has failed to demonstrate by preponderant evidence the second component of his theory,
that such a response could destroy the immune privilege of the hair follicle to cause AA. Although
Program petitioners often present homologies between vaccine components and human tissues,
such is not required to present preponderant support for a theory of molecular mimicry. However,
petitioners must present some form of preponderant evidence that a cross reaction between the
vaccine and the body part at issue can occur. Indeed, “[p]etitioners cannot simply invoke the
concept of molecular mimicry and call it a day. . . . Rather, they need to offer reliable and
persuasive medical or scientific evidence of some kind . . . that suggests the vaccine components
could interact with self structures as maintained.” Johnson v. Sec’y of Health & Hum. Servs., No.
14-254V, 2018 WL 2051760, at *26 (Fed. Cl. Spec. Mstr. Mar. 23, 2018). Petitioner has not
provided preponderant evidence that the HPV vaccine can cause AA, pursuant to Althen prong
one.
B. Althen Prong Two
Under the second prong of Althen, a petitioner must prove that the vaccine actually did
cause the alleged injury in a particular case. See Pafford, 2004 WL 1717359, at *4; Althen, 418
F.3d at 1279. The second Althen prong requires proof of a logical sequence of cause and effect,
usually supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278;
Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956 F.2d 1144, 1148 (Fed.
Cir. 1992). A petitioner does not meet this obligation by showing only a temporal association
between the vaccination and the injury; instead, the petitioner “must explain how and why the
injury occurred.” Pafford, 2004 WL 1717359, at *4 (emphasis in original). The special master in
Pafford noted petitioners “must prove [] both that her vaccinations were a substantial factor in
causing the illness . . . and that the harm would not have occurred in the absence of the
vaccination.” 2004 WL 1717359, at *4 (citing Shyface, 165 F.3d at 1352). A reputable medical or
scientific explanation must support this logical sequence of cause and effect. Hodges v. Sec’y of
Health & Hum. Servs., 9 F.3d 958, 961 (Fed Cir. 1993) (citation omitted). Nevertheless,
“[r]equiring epidemiologic studies . . . or general acceptance in the scientific or medical
communities . . . impermissibly raises a claimant’s burden under the Vaccine Act and hinders the
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system created by Congress . . . .” Capizzano, 440 F.3d at 1325–26. “[C]lose calls regarding
causation are resolved in favor of injured claimants.” Althen, 418 F.3d at 1280.
In Program cases, contemporaneous medical records and the opinions of treating
physicians are favored. Capizzano, 440 F.3d at 1326 (citing Althen, 418 F.3d at 1280). Indeed,
when reviewing the record, a special master must consider the opinions of treating physicians.
Capizzano, 440 F.3d at 1326. This is because “treating physicians are likely to be in the best
position to determine whether ‘a logical sequence of cause and effect show[s] that the vaccination
was the reason for the injury.’” Id. In addition, “[m]edical records, in general, warrant
consideration as trustworthy evidence. The records contain information supplied to or by health
professionals to facilitate diagnosis and treatment of medical conditions. With proper treatment
hanging in the balance, accuracy has an extra premium. These records are also generally
contemporaneous to the medical events.” Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d
1525, 1528 (Fed. Cir. 1993). While a special master must consider these opinions and records, they
are not “binding on the special master or court.” 42 U.S.C. § 300aa-13(b)(1). Rather, when
“evaluating the weight to be afforded to any such . . . [evidence], the special master . . . shall
consider the entire record . . . .” Id.
Petitioner has not established a logical sequence of cause and effect between his
vaccination and his AA. In his initial expert report, Dr. Gershwin asserted that “the kinetics of
appearance of cytotoxic T cells after vaccination can occur within several days.” Pet’r’s Ex. 16 at
5. In Petitioner’s case, Dr. Gershwin opined that “[o]nset within 14 days would certainly be
consistent with generation of a CD8 response,” and that there was no other immunological
challenge to Petitioner’s system during this period. Id. In a subsequent report, Dr. Gershwin argued
that Petitioner “would not have developed alopecia if he did not uniquely have an antigen in his
hair follicles that was cross-reactive with a component of the HPV vaccine.” Pet’r’s Ex. 106 at 2.
A review of Dr. Gershwin’s four expert reports reveals brief discussions of Petitioner’s specific
facts and circumstances to establish a logical sequence of cause and effect. While petitioners’
experts usually find support for specific causation within a petitioner’s medical records, there is
no requirement that medical records must be used to establish that a specific vaccine caused a
specific injury in a specific person. Here, Petitioner has failed to present preponderant evidence
that he experienced an autoimmune reaction following any of his HPV vaccinations. While this
evidence is not mandatory, evidence of such a reaction could support Petitioner’s contention that
his vaccination caused autoimmunity, which then led to his injury. Of note is Dr. Senna’s
observation that “[Petitioner] was not reported to experience even the most commonly reported
adverse effects after any of his [three] HPV vaccines, including local injection site reactions,
syncope, dizziness or other symptoms.” Resp’t’s Ex. C at 12. Petitioner’s remaining argument for
causation would be based solely on temporal proximity. It is well established in the Program that
temporal proximity between a vaccination and injury is insufficient to support causation. Moberly,
592 F.3d at 1323 (quoting Althen, 418 F.3d at 1278) (“[N]either a mere showing of a proximate
temporal relationship between vaccination and injury, nor a simplistic elimination of other
potential causes of the injury suffices, without more, to meet the burden of showing actual
causation.”); Sumner v. Sec’y of Health & Hum. Servs., No. 99-946V, 2015 WL 5173644, at *9
(Fed. Cl. Spec. Mstr. Aug. 13, 2015) (“[W]here a petitioner’s expert views the temporal
relationship as the ‘key’ indicator of causation, the claim must fail.”).
Ultimately, Dr. Gershwin was unable to identify anything in Petitioner’s medical history
besides temporal proximity to connect his vaccination and injury. See Cordova, 2021 WL 3285367,
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at *18 (finding that the petitioner did not satisfy Prong Two because “only a temporal association
links his AA onset to the first HPV dose . . . [and because t]here is no evidence of any immediate
reaction or measured autoimmune/inflammatory process that preceded onset.”). In fact, he did not
identify key symptoms, test results, or other evidence that, if present, would signal an adverse
reaction to the HPV vaccine leading to the development of AA. The fact that Petitioner’s AA began
post vaccination is not itself enough to meet the burden articulated as Althen prong two. See id.
Dr. Gershwin’s opinion also noted that “[t]he only immunological challenge within that
window was the HPV vaccination.” Pet’r’s Ex. 16 at 5. However, Dr. Senna noted that a number
of potential triggers and risk factors besides the HPV vaccine may have played a role in this case,
including “a history of atopy (allergic rhinitis, seasonal allergies), development at a young age (age
13), and AA affecting the occiput scalp or the ophiasis pattern.” Resp’t’s Ex. C at 12. She further
noted that Petitioner “had [three] of the total [eight] known associated risk factors for poor AA
prognosis, [which] unequivocally suggests that this is a patient who despite any other exogenous
influences is more likely than not to progress to severe [AA].” Id. at 13. Dr. Senna identified a
specific period in Petitioner’s life that may have triggered his AA. Petitioner’s “maternal
grandmother had been diagnosed with bladder cancer at a time that his mother was teaching and
in graduate school.” Id. at 14. Dr. Senna noted that “[a]lthough [Petitioner] is clearly a resilient
young man, it is not infrequent that stressors like this contribute to hair follicle immune collapse
in genetically predisposed patients even in the most stoic pediatric patients.” Id. While petitioners
can prevail on Prong Two without necessarily addressing alternative causes, the existence of
possible alternative causes underlies why temporal proximity alone is insufficient. See Winkler v.
Sec’y of Health & Human Servs., 88 F.4th 958 (Fed. Cir. 2023). Petitioner has not provided
preponderant evidence that Petitioner’s HPV vaccination caused him to develop AA, pursuant to
Althen prong two.
C. Althen Prong Three
To satisfy the third Althen prong, a petitioner must establish a “proximate temporal
relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This
“requires preponderant proof that the onset of symptoms occurred within a timeframe for which,
given the medical understanding of the disorder’s etiology, it is medically acceptable to infer
causation-in-fact.” de Bazan, 539 F.3d at 1352. Typically, “a petitioner’s failure to satisfy the
proximate temporal relationship prong is due to the fact that onset was too late after the
administration of a vaccine for the vaccine to be the cause.” Id. However, “cases in which onset is
too soon” also fail this prong; “in either case, the temporal relationship is not such that it is
medically acceptable to conclude that the vaccination and the injury are causally linked.” Id.; see
also Locane v. Sec’y of Health & Hum. Servs., 685 F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the
illness was present before the vaccine was administered, logically, the vaccine could not have
caused the illness.”).
Although a temporal association alone is insufficient to establish causation, under the third
prong of Althen, a petitioner must show that the timing of the injury fits with the causal theory.
See Althen, 418 F.3d at 1278. The special master cannot infer causation from temporal proximity
alone. See Thibaudeau v. Sec’y of Health & Hum. Servs., 24 Cl. Ct. 400, 403–04 (1991); see also
Grant, 956 F.2d at 1148 (“[T]he inoculation is not the cause of every event that occurs within the
ten[-]day period . . . [w]ithout more, this proximate temporal relationship will not support a finding
of causation.” (quoting Hasler v. United States, 718 F.2d 202, 205 (6th Cir. 1983))).
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Dr. Gershwin stated that “the kinetics of appearance of cytotoxic T cells after vaccination can
occur within several days[.]” Pet’r’s Ex. 16 at 5. He then opined that the “onset within l4 days
would certainly be consistent with generation of a CD8 response.” Id. Thus, he concluded that
“[b]ased on the literature, the kinetics herein are a medically appropriate time frame from exposure
to antigen challenge and the development of autoimmunity based upon on genetic susceptibility
and the generation of CD8 cytotoxic cells.” Id. However, the medical evidence and affidavits in
this case are inconsistent with Dr. Gershwin’s theory. Petitioner received his third Gardasil
vaccination on March 30, 2015, and according to Petitioner’s mother, she began to notice an
“unusual amount of hair in [Petitioner’s] bathroom” around “mid-late April” Pet’r’s Ex. 13 at ¶ 7.
She then noticed a small ball spot on Petitioner’s head on or around May 4, 2015. Petitioner’s
symptoms were noticed at the earliest, 22 days post vaccination, and at the latest, 32 days post
vaccination. While Dr. Gershwin’s theory is based on onset within 14 days of vaccination, there is
no evidence that Petitioner’s AA developed within 14 days. Petitioner has not provided
preponderant evidence that Petitioner’s onset of AA is consistent with the timeframe articulated
by Dr. Gershwin’s causation theory, pursuant to Althen prong three.
VI. Conclusion
After a careful review of the record, Petitioner has failed to prove by preponderant
evidence that his AA was caused-in-fact by his HPV vaccination. Accordingly, I DENY
Petitioner’s claim and DISMISS his petition.91
IT IS SO ORDERED.,
s/Herbrina D.S. Young
Herbrina D.S. Young
Special Master
91 Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of a notice
renouncing the right to seek review.
27