Suspected vaccination failure; Hepatitis A infection; Increasing fatigue and myalgia; Increasing fatigue and myalgia; This case was reported in a literature article and described the occurrence of vaccination failure in a 65-year-old male patient who received Hepatitis A vaccine for prophylaxis.  Concurrent medical conditions included hiv infection (diagnosed to HIV (Human immunodeficiency virus) 8 years (between HIV and HAV diagnosis), chronic kidney disease, cardiac failure chronic, disability, gonorrhea and chlamydial infection. Concomitant products included abacavir, lamivudine and raltegravir.   On an unknown date, the patient received Hepatitis A vaccine. On an unknown date, more than 2 years after receiving Hepatitis A vaccine, the patient experienced vaccination failure (serious criteria hospitalization and GSK medically significant), acute hepatitis a (serious criteria hospitalization), fatigue (serious criteria hospitalization) and myalgia (serious criteria hospitalization). On an unknown date, the outcome of the vaccination failure was unknown and the outcome of the acute hepatitis a, fatigue and myalgia were recovered/resolved.   The reporter considered the vaccination failure, acute hepatitis a, fatigue and myalgia to be related to Hepatitis A vaccine.  Additional information was provided as follows: This case was reported in a literature article and described the suspected vaccination failure in a 65 years old male patient, who was vaccinated with unspecified Hepatitis A vaccine (manufacturer unknown) for prophylaxis.  [Since 1st January 2019, 2 separate acute hepatitis A (HAV) outbreaks had identified spreading mainly via person-to-person transmission: (1) a small outbreak primarily among men who had sex with men (MSM; November 2018 to March 2019) and (2) a large outbreak beginning in April 2019, primarily among persons experiencing homelessness (PEH) or persons who use drugs (PWUD). The authors described 4 people with HIV (PWH) who acquired acute hepatitis A (HAV) infection during recent outbreaks despite documented immunity and/or vaccination. The authors identified patients with acute HAV infection during outbreak surveillance within the above noted outbreaks. Coauthors on this report initiated a discussion with local public health collaborators when some coauthors identified 2 of these cases through direct patient care at the hospital. The authors gathered data from surveillance records, case report forms, and medical records via existing public health and electronic medical records data systems]. The patient had stable housing, apartment with long-term male partner. The patient had chronic kidney disease and chronic heart failure. The patient had no known prior HAV infection and reported a remote HAV vaccination history. The patient's sexual orientation was men who have sex with men (MSM). The patient had condomless sex with a new male partner during their exposure period. The patient did not use illicit drug. The patient was disabled. The patient had diagnosed to HIV (Human immunodeficiency virus) 8 years (between HIV and HAV diagnosis). The patient's CD4 cell count nadir HIV viral load (VL) history was unknown nadir undetectable (UD) viral load (VL) since 2012.The patient had been taking antiretroviral medication (at time of HAV diagnosis) as abacavir, lamivudine, raltegravir. No information on patient's family history was provided. On an unspecified date, the patient received unspecified Hepatitis A vaccine (administration route and site unspecified; dosage unknown; batch number not provided). The patient's age at the time of vaccination was not provided. The patient's HAV vaccination status (years before HAV diagnosis) was self-reported prior vaccination (unknown date). On an unspecified date, the patient's CD4 cell count at HAV vaccination was unknown. The patient's HAV IgG positivity was 8 years before HAV diagnosis. The patient's autoimmune workup was negative antinuclear antibody (ANA) 8 years prior. The patient's CD4 cell count was 379 cells/mL and HIV VL was undetectable within year before HAV diagnosis. On an unspecified date, between January 2019 and June 2020, an unknown period after the vaccination, the patient presented with 1 week of increasing fatigue and myalgia. At the time of acute HAV infection, the patient denied drug use. The patient required hospitalization due to HAV infection. The patient's had likely source of acute HAV acquisition was condomless sex with new male partner 2 to 3 weeks prior (not long-term partner). The patient's liver function test (LFT) peak showed aspartate aminotransferase/alanine aminotransferase (AST/ALT) was 2732/5049 units/L and total bilirubin was 5.9 units/L. Radiologic findings showed normal liver ultrasound (US) (no doppler). The patient had hepatitis C virus (HCV) antibody (Ab) and polymerase chain reaction (PCR) was negative. Other workup showed hepatitis B surface antibody (HBV sAb) was positive, hepatitis B surface antigen (HBV sAg) was negative, HBV polymerase reaction (PCR) was negative, Cytomegalovirus (CMV) PCR was negative, Herpes Simplex virus (HSV) PCR was negative. The patient's sexual transmitted infection (STI) testing at admission showed urine gonorrhea (GC)/chlamydia (CT) and nucleic acid amplification test (NAATs) was negative. The patient's HAV IgM at admission was positive (positive if more than 1.0 (s/co)). The patient's HAV IgG at presentation was positive (Positive if more than 1.21 (s/co)) and Ig level was unknown. The patient's HAV PCR was positive at admission. The patient was consistently engaged in care and stable on anti-retrovirals (ARVs) and was housed in a private apartment. The patients' liver function and subjective symptoms were improved quickly with supportive care. The patient was discharged to home and returned to his baseline health status. This case has been considered as suspected vaccination failure being the full schedule was unknown. This case was considered serious due to hospitalization and suspected vaccination failure The authors commented, "All 4 PWH presented here acquired acute HAV requiring hospitalization despite documented immune response after vaccination and/or prior documentation of HAV vaccination at CD4 more than 200 cells/mL. Several factors may account for HAV infection despite presumed immunity. First, we know that protective immunity may wane over time and lead to disease acquisition and that immunosuppressed states, such as HIV, may predispose individuals to less durable immunity. Vaccination at a CD4 count more than 200 is thought to predict long-lasting immunity in PWH. Despite that, the patients in our case series were either vaccinated at a CD4 count more than 200 (Patient D) or had well-controlled HIV with long-standing undetectable HIV viral loads at the time of HAV vaccination (Patients A-C). Therefore, it is unlikely that secondary failures correlate with profound immune suppression at the time of vaccination in these patients. Accordingly, the reliance on CD4 count alone as an indicator of who will benefit from an HAV booster vaccination is insufficient. Second, a past or current positive HAV IgG titer may be an unreliable correlate of protection from acute HAV infection in PWH. Neutralizing anti-HAV IgG titers, which are thought to be associated with lifelong protection, are significantly lower after inactivated HAV vaccination as compared with natural infection. Total HAV IgG titers are correlated with neutralizing antibody titers where a level of more than 10 mIU/mL is considered a surrogate correlate of protection in vaccine trials. However, a minimum anti-HAV IgG level that confers protection in real-world situations has not been established. Three patients in our series (A-C) had positive HAV IgG titers both at the time of acute HAV infection and 3-8 years prior, which is consistent with their prior vaccination, although, admittedly, acute infection may have boosted HAV IgG titers. Further study is required to define the mechanisms of these secondary failures and may inform whether the traditional surrogate markers of immunity (ie, more than or equal to 10 mIU/mL anti-HAV IgG) should be modified for PWH. Possible mechanisms of these "breakthrough" infections could include a large inoculum related to unprotected anal intercourse, particularly with oral-anal sex, or viral escape phenomenon overcoming any existing immunity. Third, self-reported, and even well-documented, complete HAV vaccination may not be evidence of sufficient protection during an outbreak. Given the limitations of using CD4 monitoring, HAV IgG titers, and vaccination history to predict protection from acute HAV in PWH, we suggest that HAV booster vaccination be considered, especially during a local outbreak, based on risk factors for HAV acquisition irrespective of documented prior vaccination or immunity. The risk of HAV infection is higher in MSM; as such, it is possible that anal intercourse, particularly anal-oral sex, delivers a larger HAV inoculum or at least increases rates of fecal-oral transmission as compared with other exposures. In our series, Patients A to C were MSM, and Patient D identified as a transgender woman (male at birth) with similar sexual risk factors for HAV infection. Of note, a limitation of our report is the lack of risk factor analysis with comparator groups, such as persons within the local HAV outbreak not living with HIV. However, no foodborne transmission risk factors were identified in the patients reported in this series. These 4 cases serve as "proof of concept" that some form of prior immunity is not protective against acute HAV infection during local outbreaks among PWH. As such, we posit that certain sexual behaviors historically associated with MSM, such as anal-penile sex or anal-oral sex, reported by PWH should prompt consideration of an HAV booster vaccination during a local outbreak. HAV risk factors, such as homelessness (PEH), drug use (PWUD), and predisposing sexual behaviors, often coexist within individual patients and patient populations. A comprehensive social history, including a detailed history of drug use and specific sexual behaviors, will help clinicians identify PWH who may benefit from booster vaccination during an outbreak. Single booster vaccination has been shown to generate sufficient immune response in PWH. Logistical considerations, such as supply or administration during the coronavirus disease 2019 pandemic, must also be accounted for in future public health policy regarding HAV booster vaccination".  This article corresponding to this case is not available for regulatory submission due to copyright restriction. This case is 1 of the 4 cases reported in the literature article.; Sender's Comments:  US-GLAXOSMITHKLINE-US2021GSK233001:Same reporter US-GLAXOSMITHKLINE-US2021GSK232999:Same reporter US-GLAXOSMITHKLINE-US2021GSK233000:Same reporter