G. v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS No. 20-416V Filed: May 20, 2026 Reissued for public availability: September 3, 2026

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

* C.G., *

* Petitioner, *

* v. *

* SECRETARY OF HEALTH AND * HUMAN SERVICES, *

* Respondent. *

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

Michael G. McLaren, Black McLaren, et al., P.C., Memphis, TN, for Petitioner.

Emilie Williams, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION DENYING ENTITLEMENT1

Shah, Special Master:

On April 13, 2020, C.G. (“Petitioner”) filed a petition for compensation under the National Vaccine Injury Compensation Program, 42 U.S.C. §§ 300aa-10, et seq.2 (the “Vaccine Act” or “Program”). ECF No. 1 (“Pet.”). The petition alleges that Petitioner developed Guillain-Barré syndrome (“GBS”) “and/or other neurologic and physical impairments and other injuries” caused by the Hepatitis A and meningococcal vaccinations he received on July 6, 2017. Id. at 1.

For the reasons discussed in this decision, I find that the evidence did not preponderantly establish Petitioner sustained a vaccine-caused injury. The evidence did not show either of the subject vaccines can cause GBS, either independently or in combination with a cytomegalovirus (“CMV”) infection, nor did it demonstrate a logical sequence of cause and effect between the subject vaccines and Petitioner’s condition. I conclude Petitioner is not entitled to compensation. I. PROCEDURAL HISTORY

After filing his petition, Petitioner filed medical records and an affidavit. Exs. 1-14. On January 4, 2021, Respondent filed a Rule 4(c) Report, recommending that entitlement be denied. ECF No. 23 (“Report”) at 2, 8.

On February 5, 2021, Petitioner filed an expert report by M. Eric Gershwin, M.D., along with medical literature. Exs. 15-22. On July 15, 2021, Respondent filed expert reports by Brian C. Callaghan, M.D., M.S., and Robert S. Fujinami, Ph.D., along with their CVs and medical literature. Exs. A-M.

On August 23, 2021, Petitioner filed a status report indicating that he did not intend to file a responsive expert report, that Respondent “declined to participate in any mediation at this time,” and that he wished to proceed with an entitlement hearing. ECF No. 32. On September 8, 2021, Former Special Master Katherine E. Oler scheduled an entitlement hearing for January 25-26, 2023. Non-PDF Scheduling Order dated 9/8/2021.

On December 19, 2022, Special Master Oler held a status conference after Respondent advised that there was a conflict with Dr. Fujinami’s calendar and requested that the entitlement hearing be rescheduled; Petitioner objected to Respondent’s request, stating that litigation had been ongoing for over two years and that any further delay would be detrimental. ECF No. 35. Special Master Oler ordered the parties to file a joint status report on their availability to reschedule the hearing for August 2023. Id. The hearing was rescheduled for August 2-3, 2023. Non-PDF Scheduling Order dated 12/21/2022.

Petitioner filed Dr. Gershwin’s CV on March 8, 2023, and additional medical literature on June 21, 2023. Ex. 23-29. The parties filed pre-hearing briefs on July 6 and 12, 2023. ECF Nos. 44, 46.

Special Master Oler conducted the entitlement hearing on August 2-3, 2023, at which C.G. and Drs. Gershwin, Fujinami, and Callaghan testified. Minute Entry dated 8/3/2023; Tr. at 3, 133. After the hearing, the parties filed post-hearing briefs on September 28, 2023, January 12, 2024, and February 19, 2024. ECF Nos. 59, 61-62. The parties agreed that the record was complete on February 20, 2024. ECF No. 63.

This case was reassigned to me on August 14, 2024. ECF No. 64. This matter is now ripe for adjudication.

II. FACT EVIDENCE

A. C.G.’s Affidavit and Testimony Petitioner executed an affidavit on April 9, 2020. Ex. 1. He said that before the subject vaccinations, he “never suffered from pain, numbness, or tingling in [his] fingers, toes, [or] neck, nor had [he] experienced any back pain or shortness of breath or other GBS-like symptoms.” Id. at 1.

At hearing, Petitioner testified that he currently lived in Indiana, where he worked part- time at a restaurant. Tr. at 7-8. He moved to New York City several months before he received the subject vaccinations. Id. at 10. In New York, he engaged in increased sexual activity. Id. at 11. The subject vaccinations were given during a clinic visit for a refill of Pre-Exposure Prophylaxis (“PrEP”) medication. Id. at 10. The purpose of PrEP was to prevent contraction of HIV. Id.

Before moving to New York, Petitioner had never been diagnosed with a CMV infection or mononucleosis. Tr. at 13. He considered himself to be healthy at the time of the vaccinations. Id.

Petitioner said that about 11 days after the vaccinations, he felt a “lot of unusual tingling,” as well as pain in his shoulder. Tr. at 14. He went to urgent care and was sent home. Id. One or two days later, he became concerned that he was having a stroke because he could not move his left arm. Id. at 16. He had weakness that made it difficult to lift items like his wallet. Id. He called an ambulance to take him to the hospital. Id.

Petitioner testified that he had to be intubated and had a tracheostomy and placement of a feeding tube. Tr. at 19. These interventions left scars on his body. Id.

B. Medical Records Petitioner was born on October 13, 1987, and was 29 years old at the time of vaccination. Ex. 1 at 1; Ex. 2 at 5. Prior to the subject vaccinations, his medical history was significant for alcohol and drug abuse, depression, and prior hospitalizations for intoxication and “[m]edication overdose.” See Ex. 2 at 11-16; Ex. 8 at 5-6, 12, 31, 36; Ex. 12 at 21-23, 38-40.

On July 6, 2017, Petitioner presented to the Catherine M. Abate Health Center for a refill of his PrEP medication. Ex. 2 at 5-10. His physical exam was normal. Id. at 8. During his visit, he received the Hepatitis A and meningococcal vaccines, which were recommended when he reported engaging in high-risk sexual behavior. Id. at 8-9.

On July 17, 2017, 11 days after vaccination, Petitioner went to Northwell Health Urgent Care for neck pain, bilateral shoulder pain, and numbness in his hands. Ex. 3 at 5. He reported that he “[w]oke up with symptoms.” Id. On exam, he had mild bilateral trapezius tenderness, a normal musculoskeletal exam, and a normal sensory exam. Id. at 6. The assessments were neck muscle strain and numbness and tingling of both hands. Id. He was advised to rest, take ibuprofen, monitor the numbness, and follow up with his primary care provider. Id.

The next day, on July 18, 2017, Petitioner went to the Emergency Department (“ED”) at Mt. Sinai Hospital of Queens for two days of moderate thoracic back pain. Ex. 4 at 12. On exam, he had myalgias, back pain, and an abnormal gait. Id. He was admitted to the hospital after he fell in the ED. Id. at 18-20, 28, 35.

On July 19, 2017, Petitioner was seen by neurologist Gary Sclar, M.D., in the hospital. Ex. 4 at 53-57. Petitioner reported diffuse body numbness and weakness and acknowledged using alcohol and drugs. Id. A CT of the head was normal. Id. An exam revealed absent reflexes, along with symmetric weakness that was “far more prominent proximally [than] distally and was symmetric[.]” Id. at 56. Dr. Sclar’s assessment was that Petitioner seemed to have “an acute sensory motor neuropathy.” Id. at 57. A July 20, 2017 lumbar puncture revealed CSF levels consistent with GBS. Id. at 47, 73.

Petitioner began IVIG treatment on July 21, 2017, “[d]ue to high suspicion of [GBS].” Ex. 6 at 417. That same day, Petitioner experienced “acute respiratory failure from neuromuscular weakness” and was intubated on a ventilator. Ex. 4 at 76, 93; Ex. 6 at 417. Lab results revealed elevated CMV and slightly elevated Campylobacter jejuni (“C. jejuni”) antibody levels. Ex. 4 at 160-61.

Petitioner was transferred to Mt. Sinai Hospital in Manhattan on July 22, 2017, where he remained until August 24, 2017. Ex. 6 at 417. He completed five days of IVIG treatment and five days of plasmapheresis treatment. Id. He “slowly improved” with these treatments. Id. He was also treated for depression and proscribed Prozac. Id. at 417, 468, 474.

While at Mt. Sinai, Petitioner required a tracheostomy and a PEG tube. Ex. 6 at 417. He also experienced intermittent leukocytosis and was treated for thrombocytosis with Lovenox.3 Id. at 295, 330, 458.

On July 27, 2017, infectious disease specialist Nicole Bouvier, M.D., diagnosed Petitioner with a CMV infection. Ex. 6 at 446-57. Her impression was that Petitioner had either a “primary CMV infection (perhaps as GBS trigger) or latent CMV reaction in the setting of acute critical illness, which is not uncommon.” Id. at 446. Petitioner’s “serum PCR” was +2020, which was “on the low side for true CMV disease, but not entirely insignificant.” Id. Although Petitioner did not have “antecedent mono-like” symptoms, primary CMV infections are “not always symptomatic.” Id. at 446-47. Because Petitioner had already received IVIG treatment, further serological testing would not reliably determine whether he had a primary or reactive CMV infection. Id. Also, while CMV-related GBS is “typically associated with the development of antibodies to ganglioside GM2, the prior administration of IVIG makes serological testing unreliable for diagnosing specific disease entities[.]” Id. at 447.

Dr. Bouvier remarked: “Even if this was an acute CMV infection, immunocompetent individuals are able to clear their infection on their own and it is unclear that there really is a role in treating the precipitant factor in GBS overall.” Ex. 6 at 457. She did not recommend treatment for a CMV infection, as the “potential side effects of antivirals” would outweigh “the benefits of potential CMV treatment.” Id.

Because Petitioner did not have a “viable safe discharge home,” the rehabilitation team at Mt. Sinai determined that long-term care was more appropriate. Ex. 6 at 184. On August 24, 2017, he was admitted to the Henry J. Carter Specialty Hospital and Nursing Facility (“Carter”) for rehabilitation and long-term care; he remained there for seven months. Ex. 5 at 1. His diagnosis at admission was GBS, and upon exam he had abnormal and decreased muscle tone, abnormal muscle weakness, and areflexia. Id. at 1, 5. He was completely dependent for his activities of daily living. Id. at 5.

While at Carter, Petitioner slowly improved. Ex. 5 at 297, 324. His PEG tube was removed on November 30, 2017, and on December 1, 2017, he was separated from the ventilator, and his tracheostomy tube was removed. Id. at 297, 299.

On March 8, 2018, Petitioner was discharged to his mother’s care in Indiana. Ex. 5 at 1, 456. In the discharge summary from Carter, Petitioner reported that he “recall[ed] experiencing mild upper respiratory symptoms without fever” before his hospitalization, but the exact timing of these symptoms was not clear from the record. Id. at 1.

On September 18, 2018, Petitioner saw nurse practitioner Tamara Reynolds for psychiatric care. Ex. 9 at 50. He was unable to return to work after returning to Indiana due to his weakness. Id. at 52. He reported “low mood and anxiety” that had worsened since his GBS diagnosis. Id. at 53-54. He was prescribed Zoloft and Gabapentin and scheduled to follow up in 4-6 weeks. Id. at 54. He followed up with Nurse Reynolds regarding his medication on October 16, 2018, and July 3, 2019. Id. at 30, 35.

Petitioner presented to PCP Keith Harvey, M.D., on June 27, 2019, for an annual exam. Ex. 7 at 39. When asked if he had completely recovered from GBS, Petitioner reported that “he [was] more fatigued than he used to be.” Id. His lab results were unremarkable, and his physical exam did not include a musculoskeletal component. Id. at 39-49.

On October 10, 2019, Petitioner followed up with Nurse Reynolds and reported that he “[felt] tired all of the time.” Ex. 9 at 40. Labs were ordered to “evaluate fatigue” but were never completed. Id. at 44. He followed up again with Nurse Reynolds on December 5, 2019, where he reported poor sleep habits. Id. at 45, 49.

On November 8, 2019, Petitioner presented to urologist George Martin, M.D., for “frequency, hesitancy, [and] urgency of urination” that began after his GBS diagnosis. Ex. 11 at 5. He reported “[a]wakening at night to urinate more than once.” Id. His urinalysis was negative for infection, and his post-void residual volume was zero. Id. at 5-6. He was prescribed a trial of Myrbetriq4 for frequent urination, but he did not appear to follow up with this provider. Id. at 6.

There are no relevant medical records after November 2019.

III. EXPERT EVIDENCE

A. Expert Reports

1. M. Eric Gershwin, M.D.

Dr. Gershwin submitted one report in this case. Ex. 15 (“Gershwin Rep.”). He earned his M.D. from Stanford University in 1971 and is board certified in internal medicine, allergy- immunology, and rheumatology. Ex. 23 (“Gershwin CV”) at 1-2; Gershwin Rep. at 1. He joined the faculty of the University of California Medicine, Davis (“UC Davis”), in 1975 and served as the Chief of the Division of Rheumatology, Allergy, and Clinical Immunology for 38 years; he is currently the director of UC Davis’s Allergy-Clinical Immunology Program and a Distinguished Professor of Medicine in rheumatology, allergy, and clinical immunology. Gershwin CV at 1-2; Gershwin Rep. at 1. He is also the Editor-in-Chief of the Journal of Autoimmunity and serves as a co-editor-in-chief, associate editor, or reviewer for several journals. Gershwin CV at 5-7. In 2009, he became only the second American to receive an honorary Ph.D. from the University of Athens, the home of the Hippocratic Oath, for his lifetime contributions in immunology and medicine. Id. at 1; Tr. at 29.

Dr. Gershwin noted that he was “asked to specifically comment on the role of CMV in the development of GBS.” Gershwin Rep. at 2. He agreed with Petitioner’s GBS diagnosis, noting that the diagnosis did not seem to be in dispute and that Petitioner’s case was characteristic of GBS. Id.

Dr. Gershwin provided background information on GBS, quoting very extensively from a paper on which he was the lead author. Gershwin Rep. at 2-11 (citing Anil K. Jasti et al., Guillain- Barré syndrome: causes, immunopathogenic mechanisms and treatment, 12 EXPERT REV. OF CLINICAL IMMUNOLOGY 1 (2016) (Ex. 16) (“Jasti”)). He stated:

Over two thirds of patients with GBS refer symptoms of respiratory or digestive infections within six weeks of onset. In 30-40% of GBS cases Campylobacter is the infecting agent and it has been estimated that 1/1058 infections results in GBS. The association between GBS and C. jejuni was first described around 1982 in clinical anecdotes by Rhodes and Tatterfield. Other infections preceding GBS may derive from cytomegalovirus, Epstein Barr virus, Mycoplasma pneumoniae, Haemophilus influenzae and influenza A virus.

Vaccines have long been considered as a possible cause of GBS; the mechanism would be molecular mimicry.

Id. at 3.

Dr. Gershwin noted that Petitioner had “a number of environmental issues with respect to his onset of GBS,” but that he would focus on CMV. Gershwin Rep. at 12. He noted that “there are bacteria and viruses, all seemingly unrelated to each other, that have been implicated in the development of GBS,” CMV being of particular importance. Id.

Dr. Gershwin’s opinion focused on “vaccination occurring on or about the same time as either an acute or reactive CMV infection.” Gershwin Rep. at 12. He opined that “any immunological event that would amplify or increase the immune response, would facilitate loss of tolerance and the development of [GBS].” Id.5 He explained:

Essentially, my opinion is that both the hepatitis A and the meningococcal vaccination will lead to cytokine production. Such cytokines will be proinflammatory and in the presence of an acute CMV infection, will promote an aberrant dysregulated immune response . . . Although CMV alone could well have induced [GBS] in [Petitioner], the vaccination will still play a significant role in facilitating the onset of disease.

Id. Also, had Petitioner’s physicians known that he had an acute CMV infection at the time of vaccination, they would not have recommended that he receive the subject vaccinations. Id.

Dr. Gershwin recognized that there “are no epidemiologic studies” that support his theory of causation, but he quoted extensively from several articles on the potential mechanism of action. Gershwin Rep. at 12-20 (quoting José Luis Muñoz-Carrillo et al., Cytokine Profiling Plays a Crucial Role in Activating Immune System to Clear Infectious Pathogens, IMMUNE RESPONSE ACTIVATION & IMMUNOMODULATION (Rajeev K. Tyagi & Prakash S. Bisen eds., 2019) (Ex. 17.) (“Muñoz-Carrillo”); Hans-Peter Hartung, Infections and the Guillain-Barré syndrome, 66 J. OF NEUROLOGY, NEUROSURGERY & PSYCHIATRY 277 (1999) (Ex. 18) (“Hartung”); Penelope A. Morel & Michael S. Turner, Designing the optimal vaccine: the importance of cytokines and dendritic cells, 3 OPEN VACCINE J. 7 (2010) (Ex. 19) (“Morel”); Michael Lunn & Richard Hughes, The Relationship between Cytomegalovirus Infection and Guillain-Barré Syndrome, 52 CLIN. INFECT. DIS. 845 (2011) (Ex. 20) (“Lunn”); Caroline Hervé et al., The how’s and what’s of vaccine reactogenicity, 39 NATURE PARTNER JOURNALS VACCINES 1 (2019) (Ex. 21) (“Hervé”); Nikolaos Chatziandreou et al., Macrophage Death following Influenza Vaccination Initiates the Inflammatory Response that Promotes Dendritic Cell Function in the Draining Lymph Node, 18 CELL REPORTS 2427 (2017) (Ex. 22) (“Chatziandreou”)). His opinion was that “GBS is an environmentally induced autoimmune disease,” vaccination promotes an immune response, and “if given within the same window as an active CMV infection, will play a significant role in tolerance breakdown or the generation of a pathogenic immune response.” Gershwin Rep. at 20. Thus, the subject vaccinations “significantly contributed to [Petitioner’s] GBS.” Id. Dr. Gershwin also declared that “[b]ut for receiving these vaccinations, it is less likely that Petitioner would have developed GBS solely due to CMV infection.” Id. It is likely that the CMV infection “allowed” the subject vaccines to “play a significant role in starting the process of GBS.” Id.

2. Brian C. Callaghan, M.D., M.S.

Dr. Callaghan submitted one report in this case. Ex. A (“Callaghan Rep.”). He earned his M.D. from the University of Pennsylvania Medical Center in 2004, and his M.S. in Clinical Research Design and Statistical Analysis from the University of Michigan in 2011. Ex. B (“Callaghan CV”) at 1. He is currently an Associate Professor of Neurology at the University of Michigan and a neuromuscular specialist. Id.; Callaghan Rep. at 1. He is board certified in neurology, with a specialty in neurology and electrodiagnostic medicine. Callaghan CV at 1. He is also on the editorial board and Co-Section Editor for Innovations in Care Delivery, is an ad hoc reviewer for several journals, and has published more than 100 articles mostly focusing on neuropathy. Id. at 5, 12-18; Callaghan Rep. at 1. He estimated that he has seen “more than 50 patients with GBS.” Callaghan Rep. at 1.

Dr. Callaghan opined that Petitioner’s GBS was likely caused by CMV infection and that there is “no reliable support for the hypothesis that hepatitis A or meningococcal vaccines are a likely cause of GBS.” Callaghan Rep. at 4. Moreover, “there is no mechanistic evidence linking these vaccinations and GBS in general nor in the context of CMV viremia.” Id.

Dr. Callaghan agreed that Petitioner was “correctly diagnosed with GBS.” Callaghan Rep. at 3. Eleven days after receiving the subjection vaccinations on July 6, 2017, Petitioner developed back pain, numbness, weakness, and gait instability. Id. Examinations revealed “markedly reduced strength and areflexia,” a lumbar puncture revealed elevated protein with a normal white blood cell count, and imaging revealed “sural sparing consistent with a diagnosis of GBS.” Id. After his GBS diagnosis, Petitioner received IVIG and plasmapheresis treatment and “gradually improved over many months.” Id. Dr. Callaghan noted that the infectious disease team concluded that Petitioner “either had a primary CMV infection or a reactivation of a previous infection.” Id.

Regarding a “[p]ossible CMV association with GBS,” Dr. Callaghan agreed with Dr. Gershwin that “CMV had a key role in the development of [Petitioner’s] GBS.” Callaghan Rep. at 3. He noted that Dr. Gershwin provided a summary of data showing that CMV accounts “for 10-15% of [GBS] cases” and is the “predominant viral trigger of GBS.” Id. (citing Lunn). Here, Petitioner’s serum CMV PCR test revealed CMV viremia, and testing for alternative triggers was negative. Id. Moreover, “[h]omosexual men are particularly at risk for CMV infection and the [P]etitioner was engaging in high risk homosexual behavior right before his CMV infection and subsequent GBS.” Id. (citing Maher K. Gandhi & Rajiv Khanna, Human cytomegalovirus: clinical aspects, immune regulation, and emerging treatments, 4 INFECTIOUS DISEASES 725 (2004) (Ex. E) (“Ghandi”)). Additionally, “CMV triggered GBS patients are younger, have more severe disease, have more severe sensory changes, and [are] more likely to have facial palsies,” features consistent with Petitioner’s GBS presentation. Id. (citing Lunn).

Addressing a “[p]ossible vaccine association with GBS,” Dr. Callaghan disagreed with Dr. Gershwin that the subject vaccinations in combination with the CMV infection caused Petitioner’s GBS. Callaghan Rep. at 4. He opined that there is “no convincing evidence supporting a likely association” between the Hepatitis A or meningococcal vaccines and GBS. Id. For example, there is only one case report of GBS following Hepatitis A vaccination; this report establishes, at most, a temporal association which is insufficient on its own to infer causation. Id. (citing X. Roux et al., [Guillain-Barré syndrome and anti-hepatitis A vaccination], 40 MED. MAL. INFECT. 490 (2009) (Article in French) (Ex. F) (“Roux”)). Moreover, in Chen, the authors investigated whether there is an association between Hepatitis A vaccination and GBS and “did not find an increased risk for hepatitis vaccines, meningitis vaccines, or vaccines in general.” Id. (citing Yong Chen et al., Vaccines and the risk of Guillain-Barré syndrome, 35 EUR. J. OF EPIDEMIOLOGY 363 (2020) (Ex. G) (“Chen”)). Similarly, the authors in the Velentgas study concluded that there is no increased risk of GBS after receiving the meningococcal vaccine, and the de Wals paper reported that “the number of cases of GBS after the meningococcal vaccine was not higher than would be expected by chance.” Id. (citing Priscilla Velentgas et al., Risk of Guillain–Barré syndrome after meningococcal conjugate Vaccination, 21 PHARMACOEPIDEMIOLOGY & DRUG SAFETY 1350 (2012) (Ex. H) (“Velentgas”); Philippe de Wals et al., Risk of Guillain-Barré Syndrome following Serogroup C Meningococcal Conjugate Vaccine in Quebec, Canada, 46 CID e75 (2008) (Ex. I) (“de Wals”)).

Regarding a “[m]echanism linking vaccinations to GBS,” Dr. Callaghan opined that there is “no evidence” that Dr. Gershwin’s theory that “both vaccines caused increased cytokine production and in the presence of CMV led to a dysregulate immune response” occurred. Callaghan Rep. at 4. Further, although “vaccinations lead to increased cytokines, the link between increased cytokines and GBS alone or in the context of CMV is not provided.” Id. He questioned how Dr. Gershwin’s statement that “hepatitis B inflammatory markers are associated with systemic reactogenicity” was relevant to the subject vaccines and GBS. Id. He similarly questioned how the Chatziandreou article, “demonstrating macrophage death after the influenza vaccination,” related to this case. Id. (referencing Chatziandreou). After reviewing the medical literature, Dr. Callaghan concluded that “there is no evidence of a mechanism that leads from hepatitis A or meningococcal vaccinations and GBS.” Id.

3. Robert S. Fujinami, Ph.D.

Dr. Fujinami submitted one report in this case. Ex. C (“Fujinami Rep.”). He earned his Ph.D. in immunology and microbiology from Northwestern University in 1977. Ex. D. (“Fujinami CV”) at 1. At the time of hearing, he had recently retired, but he had previously served as a Professor in the Department of Pathology, Division of Cell Biology and Immunology at the University of Utah School of Medicine, with research focusing on “viral-host interactions that can lead to nervous system inflammatory disease.” Fujinami Rep. at 1; Fujinami CV at 1; Tr. at 72.

Dr. Fujinami was the first to describe “molecular mimicry” in its current context in two papers he authored in the 1980s. Tr. at 74; Fujinami CV at 22. He has researched immunologic neuroinflammation and neurovirology for roughly 50 years, has published more than 230 peer- reviewed articles, and has served on the editorial board or as a reviewer for numerous journals. Tr. at 75; Fujinami CV at 2-3, 20-38.

Dr. Fujinami opined that it is more likely than not that “the on-going CMV infection was the driving factor in the Petitioner developing GBS and not the vaccinations.” Fujinami Rep. at 7. In his view, Dr. Gershwin did not “make a compelling case” that the subject vaccinations were the cause of Petitioner’s GBS. Id. In fact, he opined that “the Hepatitis A and the Meningococcal vaccines . . . could have help[ed] limit the extent of the disease [GBS] in the Petitioner.” Id.at 2.

Summarizing Dr. Gershwin’s theory, Dr. Fujinami noted that Dr. Gershwin did not dispute “there is a clear association between CMV infection and individuals developing GBS[.]” Fujinami Rep. at 2. Instead, Dr. Gershwin was proposing that “when vaccine antigens and immune enhancers (adjuvants) are injected into the body, the innate immune system is activated leading to various cytokines being induced.” Id. Dr. Gershwin provided the example of the Hepatitis B surface antigen, adsorbed onto an aluminum adjuvant, “inducing interleukin (IL)-6 and other acute phase proteins such as C-reactive protein (CRP).” Id. Another example is the flu vaccine, which “activates macrophages which produce interferon-beta (IFN-β) which then induces IL-1α which insures dendritic cell (DC) activation and function.” Id. Dr. Gershwin’s theory was that “the Hepatitis A and Meningococcal vaccines somehow aided or enhanced the effects of CMV infection causing an inflammatory autoimmune nervous system disease that CMV could cause by itself.” Id. at 3.

Dr. Fujinami discussed some of the theories for induction of neurological disease following antigenic exposure. Fujinami Rep. at 3. One such theory is molecular mimicry. Id. He explained that Experimental Autoimmune Encephalomyelitis (“EAE”) is an animal model for multiple sclerosis (“MS”), a disease that has similarities to GBS, as “immune cells such as T and B cells/antibodies are involved in the pathogenesis of both diseases.” Id. EAE can be induced in rodents through injection of “powerful adjuvants and myelin antigens” that causes an immune response that attacks components of the animals’ nervous system. Id. These experiments show that an animal’s nervous system can be “fooled into attacking its own myelin[,] leading to clinical signs due to inflammation and demyelination.” Id.

Similarly, GBS can be caused by infection with bacteria or viruses, such as C. jejuni, CMV, Epstein-Barr virus, Mycoplasma pneumoniae, and Haemophilus influenzae. Fujinami Rep. at 3. Although it is known that there are components of the C. jejuni bacteria that have structural similarity with myelin, it is unclear whether there are mimics between the CMV antigen and myelin, or whether some other mechanism leads to CMV infection causing GBS. Id.

Dr. Fujinami pointed out that it is undisputed Petitioner had a CMV infection on July 18, 2017. Fujinami Rep. at 3 (citing Ex. 6A at 446-48). He explained:

We know that CMV infection can lead to GBS in individuals. We know that myelin components mixed with powerful adjuvants can induce EAE, a model for neuroinflammatory autoimmune disease in rodents. According to Dr. Gershwin, the Hepatitis A vaccine[,] which contains a very weak adjuvant[,] and/or the Meningococcal vaccine that does not contain adjuvant[,] contributed to the development of autoimmune neuroinflammatory demyelinating disease.

Id. at 4. While Dr. Gershwin proposed that IFN-β is the primary cytokine involved in this process, Dr. Fujinami pointed out that the scientific literature in fact shows that “IFN-β can help ameliorate the pathogenic autoimmune responses in individuals with MS,” undermining this theory. Id. He cited the Mannie paper, which demonstrated that IFN-β given with a neuroantigen (“NAg”) to animal models prevented and lessened EAE. Id. at 4-5 (citing Mark D. Mannie, Derek J. Abbott & J. Lori Blanchfield, Experimental Autoimmune Encephalomyelitis in Lewis rats: IFN-β Acts As a Tolerogenic Adjuvant for Induction of Neuroantigen-Dependent Tolerance, 182 J. OF IMMUNOLOGY 5331 (2009) (Ex. K) (“Mannie”)). He opined:

The data from the Mannie . . . study demonstrate that IFN-β and NAg both prevent disease and reduce on-going disease, thus indicating that if the Hepatitis A and Meningococcal vaccines induce IFN-β and have molecular mimicry, like NAg, then they would not contribute to GBS due to CMV infection, which can cause GBS by itself.

Id. at 5.

Next, Dr. Fujinami addressed the notion that alum used as an adjuvant could enhance the ability of CMV to cause neuroinflammatory disease. Fujinami Rep. at 5. He referenced Sicotte, where the authors immunized mice with NAg mixed with alum and reported that the mice “neither developed clinical disease nor inflammation of the nervous system.” Id. (citing Maryline Sicotte et al., Immunization with myelin or recombinant Nogo-66/MAG in alum promotes axon regeneration and sprouting after corticospinal tract lesions in the spinal cord, 23 MOLECULAR & CELLULAR NEUROSCIENCE 251 (2003) (Ex. L) (“Sicotte”)). Sicotte countered Dr. Gershwin’s hypothesis that a vaccine “containing alum and having a disease relevant molecular mimicry with peripheral nerve myelin,” such as the Hepatitis A vaccine, could induce GBS. Id.

Similarly, the Wallberg study showed that “NAg mixed with alum can reduce the extent of neuroinflammatory disease and alum by itself does nothing, neither enhancing nor protecting from disease.” Fujinami Rep. at 5 (citing Maja Wallberg, Judit Wefer & Robert A. Harris, Vaccination with myelin oligodendrocyte glycoprotein adsorbed to alum effectively protects DBA/1 mice from experimental autoimmune encephalomyelitis, 33 EUR. J. IMMUNOL 1539 (2003) (Ex. M) (“Wallberg”)). Taken together, Sicotte and Wallberg support the notion that vaccines with “disease relevant mimicry with nervous system myelin adsorbed to alum can significantly decrease the induction of disease[,] or if alum is given alone no change in the course of disease is observed.” Id. at 5-6; see also Duncheng Wang et al., IFN-β Facilitates Neuroantigen-Dependent Induction of CD25+ FOXP3+ Regulatory T Cells That Suppress Experimental Autoimmune Encephalomyelitis, 197 J. OF IMMUNOL. 2992 (2016) (Ex. N) (“Wang”) (finding “no increase in severity of neuroinflammatory disease” when animals were injected with NAg with alum or just alum).

Regarding the meningococcal vaccine, which does not contain an adjuvant, Dr. Fujinami addressed Dr. Gershwin’s position that the vaccine could contribute to “disease enhancement” by “having molecular mimicry with the peripheral nerve myelin when injected at the time of the CMV infection.” Fujinami Rep. at 6. Again, Mannie showed “that injection of NAg without adjuvant prior to the induction of EAE neither enhanced the severity of clinical signs of neuroinflammatory disease nor shortened the time to disease onset,” which does not support Dr. Gershwin’s opinion. Id. (citing Mannie).

Lastly, Dr. Fujinami reviewed the medical literature concerning Hepatitis A and/or meningococcal vaccination and GBS. Fujinami Rep. at 6. In Israeli, the authors reviewed vaccines and infections from 1976 to 2006 and found only 5 cases of GBS in individuals who received the meningococcal vaccine; this “might have been expected to occur by chance alone.” Id. (citing Eitan Israeli et al., Guillain–Barré Syndrome—A Classical Autoimmune Disease Triggered by Infection or Vaccination, 42 CLINIC. REV. ALLERG. IMMUNOL. 121 (2012) (Ex. J.) (“Israeli”)). Similarly, the authors found only one case report of GBS following the Hepatitis A vaccine in a 30-year span. Id. Dr. Fujinami opined that “there is not strong data supporting the notion that Hepatitis A and Meningococcal vaccines cause or are correlated with GBS.” Id. at 7.

B. Expert Testimony

1. Dr. Gershwin’s Testimony Dr. Gershwin was qualified as an expert in immunology, GBS, and CMV. Tr. at 34-35. He concluded that Petitioner’s vaccinations in combination with his CMV infection caused him to develop GBS. Id. at 37, 60.

Dr. Gershwin described CMV as a “fairly ubiquitous virus” that “we’re all exposed to [] by age 40.” Tr. at 31. Most people who contract it are asymptomatic; however, for “immunoincompetent” individuals, CMV manifests in “a whole variety of ways,” ranging from pneumonia to elevation of liver function with mild hepatitis. Id. Moreover, CMV has been linked to a number of autoimmune diseases, including GBS. Id. at 31, 33. Generally, a test for CMV will only be done when clinical reasons warrant it, usually with PCR technology. Id. at 36-37. Here, Petitioner’s treating physicians found the presence of the virus in his blood after examining his spinal fluid; Dr. Gershwin opined “that would be probably the sine qua non indicator that he did have active CMV.” Id. at 37.

Dr. Gershwin opined that the onset of Petitioner’s GBS coincided with the change in his lifestyle and the vaccinations. Tr. at 36. Petitioner’s lifestyle change included moving to New York City, where he engaged in unprotected homosexual activity. Id. at 35. “Homosexuals are more likely to contact CMV,” have a much higher prevalence of CMV infection, and will “develop it earlier.” Id. Moreover, Petitioner engaged in binge drinking, which will “impact the immune system and make it more likely for CMV to go from latent to an active phase.” Id. The timeline of Petitioner’s illness was important: he moved to New York in May, his sexual activity increased, he was binge drinking, he received the vaccines, and he was “finally diagnosed with [GBS] around two weeks after his vaccination.” Id. at 35-36. The onset of Petitioner’s GBS was “consistent with a timeline of a few days to a couple weeks after some initiating factor [the vaccinations] . . . which would promote the likelihood that CMV would lead to [GBS].” Id. at 36.

Dr. Gershwin acknowledged that neither of the subject vaccines alone could produce GBS. Tr. at 39. By contrast, CMV infection can trigger GBS rarely, but another trigger may also be necessary. Id. at 39. He stated:

[G]ay males have a very high incidence of CMV. But there’s no high incidence of GBS that I’m aware of in homosexuals. So certainly CMV can do it, but it suggests that maybe unlike a number of other precipitants of GBS, that maybe CMV requires other somatic events.

Id. GBS patients with CMV “tend to have a more protracted course as [Petitioner] did.” Id. at 42.

There are two possible mechanisms by which CMV could cause GBS: molecular mimicry and immune dysregulation. Tr. at 48. Dr. Gershwin used an analogy to explain molecular mimicry:

You go into a bar, and some mean guy beats you up. You come back a week later with six of your big friends, and there’s another big guy sitting in the bar. And it’s not the same guy, but he looks just like him, so you beat him up anyway. He’s a mimic.

Id. at 44. Molecular mimicry “would facilitate loss of tolerance,” which can cause an individual to develop GBS. Id. at 48, 54-55 (citing Jie Wu, Aini Xie & Wenhao Chen, Cytokine regulation of immune tolerance, 2 BURNS & TRAUMA 11 (2014) (“Wu”) (Ex. 29)). The best example of molecular mimicry is rheumatic heart disease, where, in the setting of a Streptococcus bacterial infection, the immune system attacks the bacteria and also the heart, because “the antigen or molecular structure found in strep looks like a structure found in your heart.” Id. at 44-45.

Dr. Gershwin testified that while either molecular mimicry or immune dysregulation could cause GBS following CMV infection, the “core” of his opinion was that Petitioner’s GBS was caused by immune system dysregulation involving the production of proinflammatory cytokines, which in turn was triggered by the combination of CMV infection and the vaccines. Tr. at 48. In his view, it would be malpractice for a physician to vaccinate an individual with a known CMV infection, and he did not believe any competent physician would have vaccinated Petitioner had they known he had an active CMV infection. Id. at 48-49. This is because a CMV infection causes the body to undergo an “immunological storm,” and vaccination is designed to further alter the immune response and create bystander cells that produce cytokines, augmenting the immune response. Id. at 48-49, 51. Dr. Gershwin described this “bystander activation” as follows:

You’re home, and your burglar alarm goes off, so the police come. But not only do the police come, but all your neighbors show up and they all have guns. That’s called bystander activation. And sometimes the neighbors could do more damage than is necessary.

Id. at 50. Although he did not see any evidence in the records that Petitioner had signs of immune dysregulation, such as lymph node swelling, after vaccination, the vaccines would “produce bystander activation as part of the normal immune response.” Id. at 51.

Commenting on Dr. Fujinami’s and Dr. Callaghan’s reports, Dr. Gershwin testified that they did not focus on what his report said. Tr. at 56. For example, Dr. Gershwin did not propose alum as having a role in Petitioner’s injuries, but Dr. Fujinami discussed alum extensively. Id. at 58. Dr. Fujinami also did not address the role of cytokines other than IFN-β in immune dysregulation. Id. And EAE, which was discussed by Dr. Fujinami, did not play “any role” in Dr. Gershwin’s opinions. Id. at 59.

Dr. Gershwin summarized his opinion as follows:

[T]he milestones, the chronology here of a move to New York, recent acquisition of CMV virus, documentation of viremia, meaning an active CMV infection, two weeks after the vaccination, the presence of cytokines produced following the vaccination, which would be designed to augment an immune response, would augment or alter an immune response in somebody who’s already infected with an agent that unfortunately, CMV, dysregulates the immune response and can lead to [GBS].

So I used the word earlier, an “immunological storm.” It’s like, you know, going out in a storm. The rain is coming down, and you’re just increasing the rainfall by the vaccination.

Id. at 59-60.

On cross, Dr. Gershwin said that although it is impossible to know exactly when Petitioner contracted CMV, it likely occurred after he moved to New York. Tr. at 64. However, the exact timing of when Petitioner became infected with CMV was immaterial, because, in his view, the vaccinations were given during an active CMV infection. Id.

Dr. Gershwin acknowledged that, although it would be “malpractice” to vaccinate a patient with an active CMV infection, vaccination during a latent CMV infection would acceptable. Tr. at 65. He also admitted that Petitioner did not appear to have an unusual systemic response to the vaccines, such as fever or swelling of the lymph nodes, and Petitioner’s treating physicians did not attribute his GBS to the vaccinations. Id. at 66, 71.

In response to questioning from Special Master Oler, Dr. Gershwin opined that Petitioner had an active CMV infection due to the “active virus” that was found in his blood; he said “[y]ou would not find that degree of viremia, meaning virus in the blood, in latent CMV.” Tr. at 69-70.

2. Dr. Fujinami’s Testimony Dr. Fujinami was qualified as an expert in immunology and neuroimmunology. Tr. at 79. He testified that there were no reliable studies showing an increased risk of GBS following either of the subject vaccines. Id. at 80. Nor was there meaningful molecular mimicry between either vaccine and the nervous system that could result in GBS. Id. at 80-81. By contrast, there is strong epidemiologic evidence supporting an association between CMV and GBS. Id. at 81.

The mechanism by which CMV infection could cause GBS was not as clear as the mechanism for C. jejuni-caused GBS. Tr. at 81. He agreed that “CMV would be the top agent” that could have induced Petitioner’s GBS. Id. at 83. He interpreted Dr. Gershwin to opine that CMV caused GBS via molecular mimicry. Id. at 82.

Dr. Fujinami argued that Dr. Gershwin’s opinion about vaccine causation was unpersuasive. Tr. at 83. The literature referenced by Dr. Gershwin addressed molecular mimicry in the context of infection, sometimes combined with administration of Freund’s adjuvant, which is very different from routine vaccination. Id. at 83-84.

Dr. Fujinami discussed the medical literature referenced in his report. Tr. at 84. The Israeli article summarized data over several decades to assess a possible correlation between vaccinations and GBS, and it found “no significant causal association.” Id. at 85 (citing Israeli). Similarly, the Mannie article concerned the innate cytokine response that Dr. Gershwin discussed. Id. at 86-87 (citing Mannie). Mannie showed that IFN-β given with NAg actually ameliorates neuroinflammation in animal models of EAE. Id. at 87.

Dr. Fujinami discussed several studies on the effects of alum, which is a component of the Hepatitis A vaccine. Tr. at 88, 96. These studies were done to test the potential for alum to ameliorate autoimmune diseases. Id. at 89. Sicotte showed that immunizing experimental animals with NAg and alum did not induce neuroinflammatory disease. Id. at 88-89 (citing Sicotte). The Wallberg study showed mice immunized with a combination of alum and myelin oligodendrocyte glycoprotein (“MOG”) were protected against EAE. Id. (citing Wallberg). The data from Wallberg “implicate[d] a downregulation of interferon gamma production rather than a switch from type-I to type-II cytokine production.” Id. at 90 (quoting Wallberg). Wallberg is consistent with the Wu article, cited by Dr. Gershwin, which also showed that “interferon gamma is decreased” during immunization, such that “autoimmune disease would be dampened down.” Id. at 89-90 (citing Wu (Fig. 1)). Similarly, the Wang article showed that the combination of NAg or an antigen plus alum induced IFN-β, which facilitates the production of regulatory T cells that would lessen autoimmune disease. Id. at 91 (citing Wang). Taken together, the literature addressed cytokine production following vaccination with alum-containing vaccines and showed that “they’re pushing away from autoimmune disease and more pushing towards and immune response that would either be protective or . . . not potentiate autoimmune disease.” Id. at 90-91.

Regarding Dr. Gershwin’s theory that Petitioner suffered from an “immunologic storm caused by [his] CMV infection,” Dr. Fujinami referred to the Hervé article, which showed that, though vaccines containing an adjuvant rapidly produce cytokines and chemokines, production of those molecules declines after 24 hours. Tr. at 92-93 (citing Hervé). Moreover, a patient that has a high production of cytokines would feel “lousy the day or day after vaccination.” Id. at 93. Dr. Fujinami noted that Petitioner testified that he experienced no acute reaction immediately following vaccination. Id. Dr. Fujinami opined that Petitioner did not have “this giant cytokine storm” that Dr. Gershwin discussed. Id.

Dr. Fujinami addressed the Jasti article. Tr. at 94-95. Jasti stated that a C. jejuni infection can cause an imbalance between T cells as well as cytokines; Dr. Gershwin’s view was that CMV can cause the same dysregulation of the immune system. Id. However, Dr. Fujinami opined that “CMV by itself can cause GBS.” Id. at 96. He maintained his opinion that nothing “additional” would be needed to induce GBS in the setting of a CMV infection. Id. at 96-97.

Regarding bystander activation as a proposed mechanism, Dr. Fujinami explained that, while bystander activation could lead CMV to cause GBS, the Hepatitis A and meningococcal vaccines would not cause a cytokine storm, nor could they “drive an autoimmune response like an infection does.” Tr. at 99-100. Neither of the vaccines would migrate through the body or replicate. Id. at 96. As for timing, Dr. Fujinami opined that the timing of Petitioner’s GBS was “coincidental.” Id. at 100.

On cross, Dr. Fujinami explained that the “immunologic storm” caused by CMV is “gigantic,” and the “vaccine in that context would be a drop in the bucket.” Tr. at 102. He opined that vaccination causes a “very mild cytokine reaction compared to [an] immunologic storm,” and would not be enough to trigger an already existing immunologic storm. Id. at 103-04. Dr. Fujinami explained that he discussed EAE animal models in his report to compare the pathogenesis of MS and GBS, because there are “many parallels” between the two diseases. Id. at 115-16.

In response to question from Special Master Oler about whether it would “be a bad idea to immunize someone if they were suffering from an active CMV infection,” Dr. Fujinami testified that there is a possibility of “antigen competition,” where “the immune response would be to the infection and not the vaccine.” Tr. at 126-27. There is no concern, from an immunological standpoint, that an increased immune response would overwhelm the body. Id.

3. Dr. Callaghan’s Testimony Dr. Callaghan was qualified as an expert in neurology. Tr. at 136. He agreed that Petitioner had a CMV infection, “a well-known cause of GBS,” and opined that there is no evidence supporting an association between GBS and the subject vaccinations, either alone or in combination with CMV infection. Id. at 137.

Citing the Ghandi review article on CMV, Dr. Callaghan noted that gay men generally receive more vaccinations than other populations, because they have a higher risk of certain infections, including CMV. Tr. at 137-39. Petitioner was assessed as “high risk because of his sexual behavior.” Id. at 138. Dr. Callaghan cited Lunn to point out that “patients with CMV- triggered GBS are typically younger, have more severe disease[] and more sensory changes[,] and are more likely to have facial palsies.” Id. at 137-38. These features aligned with Petitioner’s GBS presentation. Id. at 138-39.

The records show Petitioner had CMV, and he developed GBS “right after” his infection. Tr. at 139. Petitioner was on the younger side for a GBS patient, had a “very severe” case, had “very severe sensory changes,” and had facial palsies, all of which are “more common in patients with CMV-triggered GBS versus other causes of GBS.” Id. at 139-40. He was also found to have “transaminitis,”6 which Dr. Callaghan opined can be caused by CMV; his infectious disease doctors “speculated that . . . a primary infection might have led to” the transaminitis. Id. at 140. Generally, Petitioner’s treating physicians believed his GBS was related to his CMV viremia. Id.

Turning to the medical literature, Dr. Callaghan noted that the only evidence connecting either vaccine to GBS was a single case report of GBS following a Hepatitis A vaccination in France. Tr. at 141 (citing Roux). The Chen article showed “there is no association in either direction as far as we know with [H]epatitis A and GBS,” and the Velentgas article showed no association between the meningococcal vaccine and GBS. Id. at 142-43 (citing Chen; Velentgas). The de Wals article found that the incidence of GBS in 1.9 million patients given meningococcal vaccinations was actually “lower than expected.” Id. at 143-44 (citing de Wals).

Dr. Callaghan opined that there is no evidence “linking either of these vaccines specifically in a mechanism that plausibly leads specifically to GBS in this context.” Tr. at 144. The cause of Petitioner’s GBS is known; CMV is a known cause of GBS, Petitioner was at high risk for CMV, he contracted the virus, had a confirmed infection, and then developed GBS. Id. at 144-45. The only evidence of any type of relationship between the subject vaccinations and Petitioner’s GBS is that the vaccines were given before the onset of GBS. Id. at 146.

On cross, Dr. Callaghan agreed Petitioner was correctly diagnosed with GBS. Tr. at 147. His opinion would not change if Petitioner’s high-risk behavior began “long before vaccination.” Id. at 149. He acknowledged that, although gay men have a higher risk of contracting CMV infection, there is no proof that they develop GBS at a higher rate than others. Id. at 149-50. Addressing the theory that the subject vaccinations combined with CMV infection caused Petitioner’s GBS, Dr. Callaghan testified:

I’ve never seen a study trying to link that up, which is why I find this theory, you know, sort of unusual. This is not something talked about in the literature. This is not something that’s been studied epidemiologically or mechanistically. So, you know, that’s why I find it a strange mechanism to discuss.

Id. at 154.

4. Rebuttal Testimony On rebuttal, Dr. Gershwin discussed the Ferrara article, which emphasized the “multiple types of cells which can be influenced by cytokines” and explained “how important the balance of cytokine networks and regulatory cells are in immunological homeostasis.” Tr. at 159 (citing James L.M. Ferrara, Cytokines and the regulation of tolerance, 105 J. OF CLINICAL INVESTIGATION 1043 (2000) (Ex. 28) (“Ferrara”)). Similarly, the Wu article discussed how cytokines can break tolerance. Id. at 160 (citing Wu).

Dr. Gershwin also clarified the difference between an “immunological storm” and a “cytokine storm.” Tr. at 162-63. An immunological storm is when the body turns on its own tissues and produces immune cells that destroy its own nerves. Id. By contrast, a cytokine storm occurs when there is a “massive explosion of cytokines,” such as when a cancer patient receives chemotherapy drugs or in rare types of infections. Id. Dr. Gershwin clarified that he was not positing a “cytokine storm” occurred in this case. Id. at 163.

Dr. Gershwin critiqued the Wallberg paper as lacking histology, pathology, or primary data. Tr. at 164. As for the interpretation of the paper, Dr. Gershwin noted that alum does not protect against diabetes; it “only delays it.” Id. at 165 (citing Wallberg). Also, Wallberg showed “[t]he degree of protection induced by rMOG-alum . . . varies with the route of administration.” Id. (quoting Wallberg). Wallberg used an EAE model, and it would be “a leap of faith to associate EAE with [GBS].” Id. at 166.

In response to questioning from Special Master Oler, Dr. Gershwin opined that there is no evidence to support the notion of immune competition following vaccination. Tr. at 170. Regarding timing, a cytokine release following vaccination can occur within hours to days. Id. at 173 (citing Gillie A. Roth et al., Designing spatial and temporal control of vaccine responses, 7 NATURE REVS. 174 (2022) (Ex. 24) (“Roth”)). But cytokines “are not just produced in the immediate response to the vaccine”; they are also produced as the immune system “goes from IgM to an IgG response, as it goes to long-lived memory cells.” Id. He placed onset of Petitioner’s GBS within eleven days of vaccination. Id. Lastly, Dr. Gershwin clarified that an “immunologic storm” is a term he’s used while teaching to refer to when the immune system harms itself. Id. at 173-74. A “cytokine storm” is the result of the “toxicity of the cytokines, the massive about of cytokines producing massive [functional] changes,” whereas an “immunological storm” is the “clinical manifestations of the specific disease involved.” Id. at 175.

IV. APPLICABLE LAW

A. Petitioner’s Burden in Vaccine Program Cases Under the Vaccine Act, a petitioner may prevail in one of two ways. First, he may show that he suffered a Table injury within the time provided in the Table. § 11(c)(1)(C)(i). “In such a case, causation is presumed.” Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006); see § 13(a)(1)(B). Second, where the alleged injury is not listed in the Table, he may demonstrate that he suffered an “off-Table” injury that was caused-in-fact by his vaccination. § 11(c)(1)(C)(ii).

For both Table and non-Table claims, Vaccine Program petitioners bear a “preponderance of the evidence” burden of proof. § 13(a)(1). That is, a petitioner must offer evidence that leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence before [he] may find in favor of the party who has the burden to persuade the [judge] of the fact’s existence.” Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010); see also Snowbank Enter. v. United States, 6 Cl. Ct. 476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard). The petitioner must demonstrate that the vaccine was “not only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions; rather, the petition must be supported by either medical records or the opinion of a competent physician. § 13(a)(1).

In attempting to establish entitlement to a Vaccine Program award of compensation for a non-Table claim, a petitioner must satisfy all three of the elements established by the Federal Circuit in Althen v. Secretary of Health and Human Services. 418 F.3d 1274 (Fed. Cir. 2005). Althen requires a petitioner to establish by preponderant evidence that the vaccination caused his injury “by providing: (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.

Each of the Althen prongs requires a different showing. Under Althen prong one, a petitioner must provide a “reputable medical theory” demonstrating that the vaccine received can cause the type of injury alleged. Pafford, 451 F.3d at 1355-56 (citations omitted). To satisfy this prong, a petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.” Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994) (citations omitted). Such a theory must only be “legally probable, not medically or scientifically certain.” Id. at 548-49; Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991).

A petitioner may satisfy the first Althen prong without resort to medical literature, epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical theory. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing Capizzano, 440 F.3d at 1325-26). Despite their expertise, special masters are not empowered by statute to conclusively resolve what are complex scientific and medical questions, and thus scientific evidence offered to establish Althen prong one is viewed “not through the lens of the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence standard.” Id. at 1380. However, this does not negate or reduce a petitioner’s ultimate burden to establish his entitlement to compensation by preponderant evidence. W.C. v. Sec’y of Health & Hum. Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted).

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; Andreu, 569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326 (stating that “medical records and medical opinion testimony are favored in vaccine cases, as treating physicians are likely to be in the best position to determine whether a ‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”) (quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly trustworthy evidence because they are created contemporaneously with the treatment of the patient. Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). However, the existence of medical records and/or statements of treating physician views does not require the special master to adopt their conclusions per se. § 13(b)(1) (providing that “[a]ny such diagnosis, conclusion, judgment, test result, report, or summary shall not be binding on the special master or court”); Snyder v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“[T]here is nothing . . . that mandates that the testimony of a treating physician is sacrosanct–that it must be accepted in its entirety and cannot be rebutted.”). As with expert testimony offered to establish a theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as the reasonableness of their suppositions or bases. The views of treating physicians should also be weighed against other, contrary evidence in the record— including conflicting opinions among such individuals. Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742, 749 (2011) (it was not arbitrary or capricious for special master to weigh competing treating physicians’ conclusions against each other), aff’d, 698 F.3d 1355 (Fed. Cir. 2012); Veryzer v. Sec’y of Health & Hum. Servs., No. 06-522V, 2011 WL 1935813 at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review den’d, 100 Fed. Cl. 344, 356 (2011), aff’d without opinion, 475 Fed. App’x 765 (Fed. Cir. 2012).

The third Althen prong requires establishing a “proximate temporal relationship” between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the phrase “medically acceptable temporal relationship.” Id. Thus, a petitioner must offer “preponderant proof that the onset of symptoms occurred within a timeframe which, given the medical understanding of the disorder’s etiology, it is medically acceptable to infer [causation].” de Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what is a medically acceptable timeframe must also be consistent with the theory for how the relevant vaccine can cause the alleged injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health & Hum. Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand on other grounds, 105 Fed. Cl. 353 (2012), aff’d without op., 503 F. App’x 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

B. Law Governing Analysis of Fact Evidence The process for making factual determinations in Vaccine Program cases begins with analyzing the medical records, which are required to be filed with the petition. §11(c)(2). The special master is required to consider “all [] relevant medical and scientific evidence contained in the record,” including “any diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is contained in the record regarding the nature, causation, and aggravation of the petitioner’s illness, disability, injury, condition, or death,” as well as the “results of any diagnostic or evaluative test which are contained in the record and the summaries and conclusions.” §13(b)(1). The special master is then required to weigh the evidence presented, including contemporaneous medical records and testimony. See Burns v. Sec’y of Health & Hum. Servs., 3 F. 3d 415, 417 (Fed. Cir. 1993) (it is within the special master’s discretion to determine whether to afford greater weight to contemporaneous medical records than to other evidence, such as oral testimony surrounding the events in question that was given at a later date, provided that such determination is based on a rational analysis).

Medical records created contemporaneously with the events they describe are generally trustworthy, because they “contain information supplied to or by health professionals to facilitate diagnosis and treatment of medical conditions,” where “accuracy has an extra premium.” Kirby v. Sec’y of Health & Hum. Servs., 997 F.3d 1378, 1382 (Fed. Cir. 2021) (quoting Cucuras, 993 F.2d at 1528). Accordingly, if the medical records are clear, consistent, and complete, then they should be afforded substantial weight. See generally Lowrie v. Sec’y of Health & Hum. Servs., No. 03-1585V, 2005 WL 6117475 at *19 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records are often found to be deserving of greater evidentiary weight than oral testimony, especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528; see also Murphy v. Sec’y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam, 968 F.2d 1226 (Fed. Cir. 1992), cert. den’d, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United States v. U.S. Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that oral testimony which is in conflict with contemporaneous documents is entitled to little evidentiary weight.”)).

However, there are situations in which compelling oral testimony could be more persuasive than written medical records, such as where records are deemed to be incomplete or inaccurate. Campbell v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based upon common sense and experience, this rule should not be treated as an absolute and must yield where the factual predicates for its application are weak or lacking.”); Lowrie, 2005 WL 6117475, at *19 (“Written records which are, themselves, inconsistent, should be accorded less deference than those which are internally consistent.”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, the special master should assess each witness’s credibility when determining the weight their testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

In determining the accuracy and completeness of medical records, the Court of Federal Claims has listed four possible explanations for inconsistencies between contemporaneously created medical records and later testimony: (1) a person’s failure to recount to the medical professional everything that happened during the relevant time period; (2) the medical professional’s failure to document everything reported to her or him; (3) a person’s faulty recollection of the events when presenting testimony; or (4) a person’s purposeful recounting of symptoms that did not exist. LaLonde v. Sec’y of Health & Hum. Servs., 110 Fed. Cl. 184, 203- 04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014). In deciding whether to afford greater weight to contemporaneous medical records or other evidence, such as testimony, a rational analysis must be explicated. Burns, 3 F.3d at 417.

C. Analysis of Expert Testimony Establishing a sound and reliable medical theory connecting the vaccine to the injury often requires a petitioner to present expert testimony in support of his or her claim. Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579, 594-96 (1993). See 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)). “The Daubert 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 play a slightly different role in Vaccine Program cases than they do in other federal judicial proceedings. Those factors are employed by judges to exclude evidence that is unreliable and potentially confusing to a jury. In Vaccine Program cases, these factors are generally used to assess the reliability and weight of scientific evidence. 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[.]”). The flexible use of the Daubert factors to evaluate persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88 Fed. Cl. at 743.

Respondent frequently offers one or more experts of his own to rebut a petitioner’s case. Where both sides offer expert testimony, a special master’s decision may be “based on the credibility of the experts and the relative persuasiveness of their competing theories.” Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing Lampe, 219 F.3d at 1362). 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, 88 Fed. Cl. at 743 (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)). 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. Weighing the relative persuasiveness of competing expert testimony, based on a particular expert’s credibility, is part of the overall reliability analysis special masters must employ in Vaccine Program cases. Id. at 1325-26 (“[a]ssessments as to the reliability of expert testimony often turn on credibility determinations”); see also Porter v. Sec’y of Health & Hum. Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“[T]his court has unambiguously explained that special masters are expected to consider the credibility of expert witnesses in evaluating petitions for compensation under the Vaccine Act”).

D. Consideration of Medical Literature Finally, although this decision discusses some but not all the medical literature in detail, I have reviewed and considered all the medical records and literature submitted in this matter. See Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016) (“We generally presume that a special master considered the relevant record evidence even though [s]he does not explicitly reference such evidence in h[er] decision.”); Simanski v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 407, 436 (2014) (“[A] Special Master is ‘not required to discuss every piece of evidence or testimony in her decision.’”) (citation omitted), aff’d, 601 F. App’x 982 (Fed. Cir. 2015).

V. ANALYSIS

The parties here do not dispute that Petitioner developed GBS, and I agree that diagnosis is supported by the medical records. The parties’ experts also agreed that Petitioner developed an acute or reactivated CMV infection that, at least in part, caused his GBS. See Gershwin Rep. at 12; Callaghan Rep. at 3; Fujinami Rep. at 7. The parties’ dispute centered on whether the subject Hepatitis A and meningococcal vaccines, when combined with the response to the CMV infection, caused GBS. Dr. Gershwin opined that the vaccines augmented the immune response to the CMV infection, leading to dysregulation of the immune response and GBS. See Gershwin Rep. at 12; Tr. at 59-60. Respondent’s experts countered that the mechanistic, epidemiologic, and medical record evidence failed to support Dr. Gershwin’s theory; they opined the CMV infection alone was the cause of Petitioner’s condition. Callaghan Rep. at 4; Fujinami Rep. at 3. I conclude that Petitioner’s mechanistic theory of combined CMV-vaccine causation was unpersuasive, particularly in light of the epidemiologic evidence supporting CMV alone as a cause of GBS and finding no causal association between either of the subject vaccines and GBS. Furthermore, the evidence did not preponderantly show a logical connection between the subject vaccines and Petitioner’s development of GBS.

A. Althen Prong One In the context of the Program, “to establish causation, the standard of proof is preponderance of evidence, not scientific certainty.” Langland v. Sec’y of Health & Hum. Serv., 109 Fed. Cl. 421, 441 (Fed. Cir. 2013). Petitioner’s burden under Althen’s first prong is to provide a medical theory causally connecting the vaccination and the injury. Id. This theory must be sound and reliable. Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019).

According to the Jasti paper submitted by Dr. Gershwin, GBS is “the most common cause of acute flaccid symmetrical weakness of the limbs and areflexia in the post-polio era.” Jasti at 1. The condition has a range of clinical presentations but includes “acute inflammatory polyradiculoneuropathy, muscle weakness, and reduced reflexes.” Id. More than two-thirds of GBS patients report a prior respiratory or gastrointestinal infection within the six weeks before onset of GBS symptoms. Id. at 2. C. jejuni is the most common infectious cause of GBS. Id. Other bacterial and viral infections are also associated with the condition, including CMV. Id.

The experts agreed that CMV infection is associated with GBS. Gershwin Rep. at 12; Callaghan Rep. at 3; Fujinami Rep. at 2. The literature supported this proposition. Lunn, for example, discussed several studies finding such an association. Lunn at 845-46; see also Hartung at 411 (“CMV has been identified as the predominant viral cause of an infective illness preceding GBS, present in 10–15% of patients.”). GBS cases associated with CMV tend to be in younger people and are more severe, consistent with Petitioner’s presentation. Lunn at 845.

1. Petitioner’s causation theory was unpersuasive.

Dr. Gershwin expressly disclaimed the opinion that either of the subject vaccines could alone cause GBS in the absence of active CMV infection. Tr. at 39. Instead, his “core” theory was that the cytokines produced in response to Hepatitis A and meningococcal vaccinations “will be proinflammatory and in the presence of an acute CMV infection, will promote an aberrant dysregulated immune response.” Gershwin Rep. at 12; see Tr. at 48. He characterized this as an “immunological storm,” a term he coined for teaching purposes. Tr. at 173-74. He theorized that the immune response elicited by the vaccinations given during an active CMV infection could lead to “the generation of a pathogenic immune response,” leading to GBS.7 Gershwin Rep. at 20.

Dr. Gershwin quoted heavily from several articles. Gershwin Rep. at 13-20. Muñoz- Carrillo generally described the different types of cytokines produced during the response to infections, including viral infections. Muñoz-Carrillo at 1, 10-13; see Gershwin Rep. at 13 (quoting Muñoz-Carrillo). The authors pointed out that cytokines can act on different target cells and “affect the function of other cytokines in an additive, synergistic, or antagonistic manner.” Muñoz-Carrillo at 1. Muñoz-Carrillo did not characterize the cytokines produced in response to CMV infection specifically.

Other publications concerned the production of cytokines in response to vaccination. Morel reported that vaccines are being designed to elicit the types of cytokines needed to address various illnesses, including cancer, autoimmune diseases, and infections. Morel at 1; see Gershwin Rep. at 16 (quoting Morel). Vaccines can be manufactured with adjuvants to control the cytokine production for specific uses. Morel at 4.

Hervé broadly discussed the immune response to vaccination, noting that vaccines trigger the production of various cytokines, including interleukin-1 (“IL-1”), IL-6, tumor necrosis factor- alpha, and prostaglandin-E2, which enter the bloodstream and mimic the response to a natural infection. Hervé at 2; see Gershwin Rep. at 16-19 (quoting Hervé) . Cytokines are detectable in animal models as soon as three hours after vaccination. Hervé at 2; see also Roth at 176-77 (Fig. 1) (illustrating that cytokines are released and attract cells from circulation within hours of vaccination). However, “[m]ost cytokines and chemokines in muscle injected with adjuvanted vaccine decrease rapidly within [24 hours] after delivery, and reach baseline after [72 hours].” Hervé at 2. Hervé discussed studies of the production of cytokines and other inflammatory factors produced by specific vaccines, including Hepatitis B, human papillomavirus (“HPV”), H1N1 influenza (“flu”), and non-adjuvanted seasonal flu and yellow fever vaccines. Id. at 3-4. As noted, the cytokine releases measured in these studies were short-lived. Id.

Chatziandreou explored how the innate immune response following flu vaccination triggered the adaptive immune response. Chatziandreou at 2428.; see Gershwin Rep. at 19-20 (quoting Chatziandreou). The study found that macrophage activation after vaccination led to the production of IFN-β, which in turn triggered an IL-α inflammatory cascade. Chatziandreou at 2427. Audiger described the role of dendritic cells, which signal the production of cytokines, in preserving immune tolerance, but it did not tie that to GBS or the subject vaccines. Cindy Audiger et al., The importance of dendritic cells in maintaining immune tolerance, 198 J. IMMUNOL. 2223 (2017) (Author Manuscript) (Ex. 25) (“Audiger”) at 1; see also Ferrara at 1043-44 (noting that the balance of cytokine networks and regulatory cells is critical to maintaining immunological homeostasis).

These papers generally demonstrated that both infections and vaccinations lead to the production of cytokines, which play a role in the regulation of immunological homeostasis. However, this was insufficient to causally link the subject vaccinations, CMV infection, and the pathogenesis of GBS. None of the articles characterized cytokine production following Hepatitis A or meningococcal vaccination. Nor did they address how cytokines could lead to the development of GBS, aside from the general proposition that inflammation can, under some circumstances, become pathogenic. As Dr. Callaghan persuasively emphasized, Dr. Gershwin’s theory of combined CMV-vaccine pathogenesis had not been discussed in the literature or studied by the scientific community. Tr. at 154 (“I’ve never seen a study trying to link that up, which is why I find this theory, you know, sort of unusual. This is not something talked about in the literature. This is not something that's been studied epidemiologically or mechanistically. So, you know, that’s why I find it a strange mechanism to discuss.”).

Dr. Fujinami was also persuasive in countering Dr. Gershwin’s theory, pointing out that the cytokine production in response to the subject vaccines would be “a drop in the bucket” compared to the response to CMV infection. Tr. at 102. The vaccines would be insufficient to trigger an immunological storm, given their limited anatomical reach and inability to replicate. Id. at 96, 103-04. Moreover, several studies referenced by Dr. Fujinami suggested that the subject vaccines could reduce the chance of a pathogenic autoimmune reaction. For example, Mannie found that the cytokine IFN-β given along with a neuro-antigen (“NAg”) to animal models prevented and lessened EAE. Mannie at 5340. This suggests that the cytokines elicited by the subject vaccines might diminish the propensity for neuroinflammatory autoimmunity. Id.; Fujinami Rep. at 4-5; see Tr. at 86-88. Similarly, Sicotte found that mice given NAg and alum (a component of the Hepatitis A vaccine given here) did not develop either clinical EAE or nervous system inflammation. Sicotte at 251; Tr. at 88. In Wallberg, mice immunized with alum adsorbed to recombinant MOG were protected against EAE. Wallberg at 1544; Tr. at 88-90. In Wang, NAg or an antigen plus alum and IFN-β facilitated the production of regulatory T cells that inhibited EAE. Wang at 2005; see Tr. at 91-92.

Dr. Gershwin pointed out that he was not claiming alum or IFN-β were primarily responsible for triggering GBS here. Tr. at 58. He also critiqued the Wallberg paper specifically, noting, among other things, that it did not show alum fully protected against diabetes. Id. at 163- 65. Also, Wallberg showed “[t]he degree of protection induced by rMOG-alum . . . varies with the route of administration.” Id. at 165 (quoting Wallberg at 1544). And Wallberg used an EAE model, and it would be “a leap of faith to associate EAE with [GBS].” Id. at 165-66. Regardless of whether Dr. Gershwin specifically blamed these specific substances for triggering GBS, Dr. Fujinami cited a body of literature indicating that the components and products of the subject vaccines could reduce the likelihood of neuroinflammation and autoimmunity.8

Petitioner argues that in Eamick, Special Master Moran accepted a similar causation theory advanced by Dr. Gershwin to that proposed here. Pet.’s Post-Hrg. Br. at 8; Eamick v. Sec’y of Health & Hum. Servs., No. 15-519V, 2018 WL 2926048 (Fed. Cl. Spec. Mstr. May 15, 2018). In Eamick, the petitioner alleged he developed GBS caused by Hepatitis A and B vaccines. Id., at *1. The evidence showed he contracted an undefined upper respiratory infection (“URI”) 10 days before the subject vaccinations and about three weeks before developing GBS. Id. The URI worsened during the period between the vaccinations and the onset of GBS. Id. Dr. Gershwin proposed that the vaccines “could dysregulate the host’s response to the URI infection in a way that resulted in a breach of tolerance,” ultimately resulting in GBS via molecular mimicry. Id., at *5. Respondent’s expert argued that this theory was unsupported by the epidemiologic evidence, but she did not dispute that the vaccines at issue would cause a strong cytokine response in the lymph nodes. Id. Special Master Moran concluded that Althen prong one was satisfied. Id., at *6.

Eamick is not binding on me. Boatmon, 941 F.3d at 1358-59 (holding that special masters are not bound by the decisions of other special masters and, “[b]y extension, are not required to distinguish non-binding decisions of other special masters.”). Additionally, here, the experts agreed that CMV infection can cause GBS, and Dr. Gershwin disclaimed the opinion that either of the subject vaccines could alone trigger GBS. He failed to identify any specific component or product of either vaccine that could elicit a pathogenic response when combined with CMV infection. Moreover, Eamick did not reference the literature cited here by Dr. Fujinami, which added material complexity to what is known of the role of cytokines and adjuvants in autoimmunity. I conclude the theory advanced here by Dr. Gershwin was unpersuasive.

2. The epidemiologic literature does not report a causal association between either of the subject vaccines and GBS.

Although a petitioner does not need epidemiologic data to prevail on Althen prong one, such data can be considered and given weight by the special master. In Tullio, Special Master Moran explained at length why it is appropriate to give such data consideration in Vaccine Program cases. Tullio v. Sec’y of Health & Hum. Servs., No. 15-51V, 2019 WL 7580149, at *6 (Fed. Cl. Spec. Mstr. Dec. 19, 2019). First, the Federal Circuit “has endorsed special masters weighing epidemiological studies that investigated whether a vaccination is associated with an increased incidence or worsening of a disease.” Id. (discussing W.C., 704 F.3d at 1361). Second, other legal authorities have considered such data in assessing related causation questions. Id. at *7. Third, scientists rely on epidemiologic data to make determinations about causation. Id. at *7-8. I agree that epidemiologic data can be important circumstantial evidence of a causal exposure- injury association and are appropriate to assess in a Vaccine Program case.

Both parties’ experts agreed that the epidemiologic data do not support the claim that either the Hepatitis A or the meningococcal vaccine is causally associated with GBS. Dr. Gershwin, in fact, opined that he did not think either of the subject vaccines could have caused Petitioner’s GBS had he not also had a CMV infection. Tr. at 39. The epidemiologic data in the record here are reassuring.

In Chen, a nested case-control study found “no evidence of an increased risk of GBS within the 180 days after any vaccinations, as well as all vaccinations combined[.]” Chen at 368. The study assessed the potential association between each of the subject vaccines here and GBS. Id. at 367 (Table 3) (reporting non-significant results for both the Hepatitis A and meningitis vaccines).

Velentgas measured the risk of GBS following meningococcal conjugate vaccination in a population of approximately 50 million patients, with more than 1.4 million doses of the vaccine administered. Velentgas at 1356. The study identified no cases of GBS in the six weeks following vaccination in that cohort. Id. at 1355-56.

In de Wals, the investigators studied the rate of GBS following an immunization campaign in which the meningococcal conjugate vaccine was given to 1.9 million patients in Quebec. de Wals at e75. The study found no statistical association between the vaccine and development of GBS. Id. at e76 (Table 1).

Roux was a case report describing a single instance of a patient developing GBS following Hepatitis A vaccination.9 Roux at 490. The authors recognized that “GBS rarely happens after a hepatitis A vaccination. However, the responsibility of this vaccine should be considered in the clinical presentation of an acute polyradiculoneuritis.” Id. This single anecdotal report is not persuasive evidence of causation.

Because the record before me does not include preponderant evidence of a sound and reliable theory for how the subject vaccines could cause GBS, either alone or in combination with CMV infection, I conclude that Althen prong one is not satisfied.

B. Althen Prong Two Althen prong two requires proof of “a logical sequence of cause and effect showing that the vaccination was the reason for the injury.” Althen, 418 F.3d at 1278. The sequence of cause and effect must be “‘logical’ and legally probable, not medically or scientifically certain.” Andreu, 569 F.3d at 1380 (quoting Knudsen, 35 F.3d at 548-49). A petitioner is not required to show “epidemiologic studies, rechallenge, the presence of pathological markers or genetic disposition, or general acceptance in the scientific or medical communities to establish a logical sequence of cause and effect.” Capizzano, 440 F.3d at 1325. Instead, circumstantial evidence and reliable medical opinions may be sufficient to satisfy the second Althen prong. Id. Further, special masters are expected to consider the views of treating doctors. Id. at 1326. Such views are often persuasive because the doctors have direct experience with the patient whom they are diagnosing -- but they are not necessarily dispositive of the causation question. See McCulloch v. Sec’y of Health & Hum. Servs., No. 09-293V, 2015 WL 3640610, at *20 (Fed. Cl. Spec. Mstr. May 22, 2015). Finally, although a petitioner does not bear the burden of eliminating all alternative causes for his injury, it is appropriate for a special master to consider evidence relating to such alternative causes in assessing the Althen prongs. Winkler v. Sec’y of Health & Hum. Servs., 88 F.4th 958, 963 (Fed. Cir. 2023); Doe 11 v. Sec’y of Health & Hum. Servs., 601 F.3d 1349, 1357-58 (Fed. Cir. 2010); Walther v. Sec’y of Health & Hum. Servs., 485 F.3d 1146, 1151 (Fed. Cir. 2007).

All of the experts stated that Petitioner developed a CMV infection around the time of vaccination. Gershwin Rep. at 12; Callaghan Rep. at 3; Fujinami Rep. at 7. As noted, Dr. Gershwin opined that Petitioner had an acute or reactive CMV infection at about the same time he was vaccinated, and these concurrent factors led to immune dysregulation and GBS. Gershwin Rep. at 12. When Petitioner developed the CMV infection is not entirely clear, however. According to the contemporaneous records and his affidavit, he did not report any symptoms of an infection at the time of the vaccinations on July 6, 2017, nor did he develop any such symptoms in the days thereafter. See Ex. 2 at 5-10 (documenting a normal exam on the day of vaccination); Ex. 1 (Petitioner’s affidavit). Testing done in the hospital 15 days after the vaccinations revealed elevated CMV antibodies. Ex. 4 at 160-61. Infectious disease specialist Dr. Bouvier then diagnosed a CMV infection, which she believed was either a primary infection (which might have triggered Petitioner’s GBS), or a reactivation of an earlier infection “in the setting of acute critical illness.” Ex. 6 at 446. Noting Petitioner’s lack of reported symptoms, Dr. Bouvier commented that CMV infections can be asymptomatic. Id. at 446-47. Overall, although it appears that Petitioner’s CMV infection and vaccinations occurred in some temporal proximity to one another, it is not certain he had an ongoing CMV infection at the time of the vaccinations, as Dr. Gershwin presumed in delivering his causation opinion. In any event, even if Petitioner did have an acute CMV infection at the time of vaccination, he did not experience any systemic or local symptoms in the days thereafter, which undercuts the proposition that the vaccines/infection were producing a significant inflammatory response. See Tr. at 66, 71 (Dr. Gershwin’s testimony); id. at 92-93 (Dr. Fujinami’s testimony).

Furthermore, it is undisputed that none of Petitioner’s treating physicians attributed his GBS to the subject vaccinations, either alone or in combination with the CMV infection. See Tr. at 71 (Dr. Gershwin’s testimony); id. at 97-98 (Dr. Fujinami’s testimony). Dr. Bouvier mentioned the infection as a possible trigger. Ex. 6 at 446. Her supposition was in accordance with the opinions of the experts in this case, all of whom agreed that CMV infection can cause GBS. Id.; Gershwin Rep. at 12; Callaghan Rep. at 3; Fujinami Rep. at 3; see also Lunn at 845 (reporting 12.5% of GBS patients tested positive for primary CMV infection).

Lastly, because the evidence does not preponderantly support Althen prong one, it follows that there is insufficient evidence to show a logical sequence of cause and effect between the subject vaccinations and Petitioner’s GBS. Thus, I conclude Althen prong two was not met.

C. Althen Prong Three Althen prong three contains two parts. First, a petitioner must establish the “timeframe for which it is medically acceptable to infer causation,” and second, he must demonstrate that the onset of the disease occurred in this period. Shapiro, 101 Fed. Cl. at 542-43.

The evidence shows that Petitioner presented to urgent care on July 17, 2017, 11 days after the subject vaccinations. Ex. 3 at 5. He reported waking up that day with neck pain, bilateral shoulder pain, and numbness in his hands. Id. In his affidavit, Petitioner said that he woke up with numbness and tingling in both hands on July 17. Ex. 1 at 1. On July 18, 2017, Petitioner went to the Mt. Sinai ED, complaining of two days of moderate thoracic back pain. Ex. 4 at 12. These records place the onset of Petitioner’s GBS on or about July 17, 2017.

Dr. Gershwin opined: “[T]he development of [Petitioner’s] GBS after his vaccinations fits squarely within the medically acceptable timeframe expected for such an injury following vaccinations[.]” Gershwin Rep. at 20. Neither of Respondent’s experts disputed this proposition. Accordingly, I conclude that Althen prong three has been satisfied. However, because neither prong one nor prong two were preponderantly established, Petitioner is not entitled to compensation.

VI. CONCLUSION

Upon careful evaluation of all the evidence submitted in this matter, including the medical records, affidavit, testimony, expert reports, and medical literature, I conclude that the preponderant evidence does not show Petitioner is entitled to compensation under the Vaccine Act. I therefore DENY entitlement. The clerk shall enter judgment accordingly.10

IT IS SO ORDERED. s/ Jennifer A. Shah Jennifer A. Shah Special Master