               In the United States Court of Federal Claims
                                     OFFICE OF SPECIAL MASTERS
                                             No. 15-1108V
                                          (not to be published)

*************************                                                 Special Master Corcoran
GALEN L. STRONG,             *
                             *                                            Filed: January 12, 2018
                 Petitioner, *
     v.                      *                                            Entitlement; CIDP; GBS;
                             *                                            Influenza vaccine; Preexisting
SECRETARY OF HEALTH          *                                            HIV Infection; Causation; Timing
AND HUMAN SERVICES,          *
                             *
                 Respondent. *
                             *
*************************

Alexander Laufer, Eisenhower & Laufer, P.C., Fairfax, VA, Petitioner

Sarah C. Duncan, U.S. Dep’t of Justice, Washington, DC, for Respondent

                                 DECISION DENYING ENTITLEMENT1

          On October 1, 2015, Galen L. Strong filed this action seeking compensation under the
    National Vaccine Injury Compensation Program (the “Vaccine Program”).2 Mr. Strong alleges
    that he experienced Guillain-Barré syndrome (“GBS”) and/or chronic inflammatory
    demyelinating polyneuropathy (“CIDP”) as the result of receiving an influenza (“flu”) vaccine
    on September 19, 2012. Petition (“Pet.”) (ECF No. 1) at 1. Petitioner filed a motion for judgment
    on the record on June 5, 2017. See Motion for Judgment on the Administrative Record, dated
    June 5, 2017 (ECF No. 38) (“Motion”). After considering the record as a whole, and for the
    reasons explained below, I find that Petitioner has not carried his burden of proof, and is
    accordingly not entitled to an award of damages.

1
  Although this Decision has been formally designated “not to be published,” it will nevertheless be posted on the
Court of Federal Claims’s website in accordance with the E-Government Act of 2002, 44 U.S.C. § 3501 (2012). This
means the ruling will be available to anyone with access to the internet. As provided by 42 U.S.C. § 300aa-
12(d)(4)(B), however, the parties may object to the Decision’s inclusion of certain kinds of confidential information.
Specifically, under Vaccine Rule 18(b), each party has fourteen days within which to request redaction “of any
information furnished by that party: (1) that is a trade secret or commercial or financial in substance and is privileged
or confidential; or (2) that includes medical files or similar files, the disclosure of which would constitute a clearly
unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the Decision in its present form will be available.
Id.
2
 The National Vaccine Injury Compensation Program comprises Part 2 of the National Childhood Vaccine Injury Act
of 1986, Pub. L. No. 99-660, 100 Stat. 3755 (codified as amended at 42 U.S.C. § 300aa-10 through 34 (2012)).
References to sections of the Act herein shall omit the statutory prefix.

                                                           1
    I.   Factual Background

         A.      Petitioner’s Pre-Vaccination Medical History

        Mr. Strong (60 years old at the time of vaccination) had some pre-vaccination health
problems relevant to the determination of his claim. The medical records in this case reveal that
he suffered from chronic obstructive pulmonary disease (“COPD”), hypertension, high
cholesterol, recurrent bronchitis, upper respiratory infections (“URI”), and ear infections. Ex. 7
at 1-20; Ex. 11 at 1-42. (In addition, and as discussed below, in the course of treatment for the
symptoms alleged as vaccine-caused in this case, Petitioner also learned he had a previously-
undiagnosed infection that Respondent argues played a role in his injuries).

        On July 24, 2012 (two months prior to vaccination), Petitioner saw Michael Sylvester,
M.D., his primary care provider, for treatment of what he identified as five days of sinus issues,
body aches, and fatigue, along with leg pain. Ex. 7 at 1. Mr. Strong was diagnosed with a URI,
and thereafter sought follow-up treatment for it on July 30, August 3, and August 22, 2012,
respectively. Id. at 4-13. In addition, on August 23, 2012, a month prior to his vaccination, a chest
x-ray revealed a 4 cm mass in the right upper lobe of his lungs, and pathology was inconclusive.
Ex. 9 at 14; Ex. 7 at 17-20.

         B.       Vaccination and Reaction

        On September 19, 2012, petitioner saw pulmonologist Alexander Schult, M.D. At this
time, he reported that aside from his pulmonary symptoms, he was experiencing “numerous joint
aches and myalgias,” and noting the fact that he had undergone a partial right knee replacement
in 2009. Ex. 8 at 64-65. Petitioner received the flu vaccine at issue that day. See Exs. 1; 2; and 8
at 66.

        Mr. Strong alleges (in an affidavit submitted in this action) that he experienced a vaccine
reaction within the next two to three weeks (or during the first half of October 2012),
characterized by fatigue, weakness and leg pain, including a burning and prickly feeling. Ex. 2 at
¶ 3.3 However, he maintains that because his primary concern (along with physicians like Dr.
Schult) was the possibility that he might have lung cancer, the significance of such symptoms
was not sufficiently discussed and/or was broadly overlooked in the course of his treatment. Id.
Nevertheless, Petitioner’s pain and leg weakness was sufficiently severe to prevent him from
performing routine yard work that month. To corroborate the timing of these symptoms,
Petitioner noted that his sister-in-law visited the Strongs during the first week in October, and
that she commented on his inability to walk short distances without great difficulty. Id. at ¶ 4. He
also recalled a shopping trip in October to purchase a rug which he was barely able to assist his


3
  Petitioner’s wife, Shelley L. Strong, also prepared an affidavit that largely echoed the same factual assertions
contained in Mr. Strong’s affidavit. Compare Ex. 2 at ¶¶ 3-4 with Ex. 3 at ¶¶ 3-4.

                                                        2
wife in transporting home due to leg pain. Id. at ¶ 3.

        The medical records, however, do not corroborate Mr. Strong’s allegations about onset of
his purported reaction. Rather, they indicate that on November 15, 2012, Petitioner returned to
Dr. Schult for a follow-up from his September appointment. He now reported general congestion,
fatigue, and shortness of breath after exertion (although he did not provide a date on which any
such symptoms began), and also that he had awakened over the prior three days with aches and
pains in his legs plus a “prickly, hot feeling from the inside out.” Ex. 8 at 58-59. A general exam
was normal, but no neurological exam was noted. Id. Mr. Strong’s assessment was a lung mass,
COPD, and nasal discharge. Id. These records make no reference to the pain and leg weakness
Petitioner alleges he had been experiencing in October, and also do not reference any complaints
relating to a reaction to the flu vaccine.

        A month later, on December 18, 2012, Mr. Strong went back to his primary care provider,
Dr. Sylvester, to discuss diagnoses regarding his lung mass, and he reported continued wheezing
and shortness of breath, but again nothing about the purported October weakness. Ex. 7 at 21-23.
The review of symptoms was negative for paresthesias, weakness, myalgia, and arthralgias, and
his neurological exam was normal. Id. at 22. Dr. Sylvester proposed that there might have been
a reversible component or acute infectious process with respect to Mr. Strong’s COPD that would
explain his pulmonary symptoms, and discussed with Petitioner his concerns that the lung mass
could be cancerous. Id. at 23. He was prescribed a prednisone taper and inhalers. Id. Again, no
reference to ongoing or recently-experienced limb weakness or pain is set forth in these records.

       C.      2013 Treatment and Initial GBS Diagnosis

        On January 9, 2013, Petitioner returned to Dr. Sylvester complaining of a cough that had
persisted over the preceding three to four days, plus headaches and wheezing. Ex. 7 at 24-26. His
neurologic exam was normal, and no neurologic symptoms were reported or observed, but
Petitioner conveyed the stress he was suffering from due to the existence of his lung mass, and
Dr. Sylvester’s exam revealed wheezing. Id. Dr. Sylvester’s diagnosis included cough, COPD,
hypercholesterolemia (excessive cholesterol in the blood) and coronary artery disease, and
Petitioner was again prescribed steroid medication as well as an antibiotic. Id. At a follow-up
with Dr. Sylvester a little over a week later, Petitioner’s exam was negative for all problems but
the pulmonary findings. Id. at 27-29. Accordingly, almost four months since receiving the
vaccine, Mr. Strong was now reporting nothing similar, symptoms-wise, to what he purports to
have experienced two to three weeks post-vaccination.

        By February, however, the records reveal that Mr. Strong was experiencing symptoms
relevant to the claim in this case. Thus, on February 5, 2013 (now four-and-a-half months after
vaccination), Petitioner went to Dr. Sylvester’s office complaining of leg pain (beginning three
days before) severe enough to prevent sleep. Ex. 7 at 30-31. The pain was determined to be
bilateral and migratory, and involved Petitioner’s calves, thighs, and occasionally the joints, but

                                                  3
Petitioner did not report paresthesias or leg weakness. Id. at 30. Petitioner also reported that his
tongue was sore, and the examination showed oral thrush, but no focal neurological deficits. Id.
Petitioner was prescribed medicine for his leg pain. Id.

       Four days later, on February 9, 2013, Mr. Strong went to the emergency room (“ER”) at
Martha Jefferson Hospital in Charlottesville, Virginia, complaining of persistent bilateral leg pain
over several days, coupled with difficulty walking. Ex. 4 at 1-3. He reported having received
multiple courses of antibiotics for bronchitis and also prednisone. Id. at 1. The neurological
review of symptoms and neurological exam were negative. Id. The physical exam revealed
tenderness of the right calf and hip, and the ER physician noted that Petitioner’s “symptoms
sound[ed] quite muscular in nature,” but also could represent a neuropathy. Id. at 2. The ER
physician prescribed pain medication but could not identify an etiology for Petitioner’s condition.
Id. Because Mr. Strong did not appear to be in acute distress, he was released. Id.

        Mr. Strong returned to Dr. Sylvester on February 12, 2013, complaining of chronic pain,
general weakness, and severe “myalgia/arthralgia” for the last couple weeks, which Dr. Sylvester
observed was temporally related to Petitioner’s cessation of steroids (thus, Petitioner argues,
allowing for the inference that the steroid treatments suppressed these symptoms) as well as
reduction in other medications. Ex. 7 at 33-35. The review of systems was now (and for the first
time chronologically in the medical record) positive for paresthesia in a stocking glove
distribution, as well as anxiety, depression, sleep disturbance, and concentration problems. Id. at
33. Petitioner also had difficulty getting onto the exam table, and appeared tired and anxious. Id.
at 34. Dr. Sylvester discontinued Petitioner’s statin medication due to possible statin-caused
myalgia, and began a 12-day prednisone taper. Id. He also proposed (based on mildly elevated
liver test results) that Mr. Strong’s symptoms might have an infectious etiology, or reflect a
medication side effect (while also allowing that Mr. Strong could still be suffering from anxiety
relating to concern about the lung mass). Id. at 35. Petitioner was directed to follow up soon with
Dr. Sylvester, in order to gauge whether he was suffering from a post-viral syndrome, or even
possibly GBS. Id.

       D.      GBS Raised as Explanation for Symptoms

        Petitioner’s follow-up visit with Dr. Sylvester occurred on February 20, 2013. Ex. 7 at
36-38. The records from this visit note that Mr. Strong now reported a decrease in pain, and that
his weakness had also largely resolved, but that he was still experiencing paresthesias of the feet
and hands. The neurological and musculoskeletal exams were normal; gait and coordination were
intact, and except for “slight” reflexes in the lower extremities, deep tendon reflexes were
otherwise normal. Id. at 37. Dr. Sylvester noted difficulty in explaining the cause of Mr. Strong’s
symptoms. Although GBS had been a “major concern,” Dr. Sylvester felt Petitioner’s
presentation was “not a perfect fit” for GBS since he had shown improvement, and therefore they
together agreed “not [to] pursue this [diagnosis].” Id. at 38. Dr. Sylvester nevertheless prescribed


                                                 4
gabapentin for Petitioner’s leg pain and paresthesia, and recommended daily walking. Id.

        Mr. Strong visited Dr. Sylvester again on March 4, 2013, complaining of continued leg
pain for three to four weeks, cough, and fatigue. Ex. 7 at 39-41. Petitioner’s musculoskeletal and
neurological exams were again normal, with “reflexes, gait and coordination . . . all intact.” Id. at
40. Nevertheless, and noting that Petitioner’s leg pain “continue[d] to behave like improving
[GBS],” Dr. Sylvester now deemed GBS to be “probable.” Id. at 39-40. Because it appeared to
be working, Petitioner’s gabapentin dosage was increased, and he was also prescribed an
antibiotic. Id. at 41.

         Petitioner saw Dr. Sylvester two more times that month – on March 15 and March 29,
2013. At the former visit, he complained of symptoms more like those he had been experiencing
before the February ER visit (i.e., cough, shortness of breath), but reported less pain, and upon
examination he displayed none of the neurologic/neuropathic symptoms that had more recently
been the subject of his visits with Dr. Sylvester. Ex. 7 at 41-43. He was advised to continue with
gabapentin. Id. at 44. At the second visit toward the end of March, Mr. Strong reported right flank
pain for about a week and swelling on his left side, along with complaints of leg pain and
weakness much like he had voiced before. Id. at 46. Again, however, Petitioner’s neurologic and
musculoskeletal exams were negative. Id. at 47. Dr. Sylvester’s notes convey the concern that
“there may be more going on with the amount of systemic symptoms he is experiencing,”
reiterating his speculation that Mr. Strong likely had experienced GBS but was otherwise
improving. Id. at 48.

        Petitioner had more doctor’s visits with Dr. Sylvester that spring, at which time he
complained of leg and rib-midsection pain, as well as shortness of breath. See, e.g., Ex. 7 at 49-
51. Dr. Sylvester continued to watch Mr. Strong’s condition and maintained the gabapentin
prescription. Id. Petitioner also saw Dr. Schult for his pulmonary problems, and told him of
ongoing chest pain, numbness, and intermittent bilateral weakness and paresthesias in his feet
(although they were attributed more to feet positioning than to a neurologic source). Ex. 8 at 53.
He specifically informed Dr. Schult of the absence of nocturnal symptoms, as well as the fact that
gabapentin seemed to relieve his chest pain and discomfort. Id.

       On May 23, 2013, Mr. Strong saw Dr. Sylvester for an earache, but also complained of
ongoing pain and feet paresthesias since the time GBS was first proposed as a potential diagnosis
in February. Ex. 7 at 52-54. But Petitioner’s neurological exam was again normal, and the
musculoskeletal exam only revealed bilateral chest wall and epigastric tenderness. Id. Dr.
Sylvester repeated his suspicion that many of Petitioner’s symptoms were likely related to GBS,
although he expressed concern about other, different presenting symptoms, such as weight loss.
Id.




                                                  5
        E.      Summer 2013 Treatment and HIV Infection Discovery

        The medical records reveal that for almost the next two months, Petitioner sought no
additional medical care. On July 17, 2013, however, Mr. Strong went to the Martha Jefferson ER
complaining of worsening extremity and body pain plus weakness. Ex. 6 at 7-14. He reported
that he had been experiencing such symptoms since February, but that they had become “much
worse” in the previous four days. Id. at 8. His exam revealed decreased upper and lower extremity
strength and an inability to stand up without assistance. Id. The history from this visit noted that
Petitioner had similar but milder symptoms of discomfort in the arms and legs in February, and
although his usual treater (Dr. Sylvester) had thought it was “probably” GBS, he had improved
with gabapentin, and for a couple of weeks “he actually felt back to his normal self.” Id. at 7-10.
It was also noted that he had not recently had any vaccinations or experienced any illnesses. Id.
at 8.

        Ultimately, the ER treater characterized Petitioner’s condition as “a fairly rapidly
progressive lower greater than upper extremity weakness,” as well as “dysesthesias of unclear
etiology.” Ex. 6 at 10. Mr. Strong was admitted to the hospital for further work-up, and
specifically assigned for a consultation with a neurologist, Dr. Robert Adams. Id.

        Dr. Adams saw Mr. Strong that same day. Ex. 6 at 76-80. His notes include a recitation
(from Mr. Strong and his wife) of the relevant medical history. The Strongs informed Dr. Adams
that onset of Petitioner’s pain was “fairly abrupt” and had begun in February (contrary to their
statements in this action about an earlier onset). Id. at 76. Petitioner had initially experienced pain
in his legs, with tingling and paresthesias in the feet and “equivocal” symptoms of tingling and
numbness in the hands as well. Id. These records further indicate that Petitioner himself reported
that his symptoms had fluctuated in severity since February but had never dissipated entirely,
becoming acutely worse over the next several days and beginning to feature progressive
weakness. Id. Dr. Adams noted that the examination “reveal[ed] very little in the way of sensory
impairment, but clear weakness, some clearly hypoactive reflexes.” Id. at 76-77. He also noted
that it was “[u]nclear what this process is, if it is a single process beginning in February,
maintaining a fluctuating pattern for most of the time since, and then worsening substantially the
last five days. It is possible there are two independent processes.” Id. at 79. Dr. Adams did not,
however, initially theorize that Petitioner’s condition reflected GBS, CIDP, or some other
neuropathic illness, proposing instead an “inflammatory process such as vasculitis, myelitis,” or
possibly Lyme disease. Id.

        Dr. Adams proposed some testing in an effort to identify the possible cause of Mr.
Strong’s symptoms. He ordered bloodwork, which revealed that Mr. Strong suffered from a
vitamin B6 deficiency. Ex. 6 at 1192. In addition, Petitioner’s cerebrospinal fluid (“CSF”) was
drawn and analyzed, and it showed elevated proteins at 182 and 24 white blood cells, or
“lymphocytic pleocytosis” - meaning abnormal numbers of white blood cells, thereby suggesting


                                                   6
infection or inflammation in the central nervous system. Id. at 1187; Dorland’s Illustrated
Medical Dictionary 1460 (32nd ed. 2012) (hereinafter Dorland’s). More surprisingly, it was
determined from the lab work that Mr. Strong suffered from an HIV infection. Id. at 1192. From
the records and witness statements filed in this case, it appears Petitioner was not aware of this
preexisting infection.

        At this point, the records begin to reveal better-substantiated opinions as to a possible
explanation for Mr. Strong’s symptoms – and their connection to his preexisting HIV infection,
rather than having a different cause. Thus, on July 18, 2013, Mr. Strong underwent an EMG/NCS,
which “reveal[ed] evidence for an acquired, demyelinating radiculoneuropathy with lower
extremities predominantly involved, and motor > sensory nerves.” Ex. 9 at 63. Based upon these
findings, Dr. Adams now speculated that Petitioner’s condition “may represent 2nd episode
(recurrence) GBS or GBS superimposed on other more chronic neuropathic process.” Ex. 6 at
100. He recommended that Petitioner begin IVIG treatment4 immediately. Id. By July 20, 2013,
however, Dr. Adams was proposing that the GBS-like symptoms were a “likely provocation by
HIV,” and that his February symptoms were “possibly also HIV-related inflammatory
neuropathy,” which he noted explained “some [of the] atypical features in his clinical
presentation,” as well as Petitioner’s lymphocytic pleocytosis. Id. at 105.

         Other treaters echoed this conclusion. Thus, on July 22, 2013, infectious disease
specialist Keri Hall, M.D., obtained a history from Mr. Strong’s wife about his winter symptoms,
and discussed with her what possible risk factors in Petitioner’s past might have resulted in the
positive HIV finding. Ex. 6 at 115-16. Dr. Hall proposed (much like Dr. Adams) that Petitioner’s
GBS was likely “[secondary] to HIV” and recommended starting antiretroviral therapy (after
confirming his lung mass was not tuberculosis) “to treat most likely underlying cause (HIV).” Id.
at 122. Although other treaters generally continued to maintain thereafter that Petitioner had
experienced, and been recovering from, GBS, some in the summer of 2013 proposed an even
different possible etiology for his symptoms. For example, neurologist Dr. Alexander Grunsfeld
noted that in his view “GBS less likely CIDP,” although he added that he favored “GBS with pre-
existing B6 deficiency as an explanation for his acute or chronic decline versus CIDP.” Ex. 6 at
149-50.

        F.       Subsequent Treatment and Analysis of Petitioner’s Condition

       By July 21, 2013, Mr. Strong’s condition had worsened despite three courses of IVIG,
and he was intubated secondary to respiratory failure. Ex. 6 at 107. Petitioner had a bronchoscopy
(which was negative for malignancy and tuberculosis), a tracheotomy, and had a feeding tube

4
 Intravenous immunoglobulin (“IVIG”) is a blood product used to treat patients with antibody deficiencies, including
neurological     disorders.    Clinical    Uses    of    Intravenous       Immunoglobulin,        NCBI       (2005),
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809480/ (lasted visited on Aug. 28, 2017). It is commonly
prescribed to treat diseases believed to be autoimmune in nature, increasing the effectiveness of an individual's
immune response.

                                                         7
placed. Id. at 47-48, 70- 71, 89-91, 1216. He completed another IVIG treatment on July 24, 2013,
but by that date Dr. Hall had proposed antiretroviral therapy. Id. at 122. A few days later, on July
29, 2013, Mr. Strong went into cardiac arrest secondary to hypoxia and was resuscitated with
CPR. Id. at 63-66; 141. On August 10, 2013, Petitioner was discharged to University of Virginia
HealthSouth Rehabilitation Hospital and noted to be “profoundly debilitated with his Guillain-
Barre [sic] and remains quite weak.” Id. at 80-84. At that point, he had been weaned off the
ventilator and no longer required tube feeding. Ex. 5 at 1-5.

        Throughout the remainder of 2013, and then on into 2014 and 2015, Mr. Strong continued
to follow up regularly with Dr. Adams (neurology), Dr. Hall (infectious disease), Dr. Schult
(pulmonary), and Dr. Sylvester (primary care). By September 19, 2013, Petitioner was
ambulating with the support of a walking stick, and two days later he reported having used a
chainsaw to cut down trees. Ex. 8 at 44-45; Ex. 10 at 19-21. In October 2013, Petitioner
complained of leg swelling and pain, which Dr. Sylvester felt was likely medication-related. Ex.
8 at 42-43; Ex. 7 at 60-62. Throughout 2014 and 2015, Mr. Strong continued to complain of lower
extremity paresthesias and pain. See, e.g., Ex. 10 at 4-11, 13-14, 16-18; Ex. 7 at 67-72; Ex. 8 at
1-11, 13-28. Drs. Adams, Hall, and Sylvester all proposed that Petitioner’s ongoing painful
neuropathy could be related to GBS, but allowed as well that HIV neuropathy was an alternative
explanation – along with the medication he took for his HIV infection (Truvada), which his
doctors noted can cause neuropathic symptoms. Ex. 10 at 4-11; Ex. 7 at 70-72; Ex. 8 at 1-11, 13-
23.

II.    Expert Reports

       A.      Dr. Marcel Kinsbourne

        Dr. Kinsbourne offered two expert reports opining that the flu vaccine caused Petitioner
 to develop CIDP. Expert Report, filed on June 5, 2016, as Ex. 12 (ECF No. 20-1) (“Kinsbourne
 First Rep.”); Supplemental Expert Report, filed on November 21, 2016, as Ex. 13 (ECF No. 29-
 1) (Kinsbourne Second Rep.”).

        As his curriculum vitae (“CV”) indicates, Dr. Kinsbourne is board certified in pediatrics.
 See CV, dated Aug. 11, 2017 (ECF No. 40) (“Kinsbourne CV”). He received his medical degree
 in England, and he has been licensed to practice medicine in North Carolina since 1967. Id.
 From 1967 to 1974, Dr. Kinsbourne served as an associate professor in pediatrics and neurology
 and a senior research associate at Duke University Medical Center before holding a series of
 academic positions, including professorships in pediatrics, neurology, and psychology. Id. at 2.
 His clinical experience includes serving as a senior staff physician in Ontario from 1974-1980,
 and a clinical associate in neurology at Massachusetts General Hospital from 1981-1991,
 although (as noted in other cases) many years have passed since he regularly saw patients. Pope
 v. Sec’y of Health & Human Servs., No. 14-078V, 2017 WL 2460503, at *8 (Fed. Cl. Spec. Mstr.
 May 1, 2017). He has not personally studied the immunologic issues raised by theories claiming

                                                 8
    vaccine causation, and lacks specialization in the field of peripheral neuropathies (although his
    general neurologic expertise rendered him competent to discuss such matters).

           Dr. Kinsbourne’s initial report included a detailed review of Mr. Strong’s medical history
    and treatment. Kinsbourne First Rep. at 1-3. He acknowledged that Petitioner’s treaters
    consistently settled on a diagnosis of GBS. However, Dr. Kinsbourne stressed as significant the
    lengthy, up-and-down course of Petitioner’s symptoms, as well as the fact that steroid treatment
    (which is not used for GBS) was successful in ameliorating some of Mr. Strong’s symptoms. Id.
    at 4. These factors – coupled with GBS’s nature as an acute, monophasic illness – suggested to
    him that Mr. Strong likely suffered not from GBS but from CIDP, which is characterized by
    lengthy progression, relapses in symptom severity, and the responsiveness of his symptoms to
    treatments associated with CIDP rather than GBS. Id. at 4.

          Based upon this proposed counter-diagnosis, Dr. Kinsbourne was able to propose a
    causation theory involving Mr. Strong’s September 2012 flu vaccine. Borrowing from literature
    and accepted medical views about the association between GBS and the flu vaccine, Dr.
    Kinsbourne observed that “[s]ubstantial medical opinion holds that GBS and CIDP differ only
    with respect to their temporal profiles.” Kinsbourne First Rep. at 5. Thus, the two share
    immunologic mechanisms. Id.; R. Loughlin, et al., Incidence and Prevalence of CIDP and the
    Association of Diabetes Mellitus, Neurology 73: 39-45 (2009) (“Loughlin”), filed on Aug. 30,
    2016 as Ex. 12-g (ECF No. 20-8); R. Hughes, et al., Immunization and Risk of Relapse of
    Guillain-Barré Syndrome or Chronic Inflammatory Demyelinating Polyradiculoneuropathy, 16
    Muscle and Nerve:1230-1231 (1996), filed on Aug. 30, 2016 as Ex. 12-d (ECF No. 20-5).

           Because of their close association, “evidence as to influenza vaccine causation of both
    GBS and CIDP” bears equally on Petitioner’s claim. Kinsbourne First Rep. at 6. Thus, Dr.
    Kinsbourne invoked literature exploring the cross-reactive potential of components of the flu
    virus (via the mechanism of molecular mimicry – a well-accepted explanation for how the flu
    vaccine can result in GBS)5 to support his explanation for how the same process could result in
    CIDP. Id. at 7.6 He similarly referenced literature establishing CIDP’s association with
    antecedent vaccination or infection, noting that the flu vaccine had been shown (in a classic


5
  I have previously found that molecular mimicry is “a reliable explanation for how the flu vaccine would induce an
autoimmune reaction that would damage an individual’s myelin or nerves.” See Auch v. Sec’y of Health & Human
Servs., No. 12-673V, 2017 WL 1034396, at *20 (Fed. Cl. Spec. Mstr. Jan. 13, 2017); see also Stewart v. Sec'y of
Health & Human Servs., No. 06–777V, 2011 WL 3241585 (Fed. Cl. Spec. Mstr. July 8, 2011) (petitioner was entitled
to compensation in a flu/GBS case); Daily v. Sec’y of Health & Human Servs., No. 07–173V, 2011 WL 2174535 (Fed.
Cl. Spec. Mstr. May 11, 2011) (entitlement proven on a claim that the flu vaccine more likely than not caused the
petitioner to develop CIDP).
6
 Because I do not find it a contestable point to argue against the well-understood mechanisms for how the flu vaccine
can cause GBS, and because this Decision does not turn on that point, I do not include herein reference to or recitation
of the literature offered in Dr. Kinsbourne’s expert report to support this assertion.


                                                           9
    “challenge-rechallenge”7 manner) to cause recurrence or spiking of neuropathic symptoms. Id.
    at 6; D. Vellozi, et al., Safety of Trivalent Activated Influenza Vaccine in Adults: Background
    for Pandemic Influenza Vaccine Safety Monitoring, Vaccine 27: 2114-2120 (2009), filed on
    Aug. 30, 2016 as Ex. 12-n (ECF No. 21-6).

           At the same time, Dr. Kinsbourne proposed an explanation for why the autoimmune
    pathogenic process involving an identical biologic mechanism would produce a somewhat
    different disease course and outcome. Kinsbourne First Rep. at 6, citing C. Comi, Fas-Mediated
    T-Cell Apoptosis in Chronic Inflammatory Demyelinating Polyneuropathy, J. of the Peripheral
    Nervous System 16 (supplement): 45-47 (2011) (“Comi”), filed on Aug. 30, 2016 as Ex. 12-b
    (ECF No. 20-3). Dr. Kinsbourne explained that GBS’s more progressive and rapid disease
    course process was attributable to a “host variable,” such as a genetic susceptibility, but did not
    occur with CIDP, resulting in the latter disease’s “almost indefinite continuation.” Kinsbourne
    First Rep. at 6.

           With respect to the actual medical history at issue, Dr. Kinsbourne acknowledged that if
    Mr. Strong’s allegations that he began to experience symptoms in October 2012 (or within two
    or three weeks of vaccination) were accurate, then his meandering course (with no treater
    diagnosis of GBS until months later, and no short, rapid progression) was “incompatible” with
    the conclusion that in fact he had GBS. Kinsbourne First Rep. at 4. However, since CIDP must
    in Dr. Kinsbourne’s experience take at least two months to progress to nadir, the up-down, slow
    overall course of Mr. Strong’s polyneuropathic symptoms better supported CIDP as the proper
    diagnosis. Id. at 4-5. Dr. Kinsbourne also gave some weight to the steroidal treatments Mr.
    Strong was receiving, since they proved effective, thereby reflecting CIDP as the appropriate
    diagnosis, since it is deemed appropriate for CIDP but not GBS; by contrast, whenever such
    treatments were abated, his symptoms resumed. Id. at 4.

           In his first report, Dr. Kinsbourne also briefly mentioned Mr. Strong’s HIV infection. He
    admitted that HIV could cause neuropathies, but asserted (without attribution) that it was “very
    rarely” associated with CIDP. Kinsbourne First Rep. at 7. He nevertheless acknowledged the
    existence of contemporaneous treater views connecting the HIV infection to Mr. Strong’s
    polyneuropathy, allowing that it may have intensified his pain and injuries, but maintaining his
    position that the flu vaccine remained the more significant contributory factor. Id. at 7.

          Dr. Kinsbourne’s second expert report was filed in response to questions I had raised with
    the parties in light of Respondent’s expert reports. The first issue raised was why the
    contemporaneous medical records did not reflect the proposed CIDP diagnosis. Dr. Kinsbourne
    responded by speculating that Petitioner’s treaters may not have been aware of his more

7
  Re-challenge refers to the concept of an adverse event following vaccination, here the flu vaccine, which reoccurs
after a subsequent dose, “suggesting, but not confirming, a causal association” with the vaccine. Vellozi, et al., Safety
of trivalent activated influenza vaccine in adults: Background for pandemic influenza vaccine safety monitoring,
Vaccine 27: 2114-2120, at 2115 (2009).

                                                          10
    immediate, post-vaccination symptoms, and therefore failed to take into account the true course
    of his illness. Kinsbourne Second Rep. at 1. He also stressed the fact that the effectiveness of
    the steroid treatments Petitioner received further bulwarked the conclusion that a CIDP
    diagnosis was more accurate. Id. However, Dr. Kinsbourne acknowledged that if Mr. Strong’s
    symptoms were found to have begun no sooner than the winter of 2013 (and hence
    approximately four months post-vaccination) rather than when Petitioner alleges, his opinion
    that CIDP was the proper diagnosis in this case would be vitiated. Id.

           Dr. Kinsbourne’s second report also addressed the issue of the discovered HIV infection
    and its possible causal role in Petitioner’s neuropathy – another question I raised in light of
    Respondent’s expert opinions. Dr. Kinsbourne again acknowledged that both GBS and CIDP
    are associated with HIV. Kinsbourne Second Rep. at 2, citing Verma, A., Epidemiology and
    Clinical Features of HIV-1 Associated Neuropathies, J. of the Peripheral Nervous System 6: 8-
    13 (2001), filed on Nov. 17, 2016 as Ex. 13-c (ECF No. 28-3). But he otherwise referred back
    to his original opinion on this topic, declining to elaborate on why the HIV infection should be
    given less weight than the flu vaccine as a possible explanation for Mr. Strong’s symptoms. He
    also made no mention of the two expert reports Respondent had filed, both of which (as
    discussed in greater detail below) included extensive discussion in favor of this alternative
    explanation. Kinsbourne Second Rep. at 2.

          B.      Dr. Peter Donofrio

           Dr. Donofrio, one of Respondent’s two expert witnesses, prepared two expert reports in
    this case. See Report, dated September 10, 2016, filed as Ex. A (ECF No. 22-1) (“First Donofrio
    Rep.”); Report, dated February 24, 2017, filed as Ex. E (ECF No. 32-1) (“Second Donofrio
    Rep.”). As his first report and CV (filed as Ex. B (ECF No. 23) (“Donofrio CV”)) establish, Dr.
    Donofrio is a professor of neurology at the Vanderbilt University Medical Center. First Donofrio
    Rep. at 1. He received his B.S. at the University of Notre Dame, and then attended the Ohio
    State University School of Medicine for his M.D. He is board certified in neurology, internal
    medicine, electro-diagnostic medicine, and neuromuscular disorders. Donofrio CV at 2. He is
    experienced in treating peripheral neuropathies like GBS and CIDP, and is a member of
    organizations focusing on these kinds of neuropathic conditions. First Donofrio Rep. at 1.
    Among his publications is a textbook on the specific topic of peripheral neuropathy. Donofrio
    CV at 21.

           Both of Dr. Donofrio’s reports contained detailed review of Petitioner’s medical history,
    for the purpose of substantiating his opinion that Mr. Strong’s neuropathy (whether it was GBS
    or CIDP)8 could not have begun before the summer of 2013 (or about ten months from the date


8
 Dr. Donofrio’s opinion did not turn appreciably on the accuracy of the GBS diagnosis Petitioner received (especially
given his overall conclusion that the preexisting HIV infection was more likely the cause of his neuropathy). Donofrio
First Rep. at 9. He also agreed that, for present purposes, CIDP and GBS were analogous, although (as discussed

                                                         11
    of vaccination). He saw no persuasive evidence of any neuropathy in December 2012 or January
    2013, given the overall normal neurologic evaluations that Petitioner received at these times.
    First Donofrio Rep. at 9; Second Donofrio Rep. at 2. While GBS was included in Petitioner’s
    differential diagnosis, treaters did not settle on that explanation until more persuasive results
    confirmed it. Petitioner also displayed no measurable weakness in his February 2013 doctor’s
    visits. By contrast, Dr. Donofrio did not see until much later in the temporal record test results
    he would strongly associate with GBS or CIDP, such as areflexia or nerve conduction study
    results confirming the existence of demyelination.9 First Donofrio Rep. at 8. And he found
    significant the fact that Petitioner received no medical care at all between May 23, 2013, and
    July 13, 2013 – a time gap he deemed inconsistent with CIDP, which (even though chronic and
    relapsing) would likely feature some occasions of discomfort or other symptoms in such a long
    timeframe. Id. at 10.

           Dr. Donofrio discounted many of the items from the medical record cited by Dr.
    Kinsbourne in support of his proposed CIDP diagnosis. For example, Dr. Donofrio characterized
    record evidence from the winter of 2013 of complaints of weakness, or instances in which
    Petitioner expressed pain or displayed problems consistent with weakness (for example, his
    difficulty getting onto the examination table), as anecdotal or nonspecific. Second Donofrio Rep.
    at 1.10 He took particular issue with Dr. Kinsbourne’s emphasis of Petitioner’s favorable
    response to steroid treatment as circumstantially corroborating a CIDP diagnosis. He noted that
    corticosteroids were prescribed for a variety of inflammatory but non-neurologic illnesses and
    conditions, and therefore their alleged effectiveness in this case did not necessarily corroborate
    the proposed CIDP diagnosis. Id. at 3. Indeed, in Dr. Donofrio’s view, if Mr. Strong had actually
    suffered from CIDP, he would have expected a more muted response, rather than the dramatic
    improvement alleged. First Donofrio Rep. at 8.

          Dr. Donofrio deemed vastly more significant the finding of Mr. Strong’s treaters in July
    2013 that he carried an HIV infection. As Dr. Donofrio explained, it is well understood in the
    medical community that neuropathies like GBS and CIDP are associated with HIV infections.
    First Donofrio Rep. at 7. In support of this opinion, Dr. Donofrio offered several items of
    medical or scientific literature. See, e.g., A. Gabbai, et al., HIV Peripheral Neuropathy, 115
    Handbook of Clinical Neurology 515-29 (3rd. Ser. 2013), filed as Ex. A-Tab 14 (ECF No. 23-4)
    (“Gabbai”); G. Schleicher, et al., Effect of Human Immunodeficiency Virus on Intensive Care


herein) he disputed some of the evidence cited by Dr. Kinsbourne (in particular, the alleged effectiveness of steroid
treatments) to substantiate the conclusion that CIDP was the correct diagnosis.
9
 Nerve conduction studies (electroneurography) measure the functionality of peripheral nerves, which can identify
damage in the nerves. Dorland’s at 602.
10
  Dr. Donofrio also rejected evidence concerning a rash or skin problem Mr. Strong displayed in February as having
no relevance to the neuropathic injuries at issue in this case. Second Donofrio Rep. at 2.


                                                         12
 Unit Outcome of Patients with Guillain-Barré Syndrome, 31 Critical Care Medicine, 6:1848-50
 (2003), filed as Ex. A-Tab 3 (ECF No. 22-4) (“Schleicher”); T. Brannagan, et al., HIV-
 Associated Guillain-Barré Syndrome, 208 J. Neurological Sciences, 39-42 (2003), filed as Ex.
 A-Tab 4 (ECF No. 22-5) (“Brannagan”). Gabbai in particular (a textbook chapter providing a
 review of the different types of peripheral neuropathies seen in connection with HIV infection)
 provided a thorough consideration of what is known about the connection, and observed that
 “AIDP11 and CIDP occurring in HIV-positive patients are clinically and electrophysiologically
 indistinguishable from those occurring in HIV-negative individuals.” Gabbai at 521.

        Based upon Petitioner’s overall course as revealed in the medical records, Dr. Donofrio
 proposed that Mr. Strong more likely than not was suffering from “HIV associated
 polyradiculopathy.” First Donofrio Rep. at 8. Dr. Donofrio noted two things in particular from
 the record (besides the very fact of the infection itself) that he maintained corroborated his
 opinion. First, he observed that when Petitioner’s CSF was tested in July 2013 (at the time the
 most medically-defensible GBS diagnosis was made, based upon the record) he displayed
 pleocytosis, a significant finding that is highly consistent with an HIV-derived neuropathy. Id.
 at 9; Brannagan at 1; Schleicher at 1850. Second, looking at Mr. Strong’s pre-vaccination
 history, his recurring URIs and other infections were consistent with HIV immunosuppression
 (since it is highly likely that Petitioner’s HIV infection predated his vaccination by some time).
 First Donofrio Rep. at 9-10.12

           C.       Dr. Kathleen Collins

        Dr. Collins, like Dr. Donofrio, submitted two expert reports. See Report, dated July 21,
 2016, filed as Ex. C (ECF No. 24-1) (“First Collins Rep.”); Report, dated February 24, 2016,
 filed as Ex. F (ECF No. 33-1) (“Second Collins Rep.”). Her opinion largely mirrored Dr.
 Donofrio’s, although she added some additional details and viewpoints arising from her
 expertise in different medical topics.

       Dr. Collins received her medical degree and doctorate from Johns Hopkins University
 School of Medicine (after receiving an undergraduate degree from Wellesley College) in 1993.
 Ex. D (ECF No. 25-10) (“Collins CV”) at 1. She then completed her residency in internal
 medicine at Brigham and Women’s Hospital before serving as a clinical fellow of infectious
 disease at Beth Israel Hospital and served as a research fellow at Harvard University. Id. Dr.
 Collins was also a post-doctoral fellow at MIT researching the immune response to viral


11
     AIDP is an acute inflammatory demyelinating polyradiculoneuropathy, and is a GBS variant. Dorland’s at 1493.
12
  Dr. Donofrio also allowed in passing that these URI and other infections could themselves have been the source of
Mr. Strong’s neuropathy (First Donofrio Rep. at 10), although this suggestion is not favored over the HIV infection
under Dr. Donofrio’s interpretation of the record, and the record does not permit me to find this to be more likely than
not.


                                                          13
infections. Id. Dr. Collins is board certified in infectious disease, and currently works as a
professor of internal medicine and microbiology and immunology at the University of Michigan.
Id. Her opinion in this case was based on review of the medical records, along with personal
review of various medical or scientific literature. First Collins Rep. at 1.

       Dr. Collins’s first report included a review of Petitioner’s medical history consistent with
what is set forth above, along with a brief summary explanation for the diseases at issue. First
Collins Rep. at 1-7. In particular, she observed that HIV is associated closely with GBS as well
as other forms of peripheral neuropathy like CIDP, albeit usually in the earliest stages of the
infection, before an individual has become immunocompromised. Id. at 7-8; Vriesendorp,
Pathogenesis of Guillain-Barré Syndrome, UpToDate, Wolters Kluwer Health (2015), filed as
Ex. C-2 (ECF No. 24-9). Nevertheless, she maintained, HIV-associated neuropathies can also
occur on the discontinuation of antiretroviral medication (although Dr. Collins relied on case
study reports for this assertion). First Collins Rep. at 7, citing G. de Castro, et al., Episodes of
Guillain-Barré Syndrome Associated with the Acute Phase of HIV-1 Infection and with
Recurrence of Viremia, Arquivos De Neuro-psiquiatr, 64(3A), 606-8 (2006) filed as Ex. C-8
(ECF No. 24-3). She also proposed that the medical record evidence (which in her view most
strongly supports Petitioner’s neuropathy as having begun in July 2013) supported the timeframe
in which his neuropathy manifested due to the HIV infection as medically appropriate. First
Collins Rep. at 8-9.

       Dr. Collins emphasized several factual points that she maintained corroborated
Respondent’s position that Mr. Strong’s neuropathy was far more likely attributable to his HIV
infection than to the flu vaccine. She agreed with Dr. Donofrio as to the significance of
pleocytosis as corroborating the causal association in this case between the HIV infection and
Mr. Strong’s neuropathy. First Collins Rep. at 9. She also maintained that Petitioner’s symptoms
(transient decreased reflexes, bilateral lower extremity pain, and the gradual onset) were more
consistent with what is known about HIV neuropathies, while not appearing to fit the classic
clinical definition of GBS. First Collins Rep. at 9; see also Second Collins Rep. at 2. She
similarly found significant Petitioner’s responsiveness to gabapentin, which she maintained is
more effective for HIV-caused neuropathies than GBS. First Collins Rep. at 9; Hahn, K., et al.,
A Placebo-Controlled Trial of Gabapentin for Painful HIV-Associated Sensory Neuropathies,
J. Neurology 251(10), 260-6 (2004), filed as Ex. F.3 (ECF No. 33-4).

       In addition, when Petitioner’s treaters first began to evaluate his symptoms in the winter
of 2013 (at which time his underlying HIV infection was unknown), they resisted embracing a
GBS diagnosis, acknowledging the lack of fit between his presentation and what is commonly
understood to be the proper clinical indicia for GBS. First Collins Rep. at 8. Dr. Collins found
this particularly significant. To establish the accepted GBS criteria, she cited Loughlin. First
Collins Rep. at 9; Second Collins Rep. at 2. Comparing those criteria to the facts, Dr. Collins
observed that at the time Mr. Strong first purportedly began to experience neuropathic symptoms

                                                14
 in the winter of 2013, he lacked “preferential defects in motor over pain” symptomology (the
 second Loughlin criterion), and displayed no areflexia or hyporeflexia (the third criterion).
 Loughlin at 2. He also displayed worse symptoms at night. Dr. Collins opined that these
 differences were evident consistently in the medical record between November 2012 and May
 2013, bulwarking the conclusion that his neuropathy was not GBS but an HIV-associated
 neuropathy. Second Collins Rep. at 2.

        The remainder of Dr. Collins’s reports were devoted to attacking assertions made by Dr.
 Kinsbourne.13 For example, she opined that the relationship between an HIV infection and
 neuropathy was far stronger than Dr. Kinsbourne allowed. First Collins Rep. at 9. By contrast,
 she disputed Dr. Kinsbourne’s proposal (carried forward by Petitioner more generally) that an
 HIV infection would merely exacerbate a neuropathy with a different etiology, rather than be
 the actual source of it, noting the lack of literature supporting that proposal. First Collins Rep.
 at 9. She also questioned Dr. Kinsbourne’s assumption that Mr. Strong’s responsiveness to
 steroids corroborated his proposed CIDP diagnosis, arguing that this treatment’s effectiveness
 under the circumstances equally supported her counter-proposal that Petitioner’s symptoms
 were derived from his HIV infection. Id. And she stressed that gabapentin (known to be effective
 in treating an HIV neuropathy) was in fact successfully administered in this case. Id.

 III.    Procedural History

        As noted above, this case was initiated in October 2015. Petitioner thereafter began filing
 medical records, completing the process to the satisfaction of both sides by the end of March
 2016. Respondent subsequently filed a Rule 4(c) Report on May 21, 2016, contesting the
 appropriateness of an entitlement award (see ECF No. 14). Before a status conference could be
 held, Petitioner filed Dr. Kinsbourne’s first expert report,14 and I in turn ordered Respondent to
 file reports of his own in reaction. Drs. Collins’s and Donofrio’s reports, plus medical literature,
 were thereupon filed on September 14, 2016 (ECF Nos. 22-25).

         Not long after, I held a status conference with the parties on September 26, 2016, at which


13
   In a few instances, Dr. Collins makes erroneous factual assertions, or presents arguments that are not well-accepted
in the Vaccine Program (even if they possess scientific validity). For example, she mistakenly says “no” physician
ever proposed CIDP as a possible diagnosis, despite the fact that Dr. Grunsfeld did in fact include it in his differential
diagnosis. First Collins Rep. at 8. She also devotes some time attempting to rebut the concept that the flu vaccine is
reasonably associated with peripheral neuropathies like GBS or CIDP, as well as the proposed mechanisms by which
it is theorized the vaccine could produce an autoimmune response (Id. at 9-11), despite an abundance of Program case
law going the other way on this issue. These aspects of Dr. Collins’s reports did not, however, color my overall reading
of her opinion, especially since the case turned more on the significance of the preexisting HIV infection – a topic
such statements did not bear upon–as well as the record facts of Mr. Strong’s medical history.
14
   As the docket reveals, Petitioner initially filed Dr. Kinsbourne’s first report on June 5, 2016 (ECF No. 15), but at
the request of Petitioner it was stricken and refiled in August in order to be in compliance with the Vaccine Program
filing guidelines. See ECF Nos. 18 (Order granting Motion to Strike, dated Aug. 19, 2016), and 20 (refiled First
Kinsbourne Rep.).

                                                           15
time I expressed my concerns about the strength of Petitioner’s claim in light of Respondent’s
expert reports, along with the medical record. I ordered him to file a supplemental expert report
from Dr. Kinsbourne, and he did so on November 21, 2016 (ECF No. 28). This generated a
second round of supplemental expert reports from Respondent’s two experts, filed on March 7,
2017 (ECF Nos. 32-33). I thereafter proposed, by Order dated March 15, 2017 (ECF No. 34),
that the parties consider allowing me to resolve this case on the papers in light of the nature of
the questions raised rather than by hearing, and they accepted my proposal. See March 31, 2017
Joint Status Report (ECF No. 35). I set a briefing schedule that (after one request to extend the
relevant deadlines) was completed by mid-August of this year. The matter is now fully ripe for
resolution.

IV.   Parties’ Respective Arguments

       Petitioner filed his brief in support of a ruling on the record on June 5, 2017. Memorandum
in Support of Motion for Ruling on the Record (ECF No. 38) (“Mot.”). In it, he argues that Dr.
Kinsbourne’s opinion, bulwarked by the various supporting pieces of literature filed as well as
his reading of the medical record, established all of the three prongs required of claimants by
the Federal Circuit in Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir.
2005).

       Petitioner’s motion first provides his own reading of the medical records. He emphasizes
his allegations of onset of neuropathic symptoms in one to two weeks after vaccination. Mot. at
1-2, 6-7. He acknowledges that the first medical record of any problems that could be arguably
attributed to a neuropathy are from February 2013 (when leg pain is reported), but notes that the
absence of other symptoms that would render a GBS or CIDP diagnosis more conclusive should
not be given great weight, given that tests specific to these conditions were not performed at that
time. Id. at 2-3. He also purports (as per Dr. Kinsbourne’s opinion) that the steroid treatments
he was then receiving may well have suppressed his symptoms. Id. at 2. But the July 2013
records do contain a reference to CIDP (contrary to Dr. Collins’s assertion) in addition to GBS.
Id. at 3. To the extent treaters did not take into account Mr. Strong’s overall course (and in
particular whether the timeframe from alleged onset to acuity was reasonable), it was because
they did not have the benefit of the review of the entire record. Id.

       Petitioner also endeavors to diminish the significance of his inadvertently-discovered
preexisting HIV infection. He argues that (based on records from July 2013) it is likely that the
HIV infection merely exacerbated his vaccine-caused GBS, rather than was the cause of it. Mot.
at 4, citing Ex. 6 at 75. He stresses the importance of Dr. Adams’s initial view that GBS alone
was the source of Petitioner’s symptoms. Id. at 4. And he observes that treaters (aware of his
HIV diagnosis) nevertheless recommended that he not receive vaccinations in the future, thus
suggesting they placed greater weight on the vaccine’s causality than the HIV infection. Id. at
4-5, citing Ex. 8 at 51.


                                                16
        Relying on the foregoing, Petitioner maintains that he has carried his Althen burden. He
 proposes that the association between the flu vaccine and peripheral neuropathies like GBS or
 CIDP is well-supported by both medical literature and the decisions of the Vaccine Program.
 Mot. at 5. He argues that Petitioner’s course, as Dr. Kinsbourne opined, is consistent with a
 CIDP diagnosis, and that the medical record establishes that treaters considered this a valid
 explanation. Id. at 5-6. The HIV infection, by contrast, is at best a co-factor that exacerbated
 Petitioner’s neuropathy but did not primarily cause it. Id. at 5, 7, and 9. And the timing of his
 onset, considered in the context of his overall disease progression, is consistent with Dr.
 Kinsbourne’s opinion regarding CIDP. Id. at 8-9.

         Respondent’s opposition brief requests dismissal of the case entirely. Response, dated
 August 4, 2017 (ECF No. 39) (“Opp.”). Respondent primarily15 bases his position on the
 contention that Petitioner suffered not from CIPD but instead from an HIV-caused neuropathy.
 Opp. at 21. Respondent disputes the validity of Petitioner’s assertion that he first experienced
 symptoms in the fall of 2012 (something Dr. Kinsbourne’s opinion is admittedly reliant upon).
 Id. at 18-19, 25-26. In Respondent’s view, however, the medical records do not support a CIDP
 diagnosis, but instead are consistent with a more general HIV neuropathy. Id. at 21, 24.
 Petitioner has otherwise failed to establish that the flu vaccine played a more contributory role
 in causing his neuropathy, whatever it was, than his preexisting HIV infection. Id. at 24-25. And
 the timing of his symptoms (assuming they did not begin in the fall of 2012 as alleged) is not
 sufficiently medically acceptable to be linked to his flu vaccination. Id. at 25-26.

        Petitioner filed a succinct reply on August 11, 2017. Reply (ECF No. 40). In it, he largely
 summarizes his prior arguments, but gives particular emphasis to the “overlap” between the HIV
 infection and allegedly causal role of the flu vaccine for his neuropathic symptoms. Reply at 2.
 He questions whether the HIV infection could be deemed primarily causal, since it predated the
 flu vaccine and therefore should have caused similar symptoms long before. Id. at 2-3.
 Characterizing the infection and the vaccine as “two snakes” that had bitten him, Petitioner
 maintains that the interplay between the two and their effects on his heath cannot be easily
 separated, but that the standards of the Vaccine Program require that he receive the evidentiary
 “benefit of the doubt” in favor of a causation determination. Id. at 3.

 V.     Relevant Legal Standards

        A.       Petitioner’s Overall Burden in Vaccine Program Cases

       To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
 she suffered a “Table Injury” – i.e., an injury falling within the Vaccine Injury Table –

15
   Respondent also argues that Petitioner has not met her Althen prong burdens, and reviews each individually. Opp.
at 21-26. As noted below, however, not all of these prongs are integral to my resolution of this case, regardless of
whether they were satisfied.


                                                        17
 corresponding to one of the vaccinations in question within a statutorily prescribed period of
 time or, in the alternative, (2) that her illnesses were actually caused by a vaccine (a “Non-Table
 Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §
 11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321
 (Fed. Cir. 2010); Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir.
 2006).16 In this case, Petitioner does not assert a Table claim.

        For both Table and Non-Table claims, Vaccine Program petitioners bear a
 “preponderance of the evidence” burden of proof. Section 13(1)(a). 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, 592 F.3d at 1322 n.2; see also Snowbank Enter. v.
 United States, 6 Cl. Ct. 476, 486 (1984) (mere conjecture or speculation is insufficient under a
 preponderance standard). Proof of medical certainty is not required. Bunting v. Sec’y of Health
 & Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). In particular, a 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 &
 Human Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human
 Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). A petitioner may not receive a Vaccine Program
 award based solely on her assertions; rather, the petition must be supported by either medical
 records or by the opinion of a competent physician. Section 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: “(1) a medical theory causally connecting the vaccination and the injury; (2)
 a logical sequence of cause and effect showing that the vaccination was the reason for the injury;
 and (3) a showing of a proximate temporal relationship between vaccination and injury.” Althen,
 418 F.3d at 1278.

        Each of the Althen prongs requires a different showing. Under Althen prong one,
 petitioners 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 & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994).
 Such a theory must only be “legally probable, not medically or scientifically certain.” Id. at 549.

         Petitioners may satisfy the first Althen prong without resort to medical literature,

16
  Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121,
124 (2003), aff’d, 104 F. App’x 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-
159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

                                                         18
 epidemiological studies, demonstration of a specific mechanism, or a generally accepted
 medical theory. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1378-79 (Fed. Cir.
 2009) (citing Capizzano, 440 F.3d at 1325-26). Special masters, despite their expertise, are not
 empowered by statute to conclusively resolve what are essentially thorny 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. Accordingly, special masters must take care not
 to increase the burden placed on petitioners in offering a scientific theory linking vaccine to
 injury. Contreras v. Sec’y of Health & Human Servs., 121 Fed. Cl. 230, 245 (2015)
 (“[p]lausibility . . . in many cases may be enough to satisfy Althen prong one” (emphasis in
 original)), appeal docketed, No. 2015-5097 (Fed. Cir. June 19, 2015). But this does not negate
 or reduce a petitioner’s ultimate burden to establish her overall entitlement to damages by
 preponderant evidence. W.C. v. Sec’y of Health & Human Servs., 704 F.3d 1352, 1356 (Fed.
 Cir. 2013) (citations omitted).17

        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; Grant v. Sec’y of Health & Human
 Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury,
 the opinions and views of the injured party’s treating physicians are entitled to some weight.
 Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d at 1326 (“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, since they are created contemporaneously with the
 treatment of the patient. Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed.
 Cir. 1993).

        However, medical records and/or statements of a treating physician’s views do not per se
 bind the special master to adopt the conclusions of such an individual, even if they must be
 considered and carefully evaluated. Section 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 & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there
 is nothing . . . that mandates that the testimony of a treating physician is sacrosanct – that it must

17
   There is ample contrary authority for the more straightforward proposition that the first Althen prong, like the overall
test itself, simply applies a preponderance standard when evaluating if a reliable and plausible causal theory has been
established. Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1350 (Fed. Cir. 2010). For purposes of
the present analysis, I am stressing those cases focusing on the plausibility of the causal theory proposed, as opposed
to whether preponderant evidence supports it, in order to avoid imposing on Petitioners a greater evidentiary burden
than the law requires. This does not, however, change the fact that any theory’s plausibility, for purposes of satisfying
the Althen test, is properly analyzed by subjecting its components to the Daubert tests for scientific reliability. Terran
v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999).

                                                           19
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 also present in the record – including conflicting
opinions among such individuals. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742,
749 (2011) (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); Caves v. Sec’y
of Dep't of Health & Human Servs., 100 Fed. Cl. 119, 136 (2011), aff'd, 463 F. App'x 932 (Fed.
Cir. 2012); Veryzer v. Sec’y of Health & Human 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. 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.”
Bazan v. Sec'y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The
explanation for what is a medically acceptable timeframe must also coincide with the theory of
how the relevant vaccine can cause an injury (Althen prong one’s requirement). Id. at 1352;
Shapiro v. Sec’y of Health & Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after
remand, 105 Fed. Cl. 353 (2012), aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v.
Sec'y of Health & Human Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May
30, 2013), mot. for review den’d (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

      B.      Law Governing Analysis of Fact Evidence

       The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 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.” Section
13(b)(1)(A). The special master is then required to weigh the evidence presented, including
contemporaneous medical records and testimony. See Burns v. Sec’y of Health & Human 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 a determination is evidenced by a rational determination).

      Medical records that are created contemporaneously with the events they describe are

                                                20
presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s
health problems). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Human Servs., 95
Fed. Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner’s testimony and his
contemporaneous medical records, the special master’s decision to rely on petitioner’s medical
records was rational and consistent with applicable law”), aff’d, Rickett v. Sec’y of Health &
Human Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption
is based on the linked propositions that (i) sick people visit medical professionals; (ii) sick people
honestly report their health problems to those professionals; and (iii) medical professionals
record what they are told or observe when examining their patients in as accurate a manner as
possible, so that they are aware of enough relevant facts to make appropriate treatment decisions.
Sanchez v. Sec’y of Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl.
Spec. Mstr. Apr. 10, 2013); Cucuras v. Sec'y of Health & Human Servs., 26 Cl. Ct. 537, 543
(1992), aff'd, 993 F.2d 1525 (Fed. Cir. 1993) (“[i]t strains reason to conclude that petitioners
would fail to accurately report the onset of their daughter’s symptoms. It is equally unlikely that
pediatric neurologists, who are trained in taking medical histories concerning the onset of
neurologically significant symptoms, would consistently but erroneously report the onset of
seizures a week after they in fact occurred”).

       Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec’y of Health & Human Servs., No. 03-1585V, 2005
WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneously medical
records are generally 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 & Human Servs., 23 Cl. Ct. 726, 733 (1991), aff'd, 968 F.2d
1226 (Fed. Cir.), cert. den’d, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United States v.
United States 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 may be more persuasive
than written records, such as where records are deemed to be incomplete or inaccurate. Campbell
v. Sec’y of Health & Human Servs., 69 Fed. Cl. 775, 779 (2006) (“like 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 (“[w]ritten records which are, themselves, inconsistent, should be accorded less
deference than those which are internally consistent”) (quoting Murphy v. Sec’y of Health &
Human Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam, 968 F.2d 1226 (Fed. Cir. 1992)).
Ultimately, a determination regarding a witness’s credibility is needed when determining the
weight that such testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of
Health & Human Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).


                                                 21
      C.      Analysis of Expert Testimony

       Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Human 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 & Human Servs., 617 F.3d
1328, 1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Human 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
when applied in other federal judicial fora (such as the district courts). Daubert factors are
usually employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude
evidence that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast,
these factors are used in the weighing of the reliability of scientific evidence proffered. Davis v.
Sec’y of Health & Human Servs., 94 Fed. Cl. 53, 66-67 (2010) (“uniquely 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 the persuasiveness and reliability of expert testimony has routinely been upheld. See,
e.g., Snyder, 88 Fed. Cl. at 742-45. In this matter (as in numerous other Vaccine Program cases),
Daubert has not been employed at the threshold, to determine what evidence should be admitted,
but instead to determine whether expert testimony offered is reliable and/or persuasive.

       Respondent frequently offers one or more experts of her own in order 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 & Human Servs., 618 F.3d 1339, 1347 (Fed. Cir.
2010) (citing Lampe, 219 F.3d at 1362). However, 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. 146 (1997)); see also Isaac v. Sec’y
of Health & Human Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July
30, 2012), mot. for review den’d, 108 Fed. Cl. 743 (2013), aff’d, 540 Fed. App’x 999 (Fed. Cir.
2013) (citing Cedillo, 617 F.3d at 1339).

      Weighing the relative persuasiveness of competing expert testimony, based on a particular
expert’s credibility, is part of the overall reliability analysis to which special masters must

                                                22
subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d 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 & Human Servs., 663 F.3d 1242, 1250 (Fed.
Cir. 2011) (“this 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”). It is in the exercise of my duties as a special master to weigh competing expert
testimony. Copenhaver v. Sec’y of Health & Human Servs., No. 13-1002V, 2016 WL 6947389,
at *5 (Fed. Cl. Oct. 20, 2016) (“Special Masters may use their discretion in weighing expert
testimony, and case law supports that discretion”).

       In determining whether a particular expert’s testimony was reliable or credible, I may
consider whether the expert offers an opinion that exceeds his training or competence. Walton
v. Sec’y of Health & Human Servs., No. 04-503V, 2007 WL 1467307, at *17-18 (Fed. Cl. Spec.
Mstr. Apr. 30, 2007) (otolaryngologist not well suited to testify about disciplines other than her
own specialty). While (in keeping with the liberality with which evidence offered in Vaccine
Program cases is treated) I heard and have considered all of the testimony of the experts offered
at the entitlement hearing, I may properly evaluate, and give appropriate weight to, whether
certain testimony is beyond a particular expert’s purview. See, e.g., King v. Sec’y of Health &
Human Servs., No. 03-584V, 2010 WL 892296, at *78-79 (Fed. Cl. Spec. Mstr. Mar. 12, 2010)
(petitioner’s expert far less qualified to offer opinion on general causation issues pertaining to
autism than specific issues pertaining to the petitioner’s actual medical history, given the nature
of the expert’s qualifications).

      D.      Consideration of Medical Literature

       Both parties filed medical and scientific literature in this case, including some articles
(such as those discussing molecular mimicry and protein sequences in vaccines) that do not
factor into the outcome of this decision. I have reviewed all of the medical literature submitted
in this case, but I only discuss those articles that are most relevant to my determination and/or
are central to Petitioners’ case – just as I have not exhaustively discussed every individual
medical record filed. Moriarty v. Sec’y of Health & Human Servs., No. 2015-5072, 2016 WL
1358616, at *5 (Fed. Cir. Apr. 6, 2016) (“[w]e 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. v. Sec’y of Health & Human
Servs., 527 F. App;x 875, 884 (Fed. Cir. 2013) (“[f]inding certain information not relevant does
not lead to — and likely undermines — the conclusion that it was not considered”).

      E.      Ruling on the Record

      The parties accepted my proposal to determine entitlement based on written submissions
and evidentiary filings, including both side’s expert reports, rather than by holding a hearing.
The Vaccine Act and Rules not only contemplate but encourage special masters to decide

                                                23
petitions on the papers where (in the exercise of their discretion) they conclude that doing so
will properly and fairly resolve the case. Section 12(d)(2)(D); Vaccine Rule 8(d). The decision
to rule on the record in lieu of hearing has been affirmed on appeal. See Hooker v. Sec’y of
Health & Human Servs., No. 02-472V, 2016 WL 3456435, at *21 n.19 (Fed. Cl. Spec. Mstr.
May 19, 2016) (citing numerous cases where special masters decided on the papers in lieu of
hearing and that decision was upheld). I am simply not required to hold a hearing in every matter,
no matter the preferences of the parties. Hovey v. Sec’y of Health & Human Servs., 38 Fed. Cl.
397, 402-03 (1997) (special master acted within his discretion in denying evidentiary hearing);
Burns, 3 F.3d at 417; Murphy v. Sec’y of Health & Human Servs., No. 90-882V, 1991 WL
71500, at *2 (Ct. Cl. Spec. Mstr. Apr. 19, 1991).

      F.      Law on “Substantial Factor” Analysis

       In this case, the parties disagree as to the relative effects of two indisputable factors – the
preexisting HIV infection and Petitioner’s flu vaccination – in causing his neuropathic
symptoms. The Court of Federal Claims has recognized that “when two forces act in concert,”
it is appropriate to apply the “substantial factor” test first set forth in the Federal Circuit’s
Shyface decision, and evaluate not what cause predominates, but whether the vaccine can be
deemed a “substantial” cause. Heinzelman v. Sec’y of Health & Human Servs., No. 07-01V,
2008 WL 5479123, at *4 (Fed. Cl. Dec. 11, 2008); see also Walther v. Sec’y of Health & Human
Servs., 485 F.3d 1146, 1151 n.41 (Fed. Cir. 2007). Shyface predates the Federal Circuit’s
enunciation of the Althen test in 2005, and it has been noted that Althen largely subsumes it
within its three-prong test (and therefore the two tests are not inconsistent). Deribeaux v.Sec’y
of Health & Human Servs., 105 Fed. Cl. 583, 590 (2012), aff’d, 717 F.3d 1363 (Fed. Cir. 2013).

       Nevertheless, in cases such as the present, in which joint causes may plausibly explain
the same disease or condition, the Shyface version of the Vaccine Program standard provides a
more exact standard for measuring a claimant’s success. Heinzelman, 2008 WL 5479123, at *2-
4 (applying Shyface to demonstrate a lack of joint factors). “Substantial” has been defined as a
factor “that falls somewhere between causing the injury to a non-negligible degree and being
the ‘sole or predominant cause.’” Deribeaux, 105 Fed. Cl. at 595. I will utilize this standard in
evaluating whether the flu vaccine can in this case be deemed a “substantial factor” in injuring
Petitioner.

                                            ANALYSIS

I.    Petitioner’s HIV Infection was a More Likely Cause of his Injuries than the Flu Vaccine

       In resolving Vaccine Program cases, it is not within the special master’s domain to
propose a correct diagnosis for a given injury or disease. Porter v. Sec’y of Health & Human
Servs., 663 F.3d 1242, 1249–50 (Fed. Cir. 2011); Lombardi v. Sec'y of Health & Human Servs.,
656 F.3d 1343, 1351 (Fed. Cir. 2011); Broekelschen, 618 F.3d at 1345; Andreu, 569 F.3d at

                                                 24
 1382; Althen, 418 F.3d at 1277 n. 4, 1280–81. Rather, special masters should evaluate what
 determination the evidence best supports – and if that same evidence does not allow for the
 conclusion that the injury is vaccine-related, then the petitioner cannot prevail, even if the actual
 cause of a claimant’s injuries remains unknown. Andreu, 569 F.3d 1367, 1380.

        Here, the record evidence better supports the conclusion that Mr. Strong’s neuropathic
 symptoms, regardless of how they are classified, were more likely related to his HIV infection
 rather than vaccination. The fact of the preexisting infection, discovered around the time of
 Petitioner’s most acute symptoms in July 2013, is indisputable,18 and it is highly likely as well
 that it long predated his September 2012 flu vaccination. Moreover, Respondent’s experts
 persuasively demonstrated a high association between HIV and neuropathic symptoms much
 like Petitioner experienced. Gabbai at 521. Dr. Kinsbourne was hardly able to deny this showing,
 and did not endeavor to do so, acknowledging the known association between HIV and CIDP
 yet disavowing a connection in conclusory fashion, without reference to his own experience, or
 medical or scientific evidence, that would bulwark his view. See Second Kinsbourne Rep. at 2.

        Certain facts in the medical history are favorable to Petitioner’s position, but an overall,
 comprehensive consideration of the record better supports the conclusion that his neuropathy
 was connected with his HIV infection. As Respondent’s experts underscored, a number of test
 results or clinical symptoms experienced by Petitioner are more consistent with an HIV-caused
 neuropathy than GBS or CIDP linked to the flu vaccine. They persuasively established that
 pleocytosis would not be viewed as a finding associated with GBS normally, while at the same
 time Petitioner (at least when his symptoms first manifested in February) lacked the classic
 presenting indicia of GBS, like areflexia or weakness and parasthesias (as opposed to the pain
 he complained of at that time). First Donofrio Rep. at 8-9. In addition, and relying on the same
 factors, Petitioner’s treaters leaned to an interpretation of the medical history that embraced the
 HIV infection as the source of his symptoms; no treater, by contrast, identified the flu vaccine
 as causal.

         Petitioner was unable to rebut the above by arguing that his injuries may have been
 initially caused by the vaccine but were exacerbated by the underlying, preexisting infection.
 This assertion is not supported by any persuasive evidence – in the form of reliable scientific or
 medical literature, or testimony from Dr. Kinsbourne arising from his own expertise with
 peripheral neuropathies – that an undiscovered, likely subclinical HIV infection could lay

18
   I note that the same literature also suggests that an HIV-associated neuropathy would usually begin before an
infection’s immunosuppressive stage – meaning several weeks after the infection, when the antibodies are first
produced and rising to detectable levels, and also before the patient is prescribed anti-retroviral treatments. Gabbai at
521. Thus, it is possible that if Mr. Strong’s infection long predated his vaccination, the likelihood that the infection
was still associated with the neuropathic symptoms would be diminished. However, the record does not allow me to
conclude when that infection began, thereby preventing a determination that too long a time passed to deem the HIV
infection a more likely cause. And as discussed below, Petitioner did not otherwise establish that the vaccine was a
substantial factor in causing his injuries regardless of the HIV infection’s role.


                                                          25
 dormant and then interact later with a vaccine-caused neuropathic injury, and/or that any HIV-
 caused neuropathy was aggravated by the flu vaccine.19 And Petitioner did not demonstrate
 instances from the medical record to corroborate that this was in fact what he experienced.

        My analysis does not change if I apply the “substantial factor” analysis set forth in
 Shyface, and consider whether the vaccine was significant to Petitioner’s injuries even if the
 HIV infection is conceded to also have played a role. Petitioner has not demonstrated that the
 vaccine played any role in his injuries, given (as discussed below) the long temporal period
 between vaccination and first corroborated onset of symptoms, and the inconsistencies between
 his own allegations of onset and what the record establishes, and I therefore cannot even reach
 the point of concluding that both acted “in concert.” The strong correlation between HIV
 infection and neuropathies, coupled with the record evidence suggesting the nature of
 Petitioner’s presentation (along with certain lab results more associated with an HIV-caused
 neuropathy than a typical case of GBS) further diminish any role the flu vaccine might have
 played in Petitioner’s injuries. I therefore need not disentangle the impact of the vaccine from
 the more likely impact of the HIV infection.

 II.     Althen Prongs Analysis

        In order to explain in the clearest manner possible how my findings impact Petitioner’s
 success in establishing causation, I shall briefly review how the evidence applies to each of the
 three Althen prongs.

         A.       Althen Prong One

       Petitioner in this case successfully established what is often referred to as the “can cause”
 prong. There are many persuasive decisions discussing the association between GBS and the flu
 vaccine. See, e.g., Stitt v. Sec’y of Health & Human Servs., No. 09-653V, 2013 WL 3356791
 (Fed. Cl. Spec. Mstr. May 31, 2013); Stewart v. Sec'y of Health & Human Servs., No. 06–777V,

19
   Although Petitioner has not so alleged, Program claimants can obtain an entitlement award based upon the claim
that a vaccine significantly aggravated a preexisting condition. To do so, and in addition to proving the three Althen
prongs, petitioners must also show “1) the person’s condition prior to administration of the vaccine, (2) the person’s
current condition (or the condition following the vaccination if that is also pertinent), [and] (3) whether the person’s
current condition constitutes a “significant aggravation” of the person’s condition prior to vaccination.” See Loving v.
Sec’y of Health & Human Servs.,No. 02-469V, 2009 WL 3094883, at *2 (Fed. Cl. Spec. Mstr. July 30, 2009), recons.
granted in part on other grounds, 2010 WL 1076124 (Fed. Cl. Spec. Mstr. Mar. 2, 2010). At its simplest, the question
is “but for” the vaccine, would the petitioner’s condition have been as severe as it was with the vaccine. Id. at *11.

Here, although Mr. Strong has not formally alleged a significant aggravation claim, some of his arguments could be
interpreted to propose a similar theory—that Petitioner’s HIV infection would not have resulted in the neuropathy that
he now experiences had he never received the flu vaccine. But neither the evidence nor Petitioner’s expert reports
support this theory of recovery. The overall record would not allow the conclusion that Mr. Strong’s neuropathy would
not have been as severe but for the vaccine, given the weak relationship between that vaccination and his subsequent
health problems, plus the lack of treater support identifying the vaccine as causal in any way.


                                                          26
 2011 WL 3241585, at *16 (Fed. Cl. Spec. Mstr. July 8, 2011); see also Barone v. Sec’y of Health
 & Human Servs., No. 11-707V, 2014 WL 6834557 (Fed. Cl. Spec. Mstr. Nov. 12, 2014).
 Although I do not embrace Dr. Kinsbourne’s suggestion that CIDP is little more than GBS with
 a longer course,20 there is no doubt that both are related peripheral neuropathies characterized
 by a number of common symptoms – as well as a common pathogenesis, with one having a more
 chronic course. Accordingly, the large and persuasive body of evidence (and well-reasoned
 decisions of special masters past and present) noting the reliable connection between the flu
 vaccine and GBS has applicability herein even if CIDP were the correct diagnosis.

       Admittedly, there is less evidence and Program case law associating CIDP with the flu
 vaccine – somewhat diminishing the strength of a showing that so openly relies on comparisons
 between CIDP and GBS. But even if that rendered this case a closer call with respect to the first
 Althen prong, compelling case law counsels special masters to decide “close cases” generally in
 favor of claimants, and that same admonition applies to the individualized Althen prongs. Althen,
 418 F.3d 1274, at 1260. I therefore determine that Petitioner has established that the flu vaccine
 could cause CIDP or GBS.

        B.       Althen Prong Two

        A threshold question presented by the “did cause” analysis in this case is whether Petitioner
 had CIDP (Dr. Kinsbourne’s favored diagnosis). Petitioner’s overall course was characterized by
 some purported initial symptoms; a several-month dormancy period; and then a relapse in
 February, later progressing to his July hospitalization. Dr. Kinsbourne agrees that this course was
 too long and halting to meet the clinical criteria for GBS, a disease characterized by acute
 symptoms that resolve quickly. Second Kinsbourne Rep. at 1 (“[i]f the Court affirms Mr. Strong’s
 account, then the diagnosis of GBS is ruled out”). He instead proposes CIDP was the correct
 diagnosis, relying on (a) the immediate symptoms, (b) the longer, stop-start course, (d)
 Petitioner’s seemingly favorable response to steroidal treatments, and (d) some limited treater
 support for the alternative diagnosis from the summer of 2013, when Petitioner’s symptoms were
 obvious enough to cause treaters to embrace GBS as a credible diagnosis for the first time. Id.

        Dr. Kinsbourne’s proposed alternative diagnosis is a reasonable interpretation of the record
 (putting aside whether I accept Petitioner’s early onset allegations), and also accords with what
 is known about the relapsing/remitting character of CIDP. Blackburn v. Sec’y of Health & Human
 Servs., No. 10-410V, 2015 WL 425935, at *21-23 (Fed. Cl. Spec. Mstr. Jan. 9, 2015). Yet, even
 if there is record support for Dr. Kinsbourne’s position, it is difficult to discern in the record what
 final diagnosis for Mr. Strong’s symptoms is best supported by the evidence. Most of the treater

20
  I have previously discussed in detail the differences between GBS and CIDP. See, e.g., Blackburn v. Sec’y of Health
& Human Servs., No. 10-410V, 2015 WL 425935, at *21-23 (Fed. Cl. Spec. Mstr. Jan. 9, 2015) (“CIDP and GBS
represent two separate (if related) conditions rather than opposing points on the same disease spectrum—and that as
such it would be incorrect to view CIDP simply as a chronic form of GBS”).

                                                         27
 notes from the winter of 2013 characterized his condition as GBS or at least like it. See, e.g., Ex.
 10 at 4-11; Ex. 7 at 38-40, 70-72; Ex. 8 at 1-11, 13-23. But those views did not take into account
 Mr. Strong’s current assertions of an earlier onset closer in time to the vaccine administration
 (and the fact that these alleged symptoms appear not to have been mentioned to treaters cuts
 against accepting them as accurate). Also, as Respondent’s experts observed, Petitioner’s
 presentation was in many ways inconsistent with GBS (for example, the lack of areflexia), while
 being more consistent with an HIV-derived neuropathy. First Donofrio Rep. at 8. And as noted
 above, various testing results were also more consistent with an HIV-caused neuropathy than a
 vaccine-induced GBS.

        Later, some references to CIDP can be found in the record from around the time that
 Petitioner sought urgent care for his symptoms in July 2013. See, Ex. 6 at 79, 149-150. Ordinarily,
 such treater opinions would be important in evaluating if preponderant evidence supported one
 diagnosis over an alternative. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d at 1326. But at best,
 this record reveals that treaters merely included CIDP as part of a differential diagnosis – they
 never fully embraced it later, even as the record of Petitioner’s treatment and responses continued
 to unfold. There is better evidence supporting the conclusion that treaters ultimately associated
 Petitioner’s symptoms with his HIV infection. See, e.g., Ex. 6 at 105, 115-16. And there is nothing
 in the record in which a treater proposes that the flu vaccine had anything to do with Mr. Strong’s
 illness.

        This highlights a more fatal problem with Petitioner’s claim when his theory is evaluated
 in light of the record. Dr. Kinsbourne forthrightly acknowledged that his proposed CIDP
 diagnosis hinges upon the acceptance of Petitioner’s after-the-fact assertions about onset of
 symptoms beginning in the fall of 2012. Second Kinsbourne Rep. at 2 (“[i]f the Court issues a
 finding to the effect that Mr. Strong’s symptoms began no earlier than January 2013, then my
 diagnosis of CIDP would be inapplicable and so would my opinion as to vaccine causation”)
 (emphasis added). But I do not find that those assertions, uncorroborated as they are by
 circumstantial evidence, should be credited.21 Rather, I determine herein that Mr. Strong’s
 neuropathic symptoms in fact began no sooner than February 2, 2013, based upon his assertions
 to Dr. Sylvester at a February 5th visit that his leg pain had begun around three days before (but
 over four months from the date of vaccination). Ex. 7 at 30-31. Mr. Strong repeated such onset
 claims to Dr. Adams in July 2013. Ex. 6 at 76. Medical records, as noted above, are entitled to
 presumptions of truthfulness in the Program, and Petitioner has not established a basis for finding
 otherwise in this case. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d at 1326.22

21
  Mr. Strong’s preexisting health problems – CODP plus a lung mass that appears to have caused him considerable
anxiety – may better explain any physical symptoms he experienced closer in time to the vaccination, although I do
not herein determine any explanation for these alleged symptoms.
22
  Dr. Kinsbourne’s written admission on the scope of his opinion is not the only reason for me to reject his proposed
diagnosis. I note as well that literature submitted by the parties regarding CIDP also suggests that the condition would

                                                          28
        Accordingly, I do not find sufficient preponderant evidence exists in this case to support
 Petitioner’s contention that the flu vaccine “did cause” him to experience CIDP. Petitioner has
 not established a “logical sequence of cause and effect,” because the time period that passed from
 vaccination to initial neuropathic symptoms reflected by the record is too attenuated. Vaccine-
 caused GBS is also ruled out for much the same reason. Rather, as noted above, Petitioner’s
 preexisting HIV infection was a more likely causal factor than a vaccine received more than four
 months before initial symptoms began, and various testing results are more corroborative of HIV
 as the source of Mr. Strong’s symptoms than a vaccine-induced injury. And there is no treater
 support at all for the conclusion that the vaccine was connected to Mr. Strong’s various
 neuropathic symptoms, while there is ample support for the conclusion that his symptoms
 stemmed from his HIV infection.

        C.       Althen Prong Three

        Matters discussed above are relevant to why I do not find herein that Petitioner has
 established sufficient preponderant evidence supporting the conclusion that the timing of his post-
 vaccination illness was medically acceptable. As noted, I find that onset of his neuropathic
 symptoms began no sooner than February 2013 – too long, by Dr. Kinsbourne’s admission, after
 vaccination to be reliably associated with a flu vaccine-caused GBS or CIDP. The preexisting
 HIV infection compounds this analysis, and Petitioner has failed to persuasively explain why it
 should be given less causal weight than the later-in-time vaccination. And literature filed in the
 case otherwise was consistent with Dr. Kinsbourne’s admission about the most medically
 acceptable onset for CIDP after vaccination. P. Kelkar, Chronic Inflammatory Demyelinating
 Polyneuropathy (CIDP) with Rapid Progression after Influenza Vaccine, J. of Clinical
 Neuromuscular Diseases 8:20-25 (2006), filed as Ex. 12-f (ECF No. 20-7).


                                               CONCLUSION

       A Program entitlement award must be supported by a preponderant evidentiary showing.
Here, Petitioner has not made such a showing. Petitioner is therefore not entitled to compensation
under the Vaccine Program.

        In the absence of a timely-filed motion for review (see Appendix B to the Rules of the
Court), the Clerk shall enter judgment in accord with this decision.




initially present within at least four weeks of initial insult, whether by vaccine or infection. P. Kelkar, Chronic
Inflammatory Demyelinating Polyneuropathy (CIDP) with Rapid Progression after Influenza Vaccine, J. of Clinical
Neuromuscular Diseases 8:20-25 (2006), filed as Ex. 12-f (ECF No. 20-7). The onset of symptoms herein (more than
16 weeks) vastly exceeds that period.

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IT IS SO ORDERED.

                         /s/ Brian H. Corcoran
                         Brian H. Corcoran
                         Special Master




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