VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_17-vv-00714
Package ID: USCOURTS-cofc-1_17-vv-00714
Petitioner: Zacharia Farag
Filed: 2017-05-31
Decided: 2023-11-01
Vaccine: HPV
Vaccination date: 2016-05-16
Condition: alopecia areata totalis
Outcome: denied
Award amount USD: 

AI-assisted case summary:
On May 31, 2017, Lynn Farag filed a petition for compensation on behalf of her son, Zacharia Farag, alleging that the human papillomavirus (HPV) vaccine administered on May 16, 2016, caused him to develop alopecia areata totalis. Zacharia Farag was 12 years old at the time of vaccination. His mother reported that he first noticed hair loss around Memorial Day weekend of 2016, approximately two weeks after the vaccination, and that his condition progressed to total hair loss by November 2016. The petition detailed Zacharia's medical history, including a diagnosis of autism and strep throat prior to vaccination. Following the vaccination, he presented with complaints of hair loss, initially diagnosed as tinea barbae and tinea capitis, but later assessed as alopecia areata (AA) by a dermatologist. His condition worsened over time, leading to complete loss of scalp, brow, lash, and body hair by November 2016. Various treatments were attempted, including topical corticosteroids, sulfasalazine, and later immunotherapy with SADBE and diphenylcyclopropenone (DPCP), with limited success and some adverse effects like anemia and behavioral changes. Petitioner's expert, M. Eric Gershwin, M.D., proposed a theory of molecular mimicry, suggesting the HPV vaccine triggered cytotoxic T cells that attacked hair follicles. Respondent's expert, Mehrdad Matloubian, M.D., Ph.D., argued that the link between the HPV vaccine and alopecia areata is speculative and not supported by scientific literature, pointing to genetics and other potential triggers like stress or microbiome changes. The Special Master, Herbrina Sanders, reviewed the evidence, including medical records, affidavits, and expert testimony. The court found that Petitioner failed to establish a medical theory causally connecting the vaccine to the injury (Althen Prong One) or a logical sequence of cause and effect (Althen Prong Two). While a proximate temporal relationship was met (Althen Prong Three), the overall claim was denied because Petitioner did not prove by a preponderance of the evidence that the HPV vaccine caused his alopecia areata totalis. The petition was dismissed. Petitioner was represented by Mark T. Sadaka of the Law Offices of Sadaka Associates, LLC, and Respondent was represented by Dorian Hurley of the United States Department of Justice.

Theory of causation field:
Petitioner alleged that the HPV vaccine administered on May 16, 2016, caused Zacharia Farag to develop alopecia areata totalis (AA) through a theory of molecular mimicry. Petitioner's expert, Dr. M. Eric Gershwin, proposed that the vaccine produced cytotoxic T cells that cross-reacted with hair follicles, leading to AA. Dr. Gershwin cited the mouse model of AA and the presence of CD8+ T cells in affected follicles as support. He acknowledged that the HPV vaccine is not designed to produce CD8 T cells but argued it was theoretically possible for Petitioner to be a rare individual who experienced such a response. Dr. Gershwin also submitted case reports and studies linking various vaccines and viral infections (including HPV infection) to hair loss and AA, but acknowledged limitations in these studies and the difficulty in proving molecular mimicry. Respondent's expert, Dr. Mehrdad Matloubian, countered that there is no scientific literature supporting the HPV vaccine's ability to induce cytotoxic T cells or a link between the HPV vaccine and AA. Dr. Matloubian emphasized the strong genetic component of AA, the lack of established environmental triggers, and the implausibility of molecular mimicry with HPV vaccine components given the differences between HPV and the vaccine's antigens. He suggested alternative causes like stress or microbiome changes. The Special Master found that Petitioner failed to provide preponderant evidence that the HPV vaccine can induce cytotoxic T cells or that it caused AA via molecular mimicry, thus failing Althen Prong One. The Special Master also found Petitioner failed to establish a logical sequence of cause and effect (Althen Prong Two), relying solely on temporal proximity. The proximate temporal relationship (Althen Prong Three) was met, with symptoms appearing approximately two weeks post-vaccination. Ultimately, the petition was denied because Petitioner did not prove causation by a preponderance of the evidence.

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_17-vv-00714-1
Date issued/filed: 2023-11-01
Pages: 34
Docket text: PUBLIC DECISION (Originally filed: 09/29/2023) regarding 86 DECISION of Special Master. Signed by Special Master Herbrina Sanders. (rig) Service on parties made.
--------------------------------------------------------------------------------
Case 1:17-vv-00714-UNJ Document 88 Filed 11/01/23 Page 1 of 34
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: September 29, 2023
* * * * * * * * * * * * * * *
ZACHARIA FARAG, * No. 17-714V
*
Petitioner, * Special Master Sanders
*
v. *
*
SECRETARY OF HEALTH *
AND HUMAN SERVICES, *
*
Respondent. *
* * * * * * * * * * * * * * *
Mark T. Sadaka, Law Offices of Sadaka Associates, LLC, Englewood, NJ, for Petitioner.
Dorian Hurley, United States Department of Justice, Washington, DC, for Respondent.
DECISION ON ENTITLEMENT1
On May 31, 2017, Lynn Farag filed a petition for compensation in the National Vaccine
Injury Compensation Program (“the Program”)2 on behalf of her then-minor son Zacharia Farag
(“Petitioner”). Pet., ECF No. 1. Ms. Farag alleged that the human papillomavirus (“HPV”) vaccine
Petitioner received on May 16, 2016, caused him to suffer from alopecia areata (“AA”)3 totalis.4
See generally id.
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 (2012).
3 Alopecia areata is “patchy, nonscarring, asymmetric hair loss, sometimes reversible, occurring in
sharply defined areas of the scalp or beard.” Dorland’s Illustrated Medical Dictionary 53 (33rd ed. 2020)
[hereinafter “Dorland’s”].
4 Total alopecia, or alopecia totalis, is “complete loss of hair from the entire scalp, resulting from
progression of alopecia areata.” Dorland’s at 53.

Case 1:17-vv-00714-UNJ Document 88 Filed 11/01/23 Page 2 of 34
After carefully analyzing and weighing all the evidence and testimony presented in this
case in accordance with the applicable legal standards,5 I find that Petitioner has failed to provide
preponderant evidence that the HPV vaccine he received on May 16, 2016, caused him to develop
alopecia. Accordingly, Petitioner is not entitled to compensation.
I. Procedural History
Ms. Farag filed a petition on behalf of Petitioner on May 31, 2017. Pet. Ms. Farag filed
medical records on June 6, 2017, as well as additional medical records and a statement of
completion on July 11, 2017. Pet’r’s Exs. 1–2, ECF No. 6; Pet’r’s Exs. 3–4, ECF No. 8; ECF No.
9.
On September 19, 2017, Respondent filed his Rule 4(c) report recommending that
compensation be denied. Resp’t’s Report, ECF No. 11. Following a Rule 5 conference held on
October 17, 2017, I directed Ms. Farag to file an expert report. Order at 1, ECF No. 12. On October
18, 2017, Ms. Farag filed photographs documenting Petitioner’s injury. Pet’r’s Ex. 5, ECF No. 13-
1. She then filed her affidavit on November 9, 2017. Pet’r’s Ex. 6, ECF No. 14-1.
On November 21, 2017, Ms. Farag filed an expert report from M. Eric Gershwin, M.D.
Pet’r’s Ex. 7, ECF No. 15-1. Ms. Farag submitted medical literature on December 6, 2017. Pet’r’s
Exs. 8–17, ECF No. 17; Pet’r’s Exs. 18–27, ECF No. 18; Pet’r’s Exs. 28–37, ECF No. 19; Pet’r’s
Exs. 38–47, ECF No. 20. Pet’r’s Exs. 48–57, ECF No. 21; Pet’r’s Exs. 58–67, ECF No. 22; Pet’r’s
Exs. 68–77, ECF No. 23; Pet’r’s Exs. 78–80, ECF No. 24. Respondent filed an expert report from
Mehrdad Matloubian, M.D., Ph.D., as well as his curriculum vitae (“CV”) and accompanying
medical literature, on February 23, 2018. Resp’t’s Exs. A, A, Tabs 1–9, ECF No. 29; Resp’t’s Exs.
A, Tabs 10–16, B, ECF No. 30. Ms. Farag filed a supplemental expert report from Dr. Gershwin
and accompanying medical literature on March 22, 2018. Pet’r’s Exs. 81–90, ECF No. 32.
Respondent followed with a supplemental expert report from Dr. Matloubian on June 20, 2018.
Resp’t’s Ex. C, ECF No. 35-1.
I held a status conference in this case on August 7, 2018, and the parties agreed that Ms.
Farag would submit a settlement demand. Order at 1, ECF No. 38. After Ms. Farag submitted a
settlement demand, Respondent filed a status report on December 21, 2018, stating that he was not
interested in pursuing settlement. ECF No. 42. On December 24, 2018, Ms. Farag filed a status
report requesting that this case be set for an entitlement hearing. ECF No. 43. Ms. Farag filed an
additional medical record on February 22, 2021. Pet’r’s Ex. 91, ECF No. 51-1. On June 28, 2021,
I issued a decision awarding Petitioner’s counsel interim attorneys’ fees and costs. ECF No. 52.
On January 25, 2022, I set an entitlement hearing in this case for July 25–July 26, 2022.
Hearing Order, ECF No. 56. Ms. Farag filed a prehearing brief on May 27, 2022. Pet’r’s Prehearing
Br., ECF No. 58. She filed Dr. Gershwin’s CV on June 13, 2022. Pet’r’s Ex. 92, ECF No. 60-1.
5 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.”).
2

Case 1:17-vv-00714-UNJ Document 88 Filed 11/01/23 Page 3 of 34
Respondent submitted his prehearing brief on June 27, 2022. Resp’t’s Prehearing Br., ECF No.
61. On June 28, 2022, I directed the clerk of court to amend the caption in this case because
Petitioner reached the age of majority. Order at 1, ECF No. 62. Respondent filed Dr. Matloubian’s
updated CV and medical literature on July 18, 2022. Resp’t’s Exs. D–E, ECF No. 64. Petitioner
filed additional medical literature and updated photos of his injury on July 18, 2022. Pet’r’s Exs.
93–99, ECF No. 70; Pet’r’s Ex. 100, ECF No. 71-1. Petitioner filed an affidavit on July 21, 2022,
and an additional piece of medical literature on July 22, 2022. Pet’r’s Ex. 101, ECF No. 74-1;
Pet’r’s Ex. 102, ECF No. 75-1.
An entitlement hearing was held remotely on July 25, 2022. Min. Entry, docketed July 25,
2022. Petitioner filed additional medical literature and a post-hearing brief on October 18, 2022.
Pet’r’s Exs. 103–09, ECF No. 81; Pet’r’s Post-hearing Br., ECF No. 82. Respondent filed a
responsive brief and medical literature on December 5, 2022. Resp’t’s Post-hearing Br., ECF No.
83; Resp’t’s Exs. F–H, ECF No. 84. Petitioner filed a reply on January 4, 2023. Pet’r’s Reply, ECF
No. 85.
This matter is now ripe for consideration.
II. Factual Background
A. Medical Records
Petitioner was born on February 17, 2004, and his pre-vaccination medical history is
significant for autism. Pet’r’s Ex. 2 at 6, ECF No. 6-2. On September 25, 2013, Petitioner’s
pediatrician indicated that “vaccine reactions have been reviewed.”6 Id. On March 8, 2016,
Petitioner was diagnosed with strep throat and prescribed antibiotics by a pediatrician. Id. at 21–
22. He received the Gardasil vaccine at issue during a well-child visit with his pediatrician, Dr.
Jean Makhlouf, on May 16, 2016. Id. at 2, 23–27.
On June 20, 2016, Petitioner returned to Dr. Makhlouf with “complaints of hair loss on
hairline near [his] forehead.” Id. at 28. Dr. Makhlouf’s assessment was tinea barbae7 and tinea
capitis.8 Id. at 29. She prescribed griseofulvin9 but noted that Petitioner potentially had alopecia.
Id. She advised Petitioner to return in seven to ten days for a dermatology referral if his condition
did not improve. Id.
On June 24, 2016, Petitioner presented to Dr. Andrea Kassim, a dermatologist, after
receiving a referral from Dr. Makhlouf. Pet’r’s Ex. 1 at 20, ECF No. 6-1. Petitioner reported that
he was not seeing improvement after four days of griseofulvin treatment. Id. Dr. Kassim assessed
Petitioner with AA on his scalp and directed him to discontinue griseofulvin. Id. at 22. Dr. Kassim
6 It is unclear whether this means that Petitioner experienced adverse reactions to previous vaccinations.
7 Tinea is “any of various dermaphytoses,” which are superficial fungal infections. Dorland’s at 1899.
Tinea barbae is “tinea of the bearded area of the face and neck, usually occurring in those in contact with
farm animals.” Id. at 1899–1900.
8 Tinea capitis is “tinea of the scalp, or sometimes the eyebrows and eyelashes, caused by” fungi.
Dorland’s at 1900.
9 Griseofulvin is an antibiotic and antifungal medication. Dorland’s at 798.
3

Case 1:17-vv-00714-UNJ Document 88 Filed 11/01/23 Page 4 of 34
noted that Petitioner’s hair loss had been occurring for “[w]eeks” and that he had “circular areas
of hair loss[.]” Id. at 21. She stated that Petitioner’s alopecia was of moderate severity. Id.
On August 23, 2016, Petitioner returned to the dermatology office and saw a different
provider, Dr. Marc Glashofer. Id. at 16. Petitioner stated that his hair loss began two weeks after
his Gardasil vaccination and that he had “no significant life or medical stressors prior to onset of
concerns.” Id. Petitioner denied scaling, itching, or pain effecting the areas of hair loss. Id. He
reported no personal or family history of autoimmune or thyroid disorders. Id. On exam, Petitioner
had “circular areas of hair loss” on his scalp as well as sparse brows. Id. at 17. Dr. Glashofer noted
that Petitioner was “starting to loss lids[sic][.]” Id. Dr. Glashofer prescribed clobetasol
propionate10 and directed Petitioner to apply it to his scalp. Id. at 18.
Petitioner followed up with Dr. Glashofer on September 28, 2016, and presented with “no
regrowth on areas of loss[.]” Id. at 12. On exam, Petitioner had lost more than 50% of the hair on
his scalp. Id. at 13. He also had milia11 on his right cheek and eyelid. Id. Dr. Glashofer directed
Petitioner to continue his medication, and he discussed the possibility of further treatment with
sulfasalazine12 and immunotherapy. Id. at 14.
On November 16, 2016, Petitioner returned to Dr. Glashofer and presented with “complete
loss of scalp, brow, lashes, [and] body hair[.]” Id. at 8. Petitioner reported no improvement with
his topical corticosteroid. Id. The assessment was AA totalis. Id. at 10. Dr. Glashofer noted that
Petitioner’s “condition [was] severe enough to warrant the use of a[n oral] medication[,]” and Dr.
Glashofer opined that “topicals alone will not be effective.” Id. Dr. Glashofer prescribed
sulfasalazine. Id. Petitioner again followed up with Dr. Glashofer on December 28, 2016, for
“complete hair loss[.]” Id. at 4. Petitioner was directed to continue his sulfasalazine and topical
corticosteroid. Id. at 6. On January 10, 2017, blood testing revealed slightly low hemoglobin,
hematocrit, MCV, MCH, and MCHC as well as slightly high RDW and serum glucose. Id. at 24–
27.
On January 25, 2017, Petitioner followed up with Dr. Glashofer for his alopecia. Id. at 1.
Ms. Farag reported that Petitioner discontinued his topical corticosteroids because he was
experiencing increased anger. Id. at 3. Dr. Glashofer directed Petitioner to discontinue
sulfasalazine due to his bloodwork results. Id. Petitioner returned to Dr. Glashofer on March 22,
2017. Pet’r’s Ex. 3 at 1, ECF No. 8-1. Dr. Glashofer noted that Petitioner had “[s]evere” alopecia
that had been ongoing for “years[.]” Id. Dr. Glashofer directed Petitioner to continue with his
topical corticosteroid. Id. at 3. Dr. Glashofer discussed beginning topical immunotherapy with
SADBE treatment. Id.
On April 11, 2017, Petitioner presented to Dr. Makhlouf and was assessed with influenza.
Pet’r’s Ex. 4 at 13–14, ECF No. 8-2. Dr. Makhlouf noted that Petitioner had had “alopecia
10 Clobetasol propionate is “a very high potency synthetic corticosteroid[.]” Dorland’s at 367.
11 A milium is “a tiny epidermal cyst that is a round, smooth, firm, white to yellow papule just under the
skin.” Dorland’s at 1150.
12 Sulfasalazine is an antibacterial sulfonamide. Dorland’s at 1771.
4

Case 1:17-vv-00714-UNJ Document 88 Filed 11/01/23 Page 5 of 34
universalis13 for the past year [and was] not responding to treatment with steroid[s].” Id. at 13.
Petitioner followed up with Dr. Glashofer on June 25, 2017.14 Pet’r’s Ex. 91 at 18–20. Ms. Farag
indicated that Petitioner had not started SADBE yet due to insurance issues. Id. at 20.
On January 24, 2018, Petitioner returned to Dr. Glashofer. Id. at 14–17. On exam,
Petitioner had “complete hair loss and [loss of] brow/lashes with [the] exception of a fe[w] new
hairs on scalp[.]” Id. at 14. Dr. Glashofer noted that Petitioner had been suffering from alopecia
for one and a half years and that his condition “began after [G]ardasil vaccination[.]” Id. Dr.
Glashofer prescribed a “trial of [A]llegra15 based on anecdotal reports from [J]apan of benefit.”16
Id. at 16. Dr. Glashofer continued to discuss options with Petitioner for immunotherapy. Id.
Petitioner followed up with Dr. Glashofer on January 21, 2019. Id. at 11–13. Petitioner
presented with “minimal regrowth> 90% loss[ and] loss of brows[.]” Id. at 11. Ms. Farag elected
to pursue diphenylcyclopropenone (“DPCP”) treatment. Id. at 12.
On February 4, 2019, Petitioner returned to Dr. Glashofer. Id. at 8–10. Dr. Glashofer
applied DPCP to Petitioner’s scalp and noted that Petitioner declined Allegra. Id. at 9. On February
11, 2019, Dr. Glashofer increased Petitioner DPCP dosage from .01% to .1% because Petitioner
was not seeing results. Id. at 6–7. On exam during a February 18, 2019 follow-up, Petitioner had
more than 80% hair loss. Id. at 3–4. Dr. Glashofer decreased Petitioner’s DPCP strength to .05%
due to concerns about whether Petitioner could tolerate the higher dosage. Id. at 4. Dr. Glashofer
again reduced the DPCP strength on February 27, 2019, because Petitioner was experiencing
irritation. Id. at 1–2.
B. Affidavits and Fact Testimony
In her affidavit filed on November 9, 2017, Ms. Farag stated that, six days before his
Gardasil vaccination, Petitioner’s “hair was so long [that a] hair dresser put it in a small ponytail.”
Pet’r’s Ex. 6 ¶ 6. Ms. Farag recounted Petitioner’s May 16, 2016 vaccination and recalled that a
few weeks later, during Memorial Day weekend of 2016, Petitioner complained that his hair was
falling out. Id. ¶¶ 7–8. Ms. Farag recalled that Petitioner showed her a clump of hair and that she
“noticed that a part of his frontal hairline was receding upward on one side of his scalp.” Id. ¶ 8.
Ms. Farag stated that Petitioner’s hairline continued receding, creating a bald spot, in June. See id.
¶¶ 9–10. She noted that Petitioner’s alopecia continued progressing and that he was “completely
bald and [had] lost all eye brow and body hair[]” by September 7, 2016. Id. ¶ 13. Ms. Farag stated
that the medications Petitioner had tried “only result[ed] in behavioral changes and anemia[]” and
that Petitioner was no longer taking medication for his condition at that time. Id. ¶ 14.
13 Alopecia universalis, or universal alopecia, is “loss of hair over the entire body, resulting from
progression of alopecia areata.” Dorland’s at 53.
14 Petitioner’s Exhibit 91 does not indicate the dates of appointments. The dates for this exhibit refer to the
date Dr. Glashofer signed each note.
15 Allegra, or fexofenadine hydrochloride, is an antihistamine used to treat allergic rhinitis and chronic
idiopathic urticaria. Dorland’s at 688.
16 It is unclear whether Petitioner ever tried this treatment.
5

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In his affidavit filed on July 21, 2022, Petitioner recalled that he began noticing hair loss
during Memorial Day weekend of 2016. Pet’r’s Ex. 101 ¶ 6. He noted that his hair loss continued
and that he had a bald spot by his sixth-grade dance on June 9, 2016. Id. ¶ 8. Petitioner recounted
presenting to his pediatrician, who initially diagnosed him with ringworm, and then to a
dermatologist, who diagnosed Petitioner with AA. Id. ¶¶ 9–12. Like Ms. Farag, Petitioner
recounted continuing hair loss during the summer of 2016. Id. ¶¶ 14–15. Petitioner discussed the
social and emotional difficulties his hair loss had caused. See id. ¶¶ 17–24.
During the entitlement hearing, Petitioner testified that he was missing hair “[a]ll over[]”
his scalp as well as his eyebrows and eyelashes. Tr. 19:16–20:1. He also noted that he did not have
body hair. Tr. 26:8. Petitioner explained that missing his eyelashes was painful because things like
snow and sand easily got into his eyes. Tr. 20:4–13. Petitioner recalled beginning to experience
hair loss “around June[]” of 2016. Tr. 20:20–24. He explained that one day when brushing his hair,
“a clump of hair started to fall out.” Tr. 20:24–25. Like in his affidavit, Petitioner recalled initially
being diagnosed with ringworm before presenting to a dermatologist. Tr. 21:13–22:5. Petitioner
noted that his alopecia diagnosis shocked and upset his family and that his friends thought he had
cancer. Tr. 22:24–23:13. Petitioner described how his alopecia affected his confidence and the
bullying he endured. Tr. 23:14–24:14. Petitioner stated that, at the time of the hearing, he still
distanced himself from people and experienced some bullying. Tr. 24:15–25:4. Petitioner testified
that he was not taking medication for his alopecia as of the hearing date. Tr. 25:15–17. Petitioner
explained that he did not want to pursue treatment because he did not think it would be effective.
Tr. 25:23–25. He explained that he previously “took all these other treatments and everything, and
it just did[ not] work, [and his hair] barely grew back[]” before “f[alling] off again.” Tr. 26:1–3.
Petitioner testified that he recently presented to a new dermatologist, who explained that there are
new treatments for alopecia but that they can cause bad side effects. Tr. 26:24–27:2.
During my questioning, Petitioner indicated that none of his family members, including
older people, suffer from hair loss. Tr. 29:18–30:7. Petitioner explained that following his hair
loss, his scalp sometimes felt oily and sometimes felt dry. Tr. 30:15–21. Petitioner denied feeling
any kind of symptom prior to losing a patch of hair. Tr. 30:24–31:5. He explained that he “would
just wake up, and it would be out.” Tr. 31:4–5. Petitioner stated that he would “[m]aybe [feel] a
little sting when [hair] fell” because it would come out when he was brushing his hair, but he
otherwise did not feel physically unwell. Tr. 31:11–14. Petitioner noted that the hair on his scalp
sometimes fell out during brushing and sometimes on its own. Tr. 31:15–19. He also noted his
eyebrows “just fell out on their own.” Tr. 31:20–22. He stated that he did not feel any symptom
on his face before his eyebrows fell out. Tr. 31:24–32:1.
III. Experts
A. Expert Review
1. Petitioner’s Expert, M. Eric Gershwin, M.D.
Dr. Gershwin received his medical degree from Stanford University in 1971. Pet’r’s Ex.
92 at 1. 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
6

Case 1:17-vv-00714-UNJ Document 88 Filed 11/01/23 Page 7 of 34
Institutes of Health in Bethesda, Maryland. Id. at 2. He joined the faculty of the University of
California School of Medicine in Davis, California in 1975 as an assistant professor of
rheumatology and allergy. Id. He has been a full professor since 1981, and he was the chief of the
medical school’s division of rheumatology/allergy and clinical immunology for thirty-eight years.
Id.; Tr. 34:24–25. He 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.
Pet’r’s Ex. 92 at 2. 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 seventy-two books or monographs as well as an author of more than 1000 additional
publications. Id. at 9–135. Dr. Gershwin testified that his publications “overwhelmingly” involve
topics of autoimmunity. Tr. 39:7–9. Discussing his clinical experience, Dr. Gershwin testified that
he has treated “patients with very complicated immune diseases[]” for the past ten to fifteen years
and that he treats patients in rheumatology and immunology. Tr. 34:20–35:2. Dr. Gershwin
acknowledged that he is not a dermatologist and does not treat patients with AA, but he noted that
many of his patients with rheumatic diseases experience hair loss. Tr. 35:3–6. He also noted that
he has “published on alopecia[] and [ ] did some of the early transplant work on alopecia skin . . .
.” Tr. 35:7–10. During the entitlement hearing, Dr. Gershwin was admitted as an expert in internal
medicine, immunology, and rheumatology. Tr. 39:21–40:4.
2. Respondent’s Expert, Mehrdad Matloubian, M.D., Ph.D.
Dr. Matloubian received his medical degree and Ph.D. in virology from the University of
California, Los Angeles in 1996. Resp’t’s Ex. D at 1, ECF No. 64-1. He completed an internship,
a residency, a rheumatology fellowship, and a post-doctoral fellowship at the University of
California, San Francisco between 1996 and 2004. Id. at 1–2. He joined the faculty of the
University of California, San Francisco medical school in 2001, and he became a full professor
three years before the entitlement hearing. Id. at 2; Tr. 99:1–2. He is a member of various
professional societies and a recipient of various awards, and he is an author of more than forty-
five publications. Resp’t’s Ex. D at 2–3, 10–15. Dr. Matloubian is board certified in internal
medicine and rheumatology. Id. at 2. He noted that his “areas of expertise include T17 and B cell18
responses, especially to viruses as well as factors that regulate lymphocyte circulation and
trafficking.” Resp’t’s Ex. A at 1, ECF No. 29-1. He “actively evaluates and treats patients with
complex autoimmune diseases at a tertiary referral center[.]” Id. Dr. Matloubian testified that he
treats patients in his own clinical practice and attends on an inpatient rheumatology consult service.
Tr. 99:7–15. He noted that he is an adult rheumatologist and often treats rheumatoid arthritis, lupus,
and various other disorders. Tr. 99:25–100:4. He further noted that he treats adults who had
“pediatric onset rheumatologic disease[.]” Tr. 100:4–5. Although he does not primarily treat
patients with alopecia, Dr. Matloubian stated that he has treated patients with autoimmune diseases
who also have alopecia. Tr. 100:18–25. During the entitlement hearing, Dr. Matloubian was
admitted as an expert in rheumatology and immunology. Tr. 103:18–24.
17 T cells, or T lymphocytes, are “the cells primarily responsible for cell-mediated immunity[.]”
Dorland’s at 1071.
18 B cells, or B lymphocytes are “bursa-dependent lymphocytes in birds and their counterparts in nonavian
vertebrates including human beings, the cells primarily responsible for humoral immunity, the precursors
of antibody-producing cells (plasma cells).” Dorland’s at 1070.
7

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B. Expert Reports and Testimony
1. Petitioner’s Expert, Dr. Gershwin
In his first expert report, Dr. Gershwin explained that “[a]lopecia areata 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. 7 at 1 (citing Pet’r’s Ex. 8 at
2, ECF No. 17-1).19 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. He
explained that “alopecia universalis is diagnosed with 100% loss of both scalp and body hair.” Id.
at 2. Dr. Gershwin stated that alopecia is a systemic disease that can affect the nails and eyes in
addition to the hair follicles. Id. (citing Pet’r’s Ex. 10, ECF No. 17-3).20
He wrote 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. (citing Pet’r’s Ex. 11 at 1–2, ECF No. 17-4).21 He noted that 10% to 42% of alopecia
patients have a first-degree relative who is also affected. Id. Citing a paper by Martinez-Mir et
al.,22 Dr. Gershwin asserted that “[a] genome wide search for linkage of [twenty] families with
alopecia consisting of 102 affected and 118 unaffected individuals demonstrated the association
of [human leukocyte antigens (“HLA”)]23 with alopecia [ ].” Id. (citing Pet’r’s Ex. 12, ECF No.
17-5). Dr. Gershwin explained that multiple HLA class II genes are associated with alopecia and
that alopecia sometimes involves certain class I HLA alleles. Id. (citing Pet’r’s Ex. 12 at 3). He
continued that “[a]long with these HLA alleles that potentially contribute to the diagnosis of
alopecia, certain regions of the human genome are associated with more severe disease.” Id. (citing
Pet’r’s Ex. 12 at 6). He stated that certain alopecia-associated alleles “are more or less specific to
various ethnic identities, and therefore genetic associations depend on the patient’s particular
geographic location and ethnic background [ ].” Id.
In addition to genetic factors, Dr. Gershwin noted that “[c]linical and experimental studies
showed that environmental insults such as emotional/physical stressors, hormones[,] and
infections contribute to autoimmunity [ ].” Id. He explained that stress hormones “are known to
affect alopecia” and that stressors including “exposure to ultraviolet light, natural and chemical
bodily offenses, physical injury, and emotional distress[]” have been linked to alopecia. Id.
19 Naseeha Islam et al., The autoimmune basis of alopecia areata: A comprehensive Review, 14
AUTOIMMUNITY REVIEWS 81 (2015).
20 Shabnam Madani & Jerry Shapiro, Alopecia areata update, 42(4) J. AM ACAD DERMATOL 549 (2000).
21 Lawrence Scerri & Joseph L. Pace, Identical twins with identical alopecia areata, 27(5) J. AM ACAD
DERMATOL 766 (1992).
22 Amalia Martinez-Mir et al., Genomewide Scan for Linkage Reveals Evidence of Several Susceptibility
Loci for Alopecia Areata, 80 AM J. HUMAN GENETICS 316 (2007).
23 HLA are “histocompatibility antigens governed by genes of the HLA complex (the human major
histocompatibility complex), a region on the short arm of chromosome 6 containing several genetic loci,
each having multiple alleles.” Dorland’s at 103.
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Dr. Gershwin noted that cytomegalovirus (“CMV”) has been associated with alopecia but
that this association has been refuted. Id. at 3 (citing Pet’r’s Exs. 32–33, ECF Nos. 19-5–19-6).24
He explained that other viruses, such as “hepatitis B, hepatitis C, Epstein-Barr, and swine flu have
also been suggested to trigger alopecia [ ].” Id. He continued 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 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.
Explaining the evidence that alopecia is an autoimmune disease, Dr. Gershwin noted that
patients with alopecia often have one or more other autoimmune disorders. Id. He explained that
the effectiveness of immunosuppressive agents in treating alopecia indicates that it is autoimmune
and that HLA “has been reported to play a major role in the etiology of autoimmunity [ ].” Id. He
averred that “[a] confirmation of this specific hypothesis in alopecia lies in 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. He stated that “[t]he
most widely affected hypothesis for the effector mechanism of alopecia is the destruction of the
[hair follicle], an immune privilege site.” Id. He continued that while individuals without alopecia
maintain immune privilege within the hair follicle “in multiple ways, such as omitting [major
histocompatibility complex (“MHC”)]25 class 1 in the proximal outer root sheath [ ,] patients
identified with alopecia have a strong association with those same MHC class 1 alleles.” Id. He
explained that “[a]utoreactive cytotoxic T cells26 target specific autoantigens, especially
melanogenesis-associated peptides expressed by anagen [hair follicles] that produce melanin
pigment [ ].” Id. Cytokines27 as well as natural killer (“NK”) cells28 have also been implicated in
the breakdown of immune privilege in alopecia. Id. at 3–4.
Dr. Gershwin also discussed the “C3H/HeJ mouse[, which] is a 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. He cited a study by Sundberg et al.,29 who wrote that “[a] disease closely resembling human
[AA] was found in a large production colony of C3H/HeJ mice that had no evidence of thyroid
24 Robert B. Skinner, Jr., et al., Alopecia Areata and Prescence of Cytomegalovirus DNA, 273(18) JAMA
1419 (1995); María J. García-Hernández et al., No Evidence of Cytomegalovirus DNA in Alopecia Areata,
110(2) J. INVEST DERMATOL 185 (1998).
25 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.
26 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.
27 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.
28 NK cells are “cells capable of mediating cytotoxic reactions without prior sensitization against the
target.” Dorland’s at 316.
29 John P. Sundberg et al., Alopecia Areata in Aging C3H/HeJ Mice, 102 J. INVEST DERMATOL 847
(1994).
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dysfunction or an infectious etiology.” Pet’r’s Ex. 66 at 1, ECF No. 22-9. The authors noted that
they obtained the mice from a laboratory where many of the mice colonies “are housed in strict
quarantine to maintain their specific pathogen-free status[]” and where “[e]xtensive quarterly
monitoring of all mouse rooms and representative mice is done to verify the microbiologic status
of mice within rooms.” Id. at 8. They also noted that “[r]outine bacterial and mycotic cultures were
prepared from skin biopsies and plucked hair from C3H/HeJ mice with and without alopecia[, and
n]o pathogens were isolated nor were any visualized in histologic selections of skin using special
stains in the mice cultured or in others from the production of breeding colonies.” Id. Sundberg et
al. wrote that “the changes in this non-scarring alopecia were limited to anagen follicles that were
surrounded by mononuclear cells[, and t]his infiltrate, composed primarily of cytotoxic (CD8+)
and helper (CD4+) T cells,30 was associated with follicular and hair shaft dystrophy.” Id. at 1. The
“infiltrate was markedly reduced by intralesional injection of triamcinolone acetonide with
subsequent hair regrowth in the affected site.” Id. The authors concluded that “[p]edigree tracing
of [the affected] mice suggests that this non-scarring alopecia may be an inherited disease.” Id.
Although Sundberg et al. did not find an infectious etiology, Dr. Gershwin testified that
“just because they have[ not] found an antigen or they have[ not] found an infection in highly
inbred mice does[ not] mean there[ is] not an infection which is present.” Tr. 181:22–25. He
concluded that “[t]here[ is something in these mice that[ is] causing them to develop[] . . . CD8 T
cells.” Tr. 182:2–3. He continued that “in every one of these papers we[ have] cited, the pathogenic
mechanism is felt to be [follicle-specific] CD8 T cells.” Tr. 182:7–9. Dr. Gershwin was “unaware
of a clinical situation where [there are] organelle-specific cytotoxic T cells in the absence of an
antigen. And just because you have[ not] found the antigen does[ not] mean it[ is] not there.” Tr.
182:11–14. Dr. Gershwin noted that “at the end of the day, it[ is] not the infection. It[ is] the
immune response which are CD8 cells.” Tr. 183:9–10. Dr. Gershwin emphasized, “the absence of
an antigen does[ not] make any difference. What[ is] critical is there[ is] a CD8 T cell response.”
Tr. 184:1–3.
Dr. Gershwin asserted that “[t]he mechanism that leads to alopecia includes [ ] genetic
susceptibility and the generation of cytotoxic CD8 T cells.” Pet’r’s Ex. 7 at 4. 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. He noted that there have been other mechanisms proposed
for AA, but he opined that the T cell reaction he discussed is the most likely mechanism. Tr. 70:25–
71:4.
When asked during the entitlement hearing what causes AA, Dr. Gershwin stated that “the
current thesis is that it[ is] autoimmune in nature, that the immune system attacks the hair follicle.”
Tr. 42:4–7. While he acknowledged that AA has a genetic basis, he stated that it is influenced by
environmental factors, “as with every autoimmune disease[.]” Tr. 43:5–11. During cross-
examination, Dr. Gershwin acknowledged that “there are probably multiple causes[]” of AA but
that it is “likely to be autoimmune.” Tr. 61:8–12. He acknowledged that emotional and physical
stressors can trigger alopecia without the introduction of a foreign antigen, but he also noted that
30 Helper T cells are “differentiated T lymphocytes whose cooperation (help) is required for the
production of antibody against most (T-dependent) antigens.” Dorland’s at 313.
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these cases “tend not to be lifelong[]” and “tend to be a little more patchy.” Tr. 61:23–62:3. He
acknowledged that acute infections are not an established cause of AA. Tr. 62:12–14.
Summarizing his medical theory in this case, Dr. Gershwin wrote that Petitioner “received
a vaccine that produced cytotoxic T cells that were directed at his hair follicles and which cross
react with an epitope31 or region of the Gardasil vaccine.” Pet’r’s Ex. 7 at 5. He continued 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.
Discussing molecular mimicry generally, Dr. Gershwin explained that it is a viable theory
in autoimmunity. Tr. 49:5–8. He explained that “homology extends beyond what[ is] called
primary sequence. It might be the folding of proteins. It might be tertiary structure, particularly
when [ ] talk[ing] about antibody.” Tr. 49:16–19. He continued that “[w]e talk about T cells, its
binding of antigen on certain immune genes which can vary between people, including their
immune genes. They[ are] very hard to define.” Tr. 49:19–22.
Despite the fact that Dr. Gershwin’s theory of molecular mimicry in this case centers on
cytotoxic T cells, Dr. Gershwin acknowledged that “[t]he Gardasil vaccine, interestingly enough,
is projected not to induce a lot of cytotoxic CD8 T cells, but there[ is] no literature that says it
does[ not] produce any.” Tr. 43:21–24. Dr. Gershwin was “unaware of a single paper that says,
you can[not] get CD8 T cells [from HPV vaccination] at all.” Tr. 183:13–15. Even if CD8 T cells
from HPV vaccination are uncommon, “it could well be that [Petitioner’s] problem is that he is
the rare individual that does get a CD8 T cell response.” Tr. 183:19–21.
On cross-examination, Dr. Gershwin acknowledged that he had seen studies showing that
“the HPV vaccine is not designed to produce CD8 T cells, and that[ is] why [he] said it could well
be the variation here is that this child did make a CD8 response, whereas most people do not.” Tr.
79:18–21. He admitted that he did not know of literature measuring CD8 T cell responses to the
HPV vaccine. Tr. 79:12–16. He submitted a paper by Stryhn et al.,32 which examined “CD8+ and
CD4+ T cell responses after primary Yellow Fever vaccination . . . .” Pet’r’s Ex. 94 at 1, ECF No.
70-2. However, Dr. Gershwin acknowledged that the yellow fever vaccine is a live attenuated
vaccine while the HPV vaccine is not. Tr. 80:2–13. Dr. Gershwin acknowledged that he did not
provide medical literature showing the CD8 response against any virus that has been associated
with alopecia. Tr. 81:1–5. He further stated that he “do[es not] have evidence that any viral
infection produces alopecia, and we have very limited data on CD8 T cells and alopecia anyway.”
Tr. 81:5–8.
Dr. Gershwin submitted a number of papers, including case reports and epidemiological
studies, to support his contention that the HPV vaccine Petitioner received can cause AA. He
submitted a paper by Wise et al.,33 discussing sixty reports of hair loss following various
31 An epitope, or antigenic determinant, is “a site on the surface of an antigen molecule to which a single
antibody molecule binds[.]” Dorland’s at 495.
32 Anette Stryhn et al., A Systematic, Unbiased Mapping of CD8+ and CD4+ T Cell Epitopes in Yellow
Fever Vaccinees, 11 FRONTIERS IN IMMUNOLOGY 1836 (2020).
33 Robert P. Wise, et al., Hair Loss After Routine Immunizations, 278 JAMA 1176 (1997).
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vaccinations, but primarily hepatitis B vaccinations, identified through the Vaccine Adverse Event
Reporting System (“VAERS”). Pet’r’s Ex. 79 at 1, ECF No. 24-2. However, “[t]he extent and
duration of hair loss varied widely among [thirty-seven] reports with sufficient data to classify.”
Id. at 2. The authors also noted that “the FDA has learned of fewer than [five] cases per year during
a decade in which Americans received roughly [one] billion vaccine doses.” Id. at 3. Because the
paper was published in 1997, it did not include data on the HPV vaccine. Tr. 73:2–5. Nevertheless,
Dr. Gershwin wrote that Wise et al.’s data “suggest[s] that HPV is the most likely initiating
immunogen herein.” Pet’r’s Ex. 7 at 5.
Dr. Gershwin also submitted a case report by Gallo et al.34 describing a thirty-one-year-old
man who reported hair loss beginning the day after his second COVID-19 vaccination and who
was diagnosed with AA. Pet’r’s Ex. 93 at 1–2, ECF No. 70-1. Dr. Gershwin discussed a set of nine
case reports of AA following COVID-19 vaccination by Scollan et al.35 Pet’r’s Ex. 98, ECF No.
70-6. The approximate time between vaccination and the alopecia flare ranged from one to two
weeks following the first dose to four months after the second dose. Id. at 2. Dr. Gershwin
submitted a case report by Chu et al. 36 of a three-year-old boy who experienced one episode of
AA following one week following a third dose of a Japanese encephalitis vaccination and a second
episode three days after the third dose of an influenza vaccination. Pet’r’s Ex. 95 at 1, ECF No.
70-3. He also discussed an article by Tuccori et al.37 discussing two case reports of telogen
effluvium38 following receipt of the bivalent HPV vaccine. Pet’r’s Ex. 99 at 1, ECF No. 70-7. Dr.
Gershwin stated that telogen effluvium is similar to AA. Tr. 58:19–20. He opined that telogen
effluvium “likely involves innate immune mechanisms and . . . is immunological in nature, but it[
is] not as common as [AA] and not as well studied.” Tr. 79:4–7.
Dr. Gershwin explained that he submitted this literature “to point out that the many [sic]
people are tuned into the possibility that alopecia can be ascribed to environmental factors,
including vaccination.” Tr. 57:15–25. Dr. Gershwin testified that these case reports support his
opinion that Petitioner’s Gardasil vaccination caused his AA. Tr. 58:23–59:1. Respondent’s
counsel asked Dr. Gershwin about various case reports he submitted, and Dr. Gershwin opined
that molecular mimicry most likely caused alopecia in these case reports. Tr. 71:10–18.
34 Guiseppe Gallo et al., Alopecia areata after COVID-19 vaccination, 11 CLIN EXP VACCINE RES 129
(2022).
35 Margaret E. Scollan et al., Alopecia areata after SARS-CoV-2 vaccination, JAAD CASE REPORTS 2022
https://doi.org/10.1016/j.jdcr.2021.11.023.
36 Chien-Ho Chu et al., Alopecia Areata After Vaccination: Recurrence with Rechallenge, 33(3)
PEDIATRIC DERMATOLOGY e218 (2016).
37 Marco Tuccori et al., Telogen Effluvium following Bivalent Human Papillomavirus Vaccine
Administration: A Report of Two Cases, 224 DERMATOLOGY 212 (2012).
38 Telogen effluvium is “the early, excessive, temporary loss of club hairs from normal resting follicles in
the scalp as a result of traumatization by some stimulus (e.g., after surgery or childbirth; with starvation,
side effects of drugs, traction on hair, high fever, or certain diseases; or with psychogenic stress).”
Dorland’s at 589.
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Petitioner submitted a paper by Tu et al.39 “investigat[ing] the correlation between a history
of [HPV] infection and [AA] risk.” Pet’r’s Ex. 102 at 1. Tu et al. noted that previous studies and
reports had associated viral agents and vaccinations with AA, and they indicated that reports of
AA following vaccinations “may be caused by a hypersensitive reaction to vaccines, including
activation of IFN-γ-producing cells while antigen presentation in the secondary lymphoid tissues
in [AA] predisposed patients [ ].” Id. at 2. The authors noted that there are more than 600,000 new
HPV infections per year worldwide and that HPV is the primary cause of nearly all cervical cancers
and is related to other cancers. Id. While HPV can cause cancer, “under immunological
surveillance of mainly effector T cells, most HPV infections undergo spontaneous clearance within
1–2 years [ ].” Id. The authors relied on Taiwan’s National Health Insurance Research Database
to construct this study. Id. at 4. They identified patients who had been diagnosed with HPV
between 2000 and 2012 using ICD-9 codes. Id. They selected patients with at least one inpatient
admission or three outpatient visits to be a part of the study, and they excluded patients who did
not receive HPV-related treatment procedures in the three months following HPV diagnosis. Id.
They included 30,001 subjects in the HPV group and the same number in the control group. Id.
The authors followed each subject “until the presence of [AA], missing, death, or the end of the
study (31 Dec 2013).” Id. Tu et al. “discovered a 155% increased risk of developing new-onset
[AA] among HPV infected patients, compared with matched controls.” Id. at 6. They noted that
this “risk was significant in both genders and prominent in those aged more than 50 years, followed
by 41-50 years old group, 18-30 years old group, and 31-40 years old group.” Id. They also
indicated that “[m]ental disordered patients were prone to develop [AA] in HPV infected patients.”
Id. Tu et al. wrote that “[t]he underlying mechanism that HPV infection increases the risk of
developing [AA] remains unclear[, but they] propose[d] the probabilities of chronic inflammation
and elevated IFN-γ induced by host immune response against HPV infection, causing immune cell
infiltration and cytokine release that will damage immune privilege of hair follicles, and later
contribute to alopecia.” Id. Although the authors stated that they “have provided ample evidence
for this positive association [of AA] among HPV symptomatic infection[,]” they acknowledged
“[s]everal limitations” in their findings. Id. at 7. They noted that “epidemiologic evaluation of
HPV infection was challenging, as many infections were not clinically recognized. Using
retrospective, ICD-9 based methods to select study groups of HPV infection might have election
bias.” Id. at 8. They acknowledged the possibility of false-positive cases but excluded patients who
did not receive treatment to mitigate this concern. Id. Because this was a “mono-country
evaluation,” Tu et al. noted that their “findings may not be applicable to non-Asian ethnic groups.”
Id. They indicated that they did not have data on whether the participants received HPV
vaccinations and how this may have impacted their immune systems, and they noted that their
findings were solely based on epidemiological evidence. Id.
Dr. Gershwin testified that he submitted the Tu et al. study to show that in “at least one
study, infection has been linked to the development of alopecia[] . . . .” Tr. 45:20–25. When
Respondent’s counsel asked about the Tu et al. study, Dr. Gershwin acknowledged that Petitioner
is not Taiwanese, but he noted that this does not necessarily mean Petitioner does not have the
same HLA alleles as the Taiwanese study subjects. Tr. 68:7–22. Dr. Gershwin acknowledged that
this paper has multiple limitations and that it does not indicate whether people developed AA soon
39 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 102618
(2021).
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after HPV infection. Tr. 69:22–70:1. Dr. Gershwin opined that autoimmune diseases likely
“involve more than one mechanism at any given point in time.” Tr. 45:16–19. He noted that the
etiology of most autoimmune diseases is unknown, but “infection is still first on the list of virtually
anyone that looks at the etiology of autoimmunity.” Tr. 45:10–15.
Petitioner filed additional articles to show that AA has been linked to infection in general.
He filed a letter to the editor by Nguyen and Tosti,40 who “conducted an online questionnaire
among patients with AA to better understand the relationship between AA and COVID-19.” Pet’r’s
Ex. 103 at 1, ECF No. 81-1. Of 152 respondents, fifty-nine reported a positive COVID test, and
twenty-five reported AA symptoms post infection. Id. He submitted a review of nine case reports
by Christensen and Jafferany,41 who concluded that AA “may be a dermatologic manifestation of
COVID-19, with cases most often appearing [one] to [two] months following infection.” Pet’r’s
Ex. 104 at 2, ECF No. 81-2. Petitioner submitted a review by Nguyen and Tosti42 that included
1826 patients with hair loss and COVID-19. Pet’r’s Ex. 105 at 1, ECF No. 81-3. 143 patients had
AA, specifically, but 136 out of those 143 patients had preexisting AA. Id. at 1, 4. He submitted a
paper by Birkett et al.,43 who wrote that “AA can be triggered by viral infections such as influenza,
[CMV], and the Epstein-Barr virus[]” and discussed eighteen patients with AA which was
“thought to have been triggered by either COVID-19 vaccination or COVID-19 infection.” Pet’r’s
Ex. 107 at 1, ECF No. 81-5. He filed an article by Wei et al.44 on hair loss following dengue virus
infection, but the paper does not mention AA specifically. See generally Pet’r’s Ex. 108, ECF No.
81-6. Petitioner also submitted a case report linking COVID-19 infection and AA. Pet’r’s Ex. 109,
ECF No. 81-7.45
Dr. Gershwin discussed various difficulties in decisively establishing that the HPV vaccine
can cause AA via molecular mimicry. He acknowledged that his “theory can[not] be proven at the
clinical bench.” Tr. 44:19–20. He noted that the best way to prove this theory would be to find
immune cells that react with Petitioner’s hair follicles, but “the time to identify [these cells] would
have had to have been very early on during this disease course, and it would have been a research
effort.” Tr. Tr. 44:20–45:6. This is because autoimmunity “may go from an adaptive response[] .
. . to perpetuation of inflammation where it just persists on its own through innate immune
mechanisms.” Tr. 44:24–45:2. He “admit[ted] that [his] thesis is entirely based on the mechanism
here that it is cytotoxic T cells, amongst other cells, that react with the hair follicle.” Tr. 50:11–14.
He continued that “their appearance within [fourteen] days is what one would expect of a T cell
response, and alopecia is thought to be a T cell response.” Tr. 50:14–17. He opined that this is
40 Betty Nguyen & Antonella Tosti, Alopecia areata after COVID-19 infection and vaccination: A cross-
sectional analysis, J. EUR ACAD DERMATOL VENEREOL (2022).
41 Rachel E. Christensen & Mohammad Jafferany, Association between alopecia areata and COVID-19:
A systematic review, 7 JAAD INTERNATIONAL 57 (2022).
42 Betty Nguyen & Antonella Tosti, Alopecia in patients with COVID-19: A systematic review and meta-
analysis, 7 JAAD INTERNATIONAL 67 (2022).
43 Liam Birkett et al., Possible Associations Between Alopecia Areata and COVID-19 Vaccination and
Infection, AESTHETIC SURGERY J. (2022).
44 Kai-Che Wei et al., Dengue Virus Infects Primary Human Hair Follicle Dermal Papilla Cells, B
FRONTIERS IN CELLULAR & INFECTION MICROBIOLOGY 268 (2018).
45 Paul Sgubbi et al., Alopecia areata in a patient with SARS-Cov-2 infection, 33 DERMATOLOGIC
THERAPY e14295 (2020).
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“deeper than just a temporal association[ because there is also a] cellular and a mechanistic
explanation for the temporal events . . . .” Tr. 50:18–23.
Discussing the medical literature he submitted, Dr. Gershwin explained that he submitted
the Stryhn et al. paper to show “how difficult it is[]” to study molecular mimicry. Tr. 52:12–15.
The authors were “trying to define reactivity at the yellow fever vaccination, to define the epitopes
that these T cells react with.” Tr. 52:15–17. However, Dr. Gershwin noted that researchers would
“have to look at hundreds of thousands of T cell responses, or at least be able to do this type of
sophisticated mapping in only those patients who developed alopecia following a vaccination.” Tr.
52:24–53:2. He emphasized that “understanding what[ is] called epitopes or structure is not only
important for understanding the host’s reaction but even in designing vaccines, meaning it[ is] still
a major research effort” involving antibodies as well as T cells. Tr. 53:6–16. He noted that a follicle
is “an organelle which likely has as many [sic] proteins in there,” and this makes it difficult to
understand “exactly what[ is] happening at the molecular level.” Tr. 54:18–21. He further wrote
in his second expert report that AA “appears to be a T cell disease, and it has been a major challenge
to identify T cell epitopes.” Pet’r’s Ex. 81 at 2, ECF No. 32-1. He averred that “any discussion of
etiology and association with vaccines must take into account that it is thus far impossible to
individually predict T cell epitopes unique to a specific individual in response to a vaccine.” Id.
He asserted that alopecia “clearly requires environmental stimulation[,]” and he “submit[ted] that
the environmental stimulation herein was the HPV vaccine . . . .” Id.
Dr. Gershwin explained that he is not relying on a homology to support his theory in this
case because he does not “even know what the structure are [sic] of the follicles, because it[ is] a
complicated organelle of multiple structures.” Tr. 89:3–10. However, he testified that molecular
mimicry is “the only logical explanation.” Tr. 89:11–12. He explained that it is a logical
explanation because “you find T cells that are cytotoxic in the area of the follicle when you do
immunohistochemistry, and in order for T cells to be there, they have to be there, recognizing
antigen. And that antigen is in the follicle and the follicle is what[ is] destroyed.” Tr. 89:13–19.
He stated that this mechanism could apply to any vaccine that can cause alopecia. Tr. 89:20–23.
When asked whether it is a fair criticism that he has not identified mimics or a homology, Dr.
Gershwin maintained that showing specific mimics is “not plausible” in this case. Tr. 55:23–56:3.
Dr. Gershwin also discussed the difficulty in linking AA to vaccination via epidemiological
studies, particularly retrospective studies. Dr. Gershwin noted that identifying a connection would
likely require “a large probably multi-national prospective study.” Tr. 59:5–16. He stated that “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.” Pet’r’s Ex. 81 at 2.
On cross-examination, Dr. Gershwin opined that finding HPV vaccine-caused AA in an
epidemiological study would likely require “boys of [Petitioner’s] age, immunized in a cohort
population likely in the millions.” Tr. 66:7–17. Dr. Gershwin explained that it is easier to identify
rare adverse effects when a large number of people are “vaccinated almost at the same time.” See
Tr. 66:18–67:12. He noted that there might not be any cases of AA found if one million boys
Petitioner’s age received the HPV vaccine. Tr. 67:13–16.
He maintained that Petitioner “developed alopecia because of his unique genetic
susceptibility.” Pet’r’s Ex. 7 at 5. Dr. Gershwin admitted on cross-examination, that there is no
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evidence in Petitioner’s medical records that he had a unique genetic susceptibility. Tr. 83:10–13.
However, Dr. Gershwin maintained that such testing “would be research efforts, and even for a
disease like lupus that we know has a genetic basis, we do[ not] test” for genetic susceptibility. Tr.
83:13–16. Citing a study involving the measles vaccine, Dr. Gershwin wrote that “it was noted
that vaccination induced upregulation of [eighty] different genes[.]” Pet’r’s Ex. 7 at 5 (citing
Pet’r’s Ex. 78 at 1, ECF No. 24-1).46 Dr. Gershwin stated that “[i]f one considers the number of
genetic variations . . . within a gene, then the multitude of genetic diversity in response to a vaccine
is truly extraordinary.” Id. Dr. Gershwin asserted that such genetic diversity “would lead to rare
events that would be below the level of detection of epidemiologic analysis.” Id.
Further discussing the time between Petitioner’s vaccination and AA onset, Dr. Gershwin
noted that the production of T cells, including CD8 cells and other T cells, would be produced
“within a period of three days to about three or four weeks” following a vaccination. Tr. 43:25–
44:4. He noted that he would not “make an immunological association” between Petitioner’s
vaccination and alopecia if the onset of his hair loss was six to eight weeks post vaccination or
within twenty-four hours of vaccination. Tr. 44:5–9. Likewise, in his expert report, Dr. Gershwin
“emphasized that kinetics of appearance of cytotoxic T cells after vaccination can occur within
several days [ ].” Pet’r’s Ex. 7 at 4. (citing Pet’r’s Ex. 68, ECF No. 23-1).47 Thus, Dr. Gershwin
concluded that “[o]nset within [fourteen] days would certainly be consistent with generation of a
CD8 response.” Id. He averred that Petitioner’s HPV vaccination was “[t]he only immunological
challenge within that window[.]” Id. When asked by Respondent’s counsel what a reasonable time
frame would be for someone to develop AA through molecular mimicry following vaccination,
Dr. Gershwin testified, that “based on data in 2022, [he] think[s] that it would primarily be a T cell
reaction, although there may be some natural killer T cell lineages as well. And [he] think[s] it
would probably be anywhere from about three weeks to about three, four, five, maybe even six
weeks.” Tr. 70:12–22.
Dr. Gershwin explain that his theory “fits quite well” with the timing of the onset of
Petitioner’s AA. Tr. 56:16–18. Dr. Gershwin noted that “there are other cell populations that
people have . . . incriminated. They might be involved in hair loss as well. They may have taken
longer to develop.” Tr. 56:19–21. He continued that “[t]here are those who postulate there should
be an innate immune response as well, but [he] think[s] cytotoxic T cells, at least now in 2022, are
the most likely . . . candidate for the predominant involvement.” Tr. 56:21–25. He noted that
“different lineages of cytotoxic T cells [are] being defined, and . . . that field is still in its infancy
as well.” Tr. 56:25–57:2
Although Dr. Gershwin noted that environmental factors are involved in AA, he did not
identify environmental factors that could have contributed to Petitioner’s AA besides the
vaccination. Tr. 57:3–11. Dr. Gershwin noted that Petitioner suffered from a strep infection on
March 8, 2016, but Dr. Gershwin did not believe that this infection contributed to Petitioner’s AA.
46 Neelam Dhiman et al., Immune Activation at Effector and Gene Expression Levels After Measles
Vaccination in Healthy Individuals: A Pilot Study, 66 HUMAN IMMUNOLOGY 1125 (2005).
47 Hannah Rabenstein et al., Differential Kinetics of Antigen Dependency of CD4+and CD8 + T Cells, 192
J. IMMUNOL 3507 (2014).
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Pet’r’s Ex. 7 at 5. In support, Dr. Gershwin cited a paper by Morales-Sánchez et al.,48 who
concluded that an association between throat carriage of bacterial pathogens and AA “appears
valid for patients with less than 25% hair loss and a course of disease under [one] year.” Pet’r’s
Ex. 7 at 5; Pet’r’s Ex. 80 at 1, ECF No. 24-3.
During my questioning, I asked Dr. Gershwin how he would look for evidence of the
immune reaction he proposed in this case. Tr. 84:5–7. He explained that, if he had the facilities
and research efforts, he would look for this reaction while it is happening by isolating infiltrating
cells from tissues and identifying the cells as “predominantly CD8 cells.” Tr. 84:8–15. Then, “[i]n
the perfect world, [he] would be able to grow in vitro the cells of his hair follicle, and in the perfect
world, be able to show a cytotoxic reaction between his T cells and the cells [ ] growing in the
culture.” Tr. 84:15–18. He explained that the clinical presentation accompanying this reaction
“would be the same . . . as anyone else with this form of acute autoimmune alopecia.” Tr. 84:19–
22. He explained that there would be no way to distinguish between vaccine-caused and idiopathic
alopecia unless he could show that “the same cells that are infiltrating his scalp were cross-reactive
with an antigen present in the vaccine or perhaps a neoantigen created during antigen processing
of that vaccine.” Tr. 84:23–85:5.
Dr. Gershwin agreed that it was fair to say that AA totalis is years in the making. Tr. 87:1–
3. He explained that “the reason for that is that in those diseases that take months to years to
develop, we can find autoantibody present . . . long before the onset of a disease, whereas in [AA],
because we[ are] not talking about an autoantibody but rather a pathogenic cytotoxic T lymphocyte
is present at the time of the disease development.” Tr. 87:3–9. He clarified that diseases that allow
the identification and measurement of autoantibodies are less likely to occur due to molecular
mimicry. Tr. 87:10–15. He explained that the difference between diseases involving
autoantibodies and cytotoxic T cells is that “when you have a disease caused by T cells, the
overwhelming number of T cells are present in the tissue. They[ are] not found in the blood . . . .
Pathology is at the local site.” Tr. 88:11–17. He opined that AA totalis, rather than AA, results
from “just high levels of cytotoxic T cells[ that are] homing . . . [and] trafficking” at the hair
follicles. Tr. 88:18–20. However, he did not know of any way to determine whether someone
would develop AA or AA totalis. Tr. 88:21–89:2.
Dr. Gershwin acknowledged that stress is a potential trigger of AA that a twelve-year-old
boy could experience, but he did not think that stress was a likely trigger in this case because of
how quickly and severely Petitioner’s AA progressed. Tr. 91:13–19. He explained that Petitioner’s
AA continued long after the alleged cross-reaction occurred likely due to “nonspecific
inflammatory perpetuation of a disease.” Tr. 91:25–92:20.
When asked to clarify whether there was no evidence of inflammation in Petitioner’s
alopecia, Dr. Gershwin noted that “[t]here is evidence in alopecia of inflammatory T cells and
other cells, and that is inflammation.” Tr. 93:2–10. However, he noted that this inflammation is
identified “under a microscope.” Tr. 93:11–15.
2. Respondent’s Expert, Dr. Matloubian
48 M.A. Morales-Sánchez et al., Immunization and Bacterial Pathogens in the Oropharynx as Risk
Factors for Alopecia Areata, 101(5) ACTAS DERMOSIFILOGR. 437 (2010).
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Dr. Matloubian noted that AA is “the most common cause of alopecia in otherwise healthy
children[]” and that its occurrence in a twelve year old “fits within the normal and acceptable
demographics for this disease.” Resp’t’s Ex. A at 3 (citing Resp’t’s Ex. A, Tab 1, ECF No. 29-
2).49 Dr. Matloubian also countered Dr. Gershwin’s characterization of AA as an uncommon
disease. Resp’t’s Ex. C at 3. Dr. Matloubian cited the Islam et al. paper, co-authored by Dr.
Gershwin, in which Dr. Gershwin and his co-authors described AA as “a relatively frequent
disease with prevalence of 0.1%-0.2% worldwide.” Id. (quoting Pet’r’s Ex. 8 at 2). Dr. Matloubian
also noted that the authors cited data to conclude that “[o]verall AA seems to account for about
0.7%-3% of all patients in the United States and about 2% in the United Kingdom.” Id. (quoting
Pet’r’s Ex. 8 at 2). He noted that AA “is thought to be an immune-mediated disorder of unclear
etiology.” Resp’t’s Ex. A at 3 (citing Resp’t’s Ex. A, Tab 2 at 1, ECF No. 29-3).50 Although genetic
and environmental factors have been proposed to play roles in AA pathogenesis, “very little is
known about the environmental stimuli, if any[,] that may be required for development of this
disease.” Id. Dr. Matloubian wrote that “[s]everal factors, such as infections, metabolic toxins,
vaccines, and stress have all been postulated to ‘trigger’ [AA], but none have been established or
universally accepted as a culprit.” Id. (citing Resp’t’s Ex. A, Tab 3 at 4, ECF No. 29-4).51 He noted
that while AA has been associated with viral infections such as CMV, such associations have not
been confirmed by follow-up studies. Id. He continued that “[s]imilarly, based on sporadic case
reports of [AA] after hepatitis B vaccination, there was some concern regarding a relationship
between the two[, but] follow[-]up studies including experiments in a mouse strain predisposed to
developing [AA] failed to establish a causal link between hepatitis B vaccine and development of”
AA. Id. (citing Pet’r’s 15 at 7–8, ECF No. 17-8).52
Dr. Matloubian noted that some of the external factors potentially involved in AA
pathogenesis, such as stress, “do not involve introduction of a foreign antigen or an exogenous
(external) immune altering agent [ ].” Id. He noted that a number of the articles Petitioner submitted
indicated that stress is a potential trigger of AA. See id. (citing Pet’r’s Ex. 8 at 4; Pet’r’s Ex. 9 at
9, ECF No. 17-2;53 Pet’r’s Ex. 26 at 4, ECF No. 18-9;54 Pet’r’s Ex. 28 at 1, ECF No. 19-1;55 Pet’r’s
Ex. 29 at 1, ECF No. 19-2;56 Pet’r’s Ex. 47 at 6, ECF No. 20-10).57 Dr. Matloubian explained that
“[t]he hypothesis that stress mediated alterations in the hypothalamic-pituitary-adrenal [ ] axis
could result in immune changes that lead to development of [AA] indicates that an infectious agent
associated antigen, usually through a hypothesis based on molecular mimicry with self-antigens[,]
49 Amos Gilhar et al., Alopecia Areata, 366 N ENGL J. MED 1515 (2012).
50 Andrew G. Messenger, Clinical manifestations and diagnosis of alopecia areata, UPTODATE (2018).
51 C. Herbert Pratt et al., Alopecia areata, 3 NAT REV DIS PRIMERS (2017).
52 K.J. McElwee et al., What causes alopecia areata?, 22 EXPERIMENTAL DERMATOLOGY 609 (2013).
53 Abdullah Alkhalifah et al., Alopecia areata update, 62(2) J. AM ACAD DERMATOL 177 (2010).
54 Taisuke Ito, Recent Advances in the Pathogenesis of Autoimmune Hair Loss Disease Alopecia Areata,
128 J. INVEST DERMATOL 1196 (2008).
55 Petra Clara Arck et al., Stress Inhibits Hair Growth in Mice by Induction of Premature Catagen
Development and Deleterious Perifollicular Inflammatory Events via Neuropeptide Substance P-
Dependent Pathways, 162(3) AM J. OF PATHOLOGY 803 (2003).
56 Alexandra Katsarou-Katsari et al., Alopecia areata and Affected Skin CRH Receptor Upregulation
Induced by Acute Emotional Stress, 203 DERMATOLOGY 157 (2001).
57 Amos Gilhar et al., Lymphocytes, neuropeptides, and genes involved in alopecia areata, 117 J. CLIN
INVEST 2019 (2007).
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may not be playing a role in this disease.” Id. He noted that “[t]his is consistent with the finding
that C3H/HeJ mouse model of [AA] develop the disease spontaneously and in the absence of
introduction of an infectious agent or immunization with a foreign peptide [ ].” Id. (citing Pet’r’s
Ex. 66) (emphasis omitted). Because Sundberg et al. were able to increase the incidence of
spontaneously occurring alopecia from 0.25% to 20% through inbreeding the mice, Dr. Matloubian
opined that this indicates “a very strong role” of genetics in alopecia pathogenesis. Id. (citing
Pet’r’s Ex. 66 at 1). Dr. Matloubian explained that the mice developed spontaneous disease and
that “if there was an infectious immunology, you would expect all of the mice in the same cage to
have it . . . [y]ou would[ not] expect just only [twenty] percent of the colony to have it.” Tr. 122:9–
18. He stated that “[t]he fact that an external trigger, infectious or otherwise[,] has not been
identified in this model [ ] suggests that a disease initiating external cue or stimulus may also not
be required for development of [AA] in humans.” Resp’t’s Ex. A at 3. In addition, Respondent
filed an article by Maglakelidze et al., 58 which reported “that 62% of C57BL/6J female Aire mice
spontaneously developed persistent AA-like lesions that displayed several hallmarks of human
AA.” Resp’t’s Ex. H at 2, ECF No. 84-3. The researchers found “infiltrate comprised of CD8+ T
cells, CD4+ T cells, CD68+ macrophages[] . . . .” Id. They explained that “[p]atients with mutations
in autoimmune regulator (AIRE) are 15x more likely to develop AA than the general population[]
. . . .” Id.
Dr. Matloubian noted that “given the complex pathogenesis of autoimmune diseases, such
as [AA], the research field is moving away from simplistic explanations, such as molecular
mimicry[,] due to infection or vaccination, because of a lack of convincing rigorously tested
evidence in their support, to other environmental risk factors, such as diet and antibiotic usage that
may affect the microbiota.” Resp’t’s Ex. A at 4. Citing a paper by Alkhalifah et al. filed by
Petitioner, that notes that dietary soy oil increased resistance to AA in mice, Dr. Matloubian stated
that “[s]ince diet has been shown to affect the microbiome, it can thus indirectly perturb the
immune system and lead to development of [AA].” Id. (citing Pet’r’s Ex. 9 at 9). Dr. Matloubian
asserted that the microbiome “has been shown to alter immune tolerance through their effects on
regulatory T cells[,]”59 which “maintain immune tolerance and prevent immune activation towards
self-antigens.” Id. Citing a paper by Ali and Rosenblum,60 he noted that changes in the gut
microbiome have been linked “with changes in the numbers and function” of such cells.” Id.
(Resp’t’s Ex. A, Tab 8, ECF No. 29-9). He continued that regulatory T cells “have been found at
the base of hair follicles indicating an important role for them in maintaining tolerance in this
specific location.” Id. (citing Resp’t’s Ex. A, Tab 8 at 6). He also cited an article by Gilhar et al.
that noted that dysfunctional regulatory T cells have been found in diseases such as psoriasis,
multiple sclerosis, and autoimmune polyglandular syndrome type 1. Pet’r’s Ex. 47 at 5. Gilhar et
al. also noted that C3H/HeJ mice with alopecia have been found to have low levels of regulatory
T cells in their skin. Id. He also cited a paper by Petukhova et al.61 filed by Petitioner to show that
58 Natella Maglakelidze et al., Aire deficiency leads to the development of alopecia areata-like lesions in
mice, J. INVEST DERMATOL (2022).
59 Regulatory T cells are “a subset of CD4+ T cells that can suppress activity of effector cells such as
helper cells and suppressor cells, and inhibit autoimmune diseases.” Dorland’s at 318. CD4 T cells are T
cells that “carry the CD4 antigen[.]” Id. at 311.
60 Niwa Ali & Michael D. Rosenblum, Regulatory T cells in skin, 152 IMMUNOLOGY 372 (2017).
61 Lynn Petukhova et al., Genome-wide association study in alopecia areata implicates both innate and
adaptive immunity, 466 NATURE 113 (2010).
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genetic studies of individuals with alopecia “have found ‘association with genomic regions
containing several genes controlling the activation and regulation of regulatory T cells [ ].’”
Resp’t’s Ex. A at 4 (quoting Pet’r’s Ex. 17 at 1, ECF No. 17-10). He concluded that, taken together,
“these studies raise the possibility that alteration in regulatory T cell numbers or function could
contribute to pathogenesis of [AA].” Id. Noting that Petitioner was treated with antibiotics before
his vaccination in March of 2016, Dr. Matloubian surmised that “this course of antibiotics
[possibly] led to alteration of his gut microbiome, which then led to disruption of regulatory T cell
function.” Id. Citing Ali and Rosenblum, Dr. Matloubian averred that this disruption could result
in AA in a genetically-susceptible individual. Id. He also cited a report of two cases by Rebello et
al.,62 which he stated “showed that restoration of gut microbiome through a fecal implant in two
individuals with [AA] led to hair regrowth without any other treatments.” Id. (citing Resp’t’s Ex.
A, Tab 9, ECF No. 29-10). One patient, a twenty-year-old man with AA causing 95–99% hair loss,
improved to 25–49% hair loss less than two years after the transplant with no other post-transplant
treatment besides two steroid injections. Resp’t’s Ex. A, Tab 9 at 1–3. Dr. Matloubian concluded
that, therefore, “a role for the microbiome in affecting hair regrowth is not speculative but has been
clearly established in the clinical setting.” Id.
Citing a review article by Grimaldi-Bensouda et al.,63 Dr. Matloubian asserted that
“multiple studies have not found any association between administration of the quadrivalent
[HPV] vaccines, including Gardasil and the development of a variety of autoimmune diseases.”
Resp’t’s Ex. A at 5 (citing Resp’t’s Ex. A, Tab 11, ECF No. 30-2). In addition to noting that several
studies had not provided “robust evidence” linking the HPV vaccine to autoimmune diseases,
Grimaldi-Bensouda et al. conducted a study of eleven to twenty-five-year-old girls and women in
France over six years. Resp’t’s Ex. A, Tab 11 at 2. They concluded that “[e]xposure to HPV
vaccine was not associated with an increased risk of [autoimmune disorders] within the time period
studied.” Id. Dr. Matloubian noted that these studies “did not specifically determine the risk of
[AA] after HPV vaccination[]” but rather “evaluate[d] for other associated autoimmune diseases
such as systemic lupus erythematosus [(“SLE”) ] and thyroiditis.” Resp’t’s Ex. A at 5. Noting that
HPV has been shown in studies to be safe and effective in people with preexisting autoimmune
disorders, including SLE, Dr. Matloubian asserted that “[t]his makes the likelihood of an
autoimmune disease occurring due to HPV immunization of a genetically predisposed person
extremely low.” Id. (citing Resp’t’s Ex. A, Tab 12, ECF No. 30-3).64 Dr. Matloubian concluded
that “[i]n the absence of an established and universally agreed upon trigger of any kind for [AA],
to implicate the Gardasil vaccine as the cause of [Petitioner’s AA] would be quite speculative and
not supported by the medical literature.” Id. at 5–6. Dr. Matloubian noted that although “HPV
infections and [AA] are quite common, no association has been recognized between the two.”
Resp’t’s Ex. C at 4.
Dr. Matloubian asserted that “none of the 71 articles submitted by Dr. Gershwin [with his
first expert report] provide a scientific basis that would support a specific causal relationship
62 Dionne Rebello et al., Hair Growth in Two Alopecia Patients after Fecal Microbiota Transplant, 4
ACG CASE REPORTS J. 1 (2017).
63 Lamiae Grimaldi-Bensouda et al., Risk of autoimmune disease and human papillomavirus (HPV)
vaccines: Six years of case-referent surveillance, 79 J. AUTOIMMUNITY 84 (2017).
64 J. Patricia Dhar, The safety and immunogenicity of Quadrivalent HPV (qHPV) vaccine in systemic
lupus erythematosus, 35 VACCINE 2642 (2017).
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between the antigenic components of the Gardasil vaccine and [AA] through a mechanism based
on molecular mimicry.” Resp’t’s Ex. A at 7. Dr. Matloubian averred that molecular mimicry “has
rarely been persuasively demonstrated as a major cause of autoimmunity in general, with a few
notable exceptions[] . . . .” Id. He continued that molecular mimicry “has become a less favorable
explanation” as understanding of the immune system has advanced and that it “is definitely not
applicable to those autoimmune diseases that are not post-infectious and thus, may not be triggered
by exposure to a foreign antigen.” Id.
Dr. Matloubian explained that “[t]he two arms of the immune system that are implicated
in autoimmunity, potentially through molecular mimicry, are B cells and T cells.” Resp’t’s Ex. A
at 7. He continued that B cells “make antibodies that are specific for one molecular pattern[]” while
T cells “only detect small linear pieces of proteins in the context of HLA molecules[, which] are
different between unrelated individuals . . . .” Id. He noted that molecular mimicry at the level of
B cells would involve specific antibodies while “[f]or a T cell mediated disease, the same T cells
that are generated against a specific pathogen-derived peptide seen in the context of an HLA
molecule also have to see peptides derived from a self-protein in the context of that same HLA [
].” Id. Dr. Matloubian thus concluded that “for a vaccine to be mechanistically associated with a
specific autoimmune disease through molecular mimicry, the pathogen that the vaccine is derived
from should also be associated with the same specific autoimmune disease [ ].” Id. In support, he
cited a paper by Schattner65 that outlines requirements for connecting vaccinations and
autoimmune diseases. Id. at 8 (citing Resp’t’s Ex. A, Tab 13, ECF No. 30-4). Schattner conducted
a search of publications between 1996 and 2004 to look for connections between autoimmune
manifestations and vaccinations. Resp’t’s Ex. A, Tab 13 at 1. She found that “[w]henever
controlled studies of autoimmunity following viral vaccines were undertaken, no evidence of an
association was found.” Id. However, she acknowledged that “very rare individual patients may
develop certain restricted patterns of autoimmune damage following some of the viral vaccines[]
. . . .” Id. at 8. Based on her findings, Schattner proposed the following guidelines:
To establish a role for viral vaccines in the subsequent development of
autoimmunity or autoimmune diseases[,] several conditions have to be met. First,
virus infections should be linked to autoimmunity. Second, a mechanism or
mechanisms whereby exposure to viral antigens (be it during infection or
vaccination) leads to autoimmunity must be established. Third, evidence must be
obtained that patients who have been vaccinated against viruses developed an
autoimmune disease, bearing in mind that association alone does not necessarily
indicate causality.
Id. at 6.
Dr. Matloubian also cited the Institute of Medicine’s (“IOM”) reasoning that
thrombocytopenia can result from the measles, mumps, rubella (“MMR”) vaccine because
thrombocytopenia can occur after a measles infection.66 Id. at 9–10. However, Dr. Matloubian
emphasized that unlike this association, “there has [sic] been no reports of an association between
65 Ami Schattner, Consequence or coincidence? The occurrence, pathogenesis and significance of
autoimmune manifestations after viral vaccines, 23 VACCINE 3876 (2005).
66 Dr. Matloubian did not cite medical literature to support this contention.
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infection with human papilloma virus and development of [AA].” Id. at 10. Because “the antigenic
components of the Gardasil vaccine are derived from the human papilloma virus” Dr. Matloubian
concluded that “it is highly unlikely and biologically implausible that the vaccine can cause [AA]
through a mechanism based on molecular mimicry with its genetically encoded components [ ].”
Id. While Dr. Matloubian acknowledged that certain autoimmune diseases, such as rheumatic heart
disease and Guillain-Barré Syndrome (“GBS”), have been found to occur within a short time after
certain infections, he also testified that “[m]ost autoimmune diseases have not been established to
occur after a specific infection in a short period of time.” Tr. 108:7–109:1.
Dr. Matloubian stated that when he searched for publications associating HPV vaccines
with AA, he was unable to find any. Resp’t’s Ex. A at 10. He also discussed the articles submitted
by Dr. Gershwin and noted that only a few of them mention molecular mimicry. Id. He cited the
Madani and Shapiro article filed by Petitioner, in which the authors wrote that “[t]he whole concept
of molecular mimicry of the hair follicle with a virus is intriguing, but the evidence for a viral
origin of AA at this time is not conclusive.” Id. (quoting Pet’r’s Ex. 10 at 4).
Dr. Matloubian noted that “[i]t is important to make the distinction between what causes
the damage to the hair follicles, which potentially could be cytotoxic T cells, and the mechanism
by which they become activated to do so.” Resp’t’s Ex. C at 4. While he acknowledged that
cytotoxic T cells have been associated with AA pathogenesis, he opined that “[t]here is no clear
scientific evidence or consensus among researchers that these cells become activated through
molecular mimicry with a foreign antigen.” Id. He explained that “there are many mechanisms that
can lead to loss of T cell or B cell tolerance.” Tr. 107:7–9. Such mechanisms include “escape of
autoreactive T cells from the thymus[]”67 and a defect in a single gene. Tr. 107:9–18.
Dr. Matloubian testified that “T cells can be divided generally into CD8 positive or
cytotoxic T cells . . . and CD4 T cells or helper T cells . . . .” Tr. 144:11–14. He explained that
CD8 T cells “kill cells that are infected by a virus or other intracellular pathogens.” Tr. 144:15–
17. However, CD4 T cells are “really good at seeing extracellular microbes, and the reason for it
is that these viruses or proteins that are floating outside or bacteria that are floating outside get
picked up by what are called macrophages or dendritic cells.” Tr. 145:9–15. Rather than killing
cells through recognizing a peptide specific to a certain infection like CD8 T cells, CD4 T cells
“secrete cytokines and activate macrophages to kill these cells.” Tr. 145:3–7, 18–19. Dr.
Matloubian asserted that “protein vaccines such as the Gardasil vaccine, they typically get picked
up by these macrophages/dendritic cells and predominantly they get presented to CD4 T cells and
activate CD4 T cells to MHC class 2.” Tr. 145:21–24. He continued that “it[ is] unlikely for them
to get presented to CD8 T cells, because the antigens that get presented in the CD8 T cells are
usually the ones that are generated in the cytoplasm.” Tr. 146:1–4. He opined that “there are really
no papers showing CD8 T cells get activated by the HPV vaccine . . . because they probably do[
not] get much activated. That[ is] not what the vaccine is designed for.” Tr. 146:9–12. Instead,
“[t]he vaccine is designed to activate CD4 T cells so it provides help to B cells . . . And these B
cells will now make antibodies to these proteins in the Gardasil vaccine.” Tr. 146:12–16. He noted
that if the HPV vaccine was good at promoting cytotoxic T cells, it would be used to treat cervical
cancer, which occurs due to HPV infection and contains HPV virus. Tr. 146:19–23. He stated that
67 The thymus is “a primary lymphoid organ consisting of two pyramidal lobes usually located in the
mediastinum.” Dorland’s at 1895. It is “the site of production of immunocompetent T lymphocytes.” Id.
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“if the Gardasil vaccine was good enough to induce cytotoxic T cells, it would be used to vaccinate
people who suffer from cervical cancer to be able to activate these cytotoxic T cells to get rid of
those [sic] cancer, but it[ is] not good enough to do that.” Tr. 147:23–148:2. Dr. Matloubian
criticized Dr. Gershwin’s use of Stryhn et al. paper to support his theory in this case because the
yellow fever vaccine, unlike the HPV vaccine, is a live attenuated vaccine. Tr. 148:17–18. He
explained that live attenuated vaccines contain “actual infection[] . . . and get inside the cells and
replicate, they induce a good cytotoxic T cell response, whereas protein vaccines are not very good
at doing that.” Tr. 148:19–24.
Dr. Matloubian discussed a paper by Xing et al.68 filed by Petitioner, in which the “authors
show that cytotoxic T cells are involved in a spontaneous mouse model of [AA] . . . .” Resp’t’s
Ex. C at 4 (citing Pet’r’s Ex. 67, ECF No. 22-10). Dr. Matloubian noted that the authors “suggest
that the T cells may recognize and kill hair follicle cells through expression of NKG2D, a natural
killer cell receptor.” Id. (citing Pet’r’s Ex. 67). Dr. Matloubian explained that “[t]he ligands for
NKG2D, such as H60 and Rae-1 are expressed on the surface of cells when they become ‘stressed’
so that natural killer cells or other cytotoxic cells expressing NKG2D can recognize and kill those
cells.” Id. He noted that unlike NKG2D ligands, “[c]omponents of the Gardasil vaccine cannot be
processed and expressed on surface of cells” and that thus, “NKG2D expressing cytotoxic T cells
cannot be activated through molecular mimicry by components of the Gardasil vaccine.” Id. at 4–
5. He stated that “Dr. Gershwin has not provided any literature to support that this mouse model
is based on molecular mimicry, with any cross-reactive T cells.” Tr. 123:21–24.
Dr. Matloubian addressed the case reports and similar papers Petitioner submitted.
Discussing the Wise et al. paper, Dr. Matloubian noted that the authors “were not looking at [AA]
specifically[]” but rather at “this passive report of hair loss after vaccination, and they found only
a few cases.” Tr. 113:4–8. Noting that the authors’ findings were equivalent to a one in twenty
million incidence of hair loss following vaccinations, Dr. Matloubian stated that the typical
incidence rate of one in 5,000 per year is much higher. Tr. 113:21–114:13 (citing Pet’r’s Ex. 79 at
3). He testified that “the point here is that people after vaccination can coincidentally have AA
because the rate is so high.” Tr. 114:13–14. Regarding the COVID-19 vaccine case reports, Dr.
Matloubian explained that coronaviruses are “very different from human papillomavirus[]” in that
coronaviruses have an RNA-based genome and a membrane while “human papillomaviruses have
DNA as their genome[]” and no membrane. Tr. 114:20–115:5. Dr. Matloubian also noted that in
the Gallo et al. case report, the individual developed AA within one day of his second COVID
vaccination, which is “not consistent with a mechanism based on molecular mimicry[.]” Tr. 115:6–
9 (citing Pet’r’s Ex. 93 at 1–2). Discussing the Scollan et al. article, Dr. Matloubian noted that “the
COVID mRNA vaccine is not the same as the HPV vaccine which is made of only proteins.” Tr.
116:13–19. He also noted some individuals in this study developed hair loss months following
their second COVID vaccine doses, which is “not consistent with a mechanism based on molecular
mimicry.” Tr. 117:2–5 (citing Pet’r’s Ex. 98 at 2). Addressing the Chu et al. case report, Dr.
Matloubian likewise noted that Japanese encephalitis is a “very different” virus and that the authors
proposed a different mechanism. Tr. 115:22–116:4.
68 Luzhou Xing et al., Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK
inhibition, 20 NATURE MEDICINE 1043 (2014).
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Addressing the Tu et al. study, Dr. Matloubian noted that this article did not change his
opinion in this case. Tr. 129:24–130:1. He stated that the study is not ideal because it is a
“population-based retrospective cohort study” using billing codes from medical records. Tr.
130:6–13. Dr. Matloubian also noted that that there are 200 types of HPV, only forty of which can
infect the genital tract. Tr. 131:12–15. He stated that “the infections [Tu et al. are] looking at are
not the same HPV [strains as] the four HPV [strains] that were in the Gardasil vaccine.” Tr.
131:19–21. He also pointed out that the authors were only looking at symptomatic HPV infections,
but most HPV infections are asymptomatic. Tr. 131:21–25. Dr. Matloubian noted that, according
to some estimates, “80 up to 100 percent of sexually active individuals have been infected with
HPV at some point.” Tr. 133:2–4. Dr. Matloubian also explained that when an individual had HPV
symptoms, such as warts, does not indicate when she was infected, as she “could have had the
infection for many years before that.” Tr. 133:24–134:5. Discussing the time between HPV
symptoms and AA onset in this study and when differences in incidence occurred between the
affected individuals and the control group, Dr. Matloubian, again noted that study participants
likely had HPV for years before diagnosis and that this timeline is not consistent with a mechanism
based on molecular mimicry. Tr. 134:15–135:7. He noted that Tu et al. “start[ed] seeing a
difference between the control group versus not, somewhere between four to six years” after HPV
diagnosis. Tr. 134:18–20. He opined that this paper does not show that AA “can happen shortly
after an HPV infection.” Tr. 140:12–15. Dr. Matloubian noted that AA is common in children, and
he cited the Gilhar et al. paper, which identified the median age of AA onset in one study as ten
years old. Tr. 140:25–141:3 (citing Resp’t’s Ex. A, Tab 1 at 1). Because the HPV infections the
Gardasil vaccine protects against are uncommon in children, Dr. Matloubian concluded that it is
unlikely that HPV infection causes AA in children. Tr. 141:23–25.
Dr. Matloubian disagreed with Dr. Gershwin’s contention that Petitioner’s AA was likely
caused by the HPV vaccine because the HPV vaccine was the only immunological challenge
Petitioner experienced in the weeks before his AA onset. Tr. 149:13–17. He opined that “[i]n the
absence of any epidemiologic or scientific evidence to link either infection or immunization with
[HPV] and the development of [AA], . . . coincidence is the most likely explanation.” Resp’t’s Ex.
A at 12. Extrapolating data from a paper by Ahmed et al.,69 Dr. Matloubian noted that “if 10,000
individuals receive the Gardasil vaccine, there is a 90% chance that one individual will develop
[AA] through coincidence alone based on its annual incidence.” Id. (citing Resp’t’s Ex. A, Tab
10). He noted that “based on the literature provided by Dr. Gershwin[,] it appears that some experts
believe that internal causes, such as changes in the microbiome, random gene expression, or even
hormonal changes that can occur, especially in a 12-year-old who is undergoing puberty can result
in immune changes and development of [AA].” Id. Dr. Matloubian concluded that Dr. Gershwin
“is relying solely on temporal relationship between vaccination and development of disease.” Id.
He disagreed with Dr. Gershwin’s contention that an examination of one million people who
received the HPV vaccine might not reveal a single case of AA. Tr. 151:10–13. Dr. Matloubian
explained, “[y]ou will see a lot, but that[ is] because of coincidence alone.” Tr. 151:13–14. Dr.
Matloubian indicated that the range of time frames between vaccination and AA onset presented
in the case reports submitted by Petitioner “does[ not] seem to support a unified theory based on
molecular mimicry.” Tr. 163:5–9. However, he agreed that CD8 positive T cells can activate and
cause dysfunction within one to two weeks. Tr. 164:11–15.
69 S. Sohail Ahmed et al., Assessing the Safety of Adjuvanted Vaccines, 3(93) VACCINES 1 (2011).
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IV. Applicable Legal Standards
To receive compensation under the Vaccine Act, a petitioner must demonstrate either that:
(1) the petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently
developing a listed injury within the 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 petitioner suffered an “off-
Table injury,” one not listed on the Table, as a result of his 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 the Dept. 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
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or condition.’” 42 U.S.C. § 300aa-13(a)(2); see also Doe v. Sec’y of Health & Hum. Servs., 601
F.3d 1349 (Fed. Cir. 2010) (stating that an idiopathic diagnosis cannot be a “factor unrelated,” as
it is idiopathic).
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). To satisfy this prong, 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.
Furthermore, establishing a sound and reliable medical theory connecting the vaccine to
the injury often requires a petitioner to present expert testimony in support of her claim. Lampe v.
Sec’y of Health & Hum. Servs., 219 F.3d 1357,1361 (Fed. Cir. 2000). The Supreme Court’s
opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), requires that
courts determine the reliability of an expert opinion before it may be considered as evidence.
However, in the Vaccine Program, the Daubert factors are used in the weighing of the reliability
of scientific evidence proffered. Davis v. Sec’y of Health & Hum. Servs., 94 Fed. Cl. 53, 66–67
(2010) (“[U]niquely in this Circuit, the Daubert factors have been employed also as an acceptable
evidentiary-gauging tool with respect to persuasiveness of expert testimony already admitted.”);
see also Cedillo v. Sec’y of Health & Hum. Servs., 617 F.3d 1328, 1339 (Fed. Cir. 2010) (citing
Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999). Under Daubert,
the
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factors for analyzing the reliability of testimony are: (1) whether a theory or
technique can be (and has been) tested; (2) whether the theory or technique has
been subjected to peer review and publication; (3) whether there is a known or
potential rate of error and whether there are standards for controlling the error; and
(4) whether the theory or technique enjoys general acceptance within a relevant
scientific community.
Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592–95).
The Daubert factors are “meant to be helpful, not definitive.” Kumho Tire Co. v.
Carmichael, 526 U.S. 137, 151 (1999). The factors do not “constitute ‘a definitive checklist or
test’” and may be applied differently depending on the facts of a particular case. Id. at 150 (quoting
Daubert, 509 U.S. at 593).
“In short, the requirement that an expert’s testimony pertain to ‘scientific knowledge’
establishes a standard of evidentiary reliability.” Daubert, 509 U.S. at 590 (citation omitted).
Thus, for Vaccine Act claims, a “special master is entitled to require some indicia of reliability to
support the assertion of the expert witness.” Moberly, 592 F.3d at 1324. Nothing requires the
acceptance of an expert’s conclusion “connected to existing data only by the ipse dixit of the
expert,” especially if “there is simply too great an analytical gap between the data and the opinion
proffered.” Snyder v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen.
Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also D’Tiole v. Sec’y of Health & Hum. Servs.,
No. 15-085V, 2016 WL 7664475, at *24 (Fed. Cl. Spec. Mstr. Nov. 28, 2016) (stating that the
Vaccine Act “require[s] a chain of reliable propositions supporting [a] petitioner’s theory[]”).
Petitioner’s proposed theory of molecular mimicry has two central components. The first
component is that Petitioner “received a vaccine that produced cytotoxic T cells[.]” Pet’r’s Ex. 7
at 5. The second is that these cytotoxic T cells “were directed at his hair follicles and [ ] cross
react[ed] with an epitope or region of the Gardasil vaccine.” Id. Accordingly, to demonstrate that
this theory is sound and reliable by a preponderant standard, Petitioner must present preponderant
evidence that the HPV vaccine he received “produce[s] cytotoxic T cells.” Petitioner cannot
prevail on Prong One because he has failed to present such evidence.
Despite filing ninety-seven pieces of medical literature, Petitioner has not filed a single
article indicating that the HPV vaccine can or does produce cytotoxic T cells. 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. Petitioner’s
own expert, Dr. Gershwin, admitted that “the HPV vaccine is not designed to produce CD8 T
cells[.]” Tr. 79:18–21. Likewise, Dr. Matloubian explained that protein vaccines like Gardasil are
designed to activate CD4 T cells rather than cytotoxic T cells. Tr. 146:9–16. Dr. Matloubian noted
that “there are really no papers showing CD8 T cells get activated by the HPV vaccine . . . because
they probably do[ not] get much activated.” Tr. 146:9–12. Dr. Matloubian supported his point by
noting that if the HPV vaccine induced cytotoxic T cells, it would be used to treat cervical cancer,
which is often caused by the HPV strains that Gardasil is designed to protect against, via activation
of cytotoxic T cells against the HPV in the cancer cells. See Tr. 146:19–23. He further explained
that while Petitioner filed the Stryhn article, which indicates that the yellow fever vaccine can
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produce cytotoxic T cells, the yellow fever vaccine is a live attenuated vaccine. Tr. 148:17–18. It
contains “actual infection,” and it “induce[s] a good cytotoxic T cell response[;] whereas protein
vaccines[, such as Gardasil,] are not very good at doing that.” Tr. 148:19–24. Rather than
presenting evidence that the Gardasil vaccine induces cytotoxic T cells, Dr. Gershwin asserted that
that there is “no literature that says [the Gardasil vaccine] does[ not] produce any [cytotoxic T
cells].” Tr. 43:21–24. He claimed that “it could well be that [Petitioner’s] problem is that he is the
rare individual that does get a CD8 T cell response.” Tr. 183:19–21. Thus, Petitioner’s response to
the dearth of evidence supporting a central component of his theory appears to be that it is
theoretically possible that the HPV vaccine could induce a CD8 T cell response in some people.
However, showing that this response is merely possible is insufficient to sustain this essential
component of Petitioner’s theory by preponderant evidence. See, e.g., Canuto v. Sec’y of Health
& Hum. Servs., 660 Fed. Appx. 955, 957 (Fed. Cir. 2016) (citing W.C. v. Sec’y of Health & Hum.
Servs., 704 F.3d at 1356 (Fed. Cir. 2013) (“[T]he petitioner must do more than demonstrate a
‘plausible’ or ‘possible’ causal link between the vaccination and the injury[.]”). Petitioner has
failed to provide preponderant evidence that this response actually can occur.
In Cordova v. Sec’y of Health & Hum. Servs., in which Dr. Gershwin was also the
petitioner’s expert, the chief special master concluded that the petitioner failed to present
preponderant evidence that the HPV vaccine could cause AA via the upregulation of cytotoxic T
cells. He reached this conclusion in part because “there [was] an overarching deficiency in Dr.
Gershwin’s contentions about the capacity of the HPV vaccine to cause an upregulation of the
cytotoxic T cells central to hair follicle destruction.” No. 17-1282V, 2021 WL 3285367, at *18
(Fed. Cl. Spec. Mstr. June 21, 2021). The chief special master wrote that “[a]lthough it is not
disputed that CD8+ T cells are central to AA’s progression, few reliable articles stand for the
proposition that the HPV vaccine causes the upregulation of this T cell in sufficient amounts to be
pathologic.” Id. Unlike in the present case, the petitioner in Cordova 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.” Id. at *17. The chief special master
found that the articles did not show that the increase in T cells “(a) is likely causal of AA, or (b)
even involves the specific kind of cytotoxic T cells that drive AA.” Id. While the petitioner in
Cordova was unsuccessful, he at least provided some evidence linking the HPV vaccine to a T cell
response, although not to a cytotoxic T cell response specifically. Thus, Petitioner’s evidence to
support that the HPV vaccine can induce cytotoxic T cells is even weaker in this case. As in
Cordova, Petitioner has failed to present preponderant evidence of this component of his theory.
Furthermore, 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 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 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). As in Cordova, “Petitioner lacks
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evidence suggesting an association between the HPV vaccine and AA, whether in the form of
literature[,] . . . studies[,] or testimony from Dr. Gershwin derived from his own research or
treatment experience.” Cordova, 2021 WL 3285367, at *16.
Petitioner submitted some case reports and papers to establish a relationship between
vaccines, including HPV, and conditions that involve hair loss, including AA. The Tuccori et al.
case reports center on the bivalent HPV vaccine, which is not the same type of HPV vaccine
Petitioner received, and telogen effluvium, which is not AA. See Pet’r’s Ex. 99. This is the only
article Petitioner filed that links any HPV vaccine and hair loss. However, it does not provide
persuasive evidence of a link between HPV vaccines and AA because the article draws from a
small number of cases and involves a different type of hair loss. See Al-Uffi vs. Sec'y of Health &
Hum. Servs., No. 13-956V, 2017 WL 1713113 at *16 (Fed. Cl. Spec. Mstr. Feb. 22, 2017)
(“Individual case studies are not themselves particularly probative in the context of establishing
the first Althen prong (especially where they involve a totally different vaccine).”). Likewise, the
Wise et al. paper does not involve the HPV vaccine and is not specific to AA. See Pet’r’s Ex. 79.
Petitioner filed some case reports linking other vaccines to AA, but these do not indicate a
relationship between the HPV vaccine and AA. These include papers linking the COVID-19
vaccine to AA, but Dr. Matloubian persuasively explained that “the COVID mRNA vaccine is not
the same as the HPV vaccine which is made of only proteins.” Tr. 116:13–19. After reviewing all
of the medical literature Petitioner submitted, I find that he has not presented preponderant
evidence of a relationship between the HPV vaccine he received and AA.
While Petitioner has not presented preponderant evidence relating the HPV vaccine and
AA, he could possibly show a potential for cross-reaction by linking HPV infection, especially
infection from the strains included in the Gardasil vaccine he received, with AA in a manner
consistent with Petitioner’s mechanism of molecular mimicry. Dr. Matloubian cited the Schattner
paper, which proposes the requirement that “virus infections should be linked to autoimmunity[]”
to demonstrate that vaccines can be implicated. See Resp’t’s Ex. A, Tab 13 at 6. This signals
Respondent’s contemplation that showing a link between HPV infection and AA may help
Petitioner establish a connection between the two, but Petitioner has not shown preponderant
evidence of such a link here.
Petitioner filed the Tu et al. paper to show that in “at least one study, [HPV] infection has
been linked to the development of alopecia[] . . . .” Tr. 45:20–25. However, this paper does not
provide preponderant support for the proposition that HPV infection could cause AA via molecular
mimicry. Tu et al. 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. See Pet’r’s Ex. 102 at 4.
Furthermore, as Tu et al. only included patients who were symptomatic and received treatment
related to their HPV in the HPV group, it is unlikely that patients in the HPV group were recently
infected with HPV. This is because, as Dr. Matloubian explained, HPV infections can take years
to cause symptoms or warrant treatment. See Tr. 133:24–135:7. Thus, the Tu et al. study does not
support that HPV infection caused AA via Petitioner’s mechanism or a similar mechanism, which
Dr. Gershwin indicated would occur within weeks of antigen exposure. In fact, Tu et al. did not
propose molecular mimicry as the possible mechanism at play in their study. They also
acknowledged that “epidemiologic evaluation of HPV infection was challenging, as many
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infections were not clinically recognized[,]” underscoring the point that patients with HPV
infections or newly-acquired HPV infections may have been excluded from the HPV group. See
Pet’r’s Ex. 102 at 7. Furthermore, the Tu et al. paper does not indicate how many patients in their
study were infected with the HPV strains contained in the Gardasil vaccine. Thus, it is unclear
whether the authors would have found an association between HPV infection and AA if their study
were limited to the HPV strains contained in the vaccine. Tu et al. also acknowledged that their
“findings may not be applicable to non-Asian ethnic groups[,]” thus implying that their findings
do not necessarily support a general association between HPV and AA. See id. at 8.
Petitioner filed additional articles, primarily centering on COVID-19 infection, in an
attempt to show that AA is associated with infection. However, these papers are mostly case
reports on a small number of cases. Nguyen and Tosti identified 143 patients who experienced
flares of AA following COVID-19 infection, but all but seven of those patients had preexisting
AA. Pet’r’s Ex. 105 at 1. Petitioner has also failed to provide preponderant evidence that AA
allegedly following COVID-19 infection is relevant to this case. Dr. Matloubian explained that
coronaviruses, like COVID-19, are “very different from human papillomavirus[]” in that
coronaviruses have an RNA-based genome and a membrane while human papillomaviruses have
no membrane and a different type of genome. Tr. 114:20–115:5. Petitioner has not responded to
this contention or explained how COVID-19 infection may be analogous to HPV infection. Birkett
et al. stated that “AA can be triggered by viral infections such as influenza, [CMV], and the
Epstein-Barr virus[,] Pet’r’s Ex. 107 at 1, but Petitioner’s own expert, after reviewing and
submitting many articles in support of Petitioner’s case, acknowledged that acute infections are
not an established cause of AA. Tr. 62:12–14. He further acknowledged that he did not provide
medical literature showing a CD8 response to any virus that has been associated with AA. Tr.
81:1–5.
To support his mechanism of molecular mimicry between components of the HPV vaccine
and self-structures involved in AA, Dr. Gershwin indicated that the implication of cytotoxic T cells
in AA suggests that an antigen is also involved. See Tr. 182:11–14. Dr. Matloubian acknowledged
that cytotoxic T cells have been implicated in AA, but he denied that AA requires the introduction
of a foreign antigen. See Resp’t’s Ex. C at 4; Tr. 107:7–18. He noted that potential triggers, such
as stress and microbiome changes, do not involve the introduction of a foreign antigen. Resp’t’s
Ex. A at 3. He also cited the Sundberg et al. mice study filed by Petitioner as an example of an
AA-like disease appearing spontaneously, without an infectious source, and appearing to be
genetics-driven. Id. In response, Dr. Gershwin acknowledged that stress is a potential trigger that
does not involve an antigen, but he asserted that cases of AA associated with these triggers are
typically “more patchy[]” and not “lifelong.” Tr. 61:23–62:3. However, he also stated that he did
not know of a way to determine whether someone would develop AA, which may be more patchy,
or AA totalis. Tr. 88:21–89:2. Regarding the Sundberg et al. study, Dr. Gershwin asserted that
“[t]here[ is] something in these mice that[ is] causing them to develop[] . . . CD8 T cells[]” and
that the fact that the researchers did not find an antigen does not mean one was not present. Tr.
181:22–182:2–3. However, Dr. Gershwin’s assertion is curious given that Sundberg et al. looked
but did not find an infection present in the mice. See Pet’r’s Ex. 66 at 8. Dr. Gershwin was
“unaware of a clinical situation where [there are] organelle-specific cytotoxic T cells in the absence
of an antigen.” Tr. 182:11–14. However, Dr. Matloubian explained that “[t]here is no clear
scientific evidence or consensus among researchers that [the cytotoxic T cells implicated in AA]
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become activated through molecular mimicry with a foreign antigen.” Resp’t’s Ex. C at 4. He cited
other potential mechanisms associated with “loss of T cell or B cell tolerance[,]” including “escape
of autoreactive T cells from the thymus[]” and a genetic defect. Tr. 107:7–18. I find Dr.
Matloubian’s explanation more persuasive than Dr. Gershwin’s because, while it is undisputed
that cytotoxic T cells have been implicated in AA, the literature filed in this case does not indicate
that researchers necessarily or consistently associate these T cells with foreign antigens.
Specifically, the Sundberg et al. study indicates the presence of T cells in mice with AA without
an infection present. Thus, Petitioner has not established by preponderant evidence that a foreign
antigen, such as HPV or the components of the HPV vaccine, are required to induce the cytotoxic
T cells associated with AA.
Ultimately when discussing whether a foreign antigen is necessary to induce cytotoxic T
cells, Dr. Gershwin emphasized that “[w]hat[ is] critical is there[ is] a CD8 T cell response.” Tr.
184:1–3. Petitioner has not provided preponderant evidence that his proposed theory can occur
because he has not shown that the HPV vaccine can induce the “critical . . . CD8 T cell response.”
Even if Petitioner were able to provide preponderant evidence for the first component of his theory,
he still has not shown preponderant evidence of the second. He has failed to provide preponderant
evidence that the HPV vaccine or HPV infection can cross-react with components of the Gardasil
vaccine. Thus, Petitioner has failed to satisfy Prong One by a preponderant standard.
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
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
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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. During his testimony, Dr. Gershwin testified that causation in this case is
“deeper than just a temporal association[ because there is also a] cellular and a mechanistic
explanation for the temporal events . . . .” Tr. 50:18–23. Petitioner has failed to provide
preponderant evidence of a “cellular and [ ] mechanistic explanation” in this case. Thus, in light
of Dr. Gershwin’s own statement, 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.”). Dr. Gershwin supported causation by stating that Petitioner’s
HPV vaccination was “[t]he only immunological challenge” between Petitioner’s HPV
vaccination and alopecia onset. Pet’r’s Ex. 7 at 4. However, Dr. Matloubian disagreed that this
indicates causation and also explained that “very little is known about the environmental stimuli,
if any[,] that may be required for development of [AA].” Resp’t’s Ex. A at 3. Dr. Matloubian
explained a number of potential triggers besides the HPV vaccine that may have played a role in
this case, including stress and Petitioner’s use of an antibiotic in March of 2016. See id. at 4, 12.
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.
Furthermore, Petitioner has failed to present preponderant evidence that he experienced an
autoimmune reaction following his HPV vaccination. 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. However, Dr. Gershwin acknowledged that there
would be no way to distinguish between vaccine-caused and idiopathic alopecia. Tr. 84:23–85:5.
He indicated that a difference could potentially be demonstrated through research efforts that have
not been undertaken, but he conceded that he did not have evidence of an autoimmune reaction in
this case. Tr. 84–85. Dr. Gershwin could not identify evidence of inflammation in Petitioner’s
alopecia, and he instead noted that such inflammation in an AA case would need to be observed
“under a microscope.” Tr. 93:2–15. 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, 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
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no evidence of any immediate reaction or measured autoimmune/inflammatory process that
preceded onset[]”). Thus, Petitioner has failed to satisfy Prong Two by a preponderant standard.
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))).
Petitioner has presented preponderant evidence that his AA symptoms began
approximately two weeks after his HPV vaccination. Dr. Gershwin stated that “onset within
[fourteen] days” is “consistent with generation of a CD8 response.” Pet’r’s Ex. 7 at 4. Dr.
Matloubian agreed that CD8 T cells can cause dysfunction within one to two weeks. Tr. 164:11–
15. Therefore, Petitioner has provided preponderant evidence of a proximate temporal relationship
pursuant to Prong Three. However, because Petitioner has not provided preponderant evidence
that the HPV vaccine can induce cytotoxic T cells and thus cause AA through molecular mimicry
or that it did so in this case, Petitioner has not established that he is entitled to compensation.
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 May 16, 2016 HPV vaccination. Accordingly, I DENY
Petitioner’s claim and DISMISS his petition.70
IT IS SO ORDERED.
70 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.
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s/Herbrina D. Sanders
Herbrina D. Sanders
Special Master
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