Sustainability of Immune Response to Hepatitis B Virus Vaccination Three Years after Vaccination among HIV-1 Infected and Uninfected Adults in Kenya

Abstract

Hepatitis B virus (HBV) infection, a leading cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma, worldwide is preventable by vaccination. Following the completion of the recommended vaccination series over 90% of adults will develop protective immune levels of anti-HBS antibodies. However, there is a paucity of data on sustained protective immune levels of Anti-HBS antibodies, among HIV-infected African adults. This study aimed at assessing if there is an immune response sustained to hepatitis B virus vaccination three years after vaccination among HIV-1 infected and uninfected adults in Kenya. A retrospective study was carried out to analyse archived serum samples. The study was conducted at the Partners PrEP Study clinic in Thika which was among sites for a phase III, multi-site, randomized, double-blind, placebo controlled trial of daily oral tenofovir-based pre-exposure prophylaxis (PrEP) for prevention of HIV-1 acquisition. The samples were randomly selected and participant’s demographic information was retrieved from case referral forms that were been filled every time participant’s visited the clinic. A total of 336 serum samples retrieved were measured for Hepatitis B surface antibody (anti-HBs) titers using ELISA kit Murex DiaSorin LIAISON anti-HBs II assay (DiaSorin, Saluggia, Italy). Those serum samples that did not have protective anti-HBs titers were further tested for Hepatitis B surface antigen (HBsAg), a marker of infection with HBV DiaSorin Murex HBsAg Version 3 assay kit (DiaSorin, S.p.A. UK). Univariate logistic regression to determine factors associated with non-response to HBV vaccination was used. Of the 336 participants serum samples tested, 176 (52.4%) were from HIV-1 infected individuals, of whom 40 (22.7%) were male. 160 samples from HIV-1 uninfected individuals of whom 125 (78.1%) were male. The mean (standard deviation) age of the study population was 34.6 (8.5) years. Of the 62 (18%) individuals who did not have protective anti-HBs titers three years post- vaccination, 50 (81%) were HIV-1 infected. HIV infected persons were more likely to have less protective anti-HBs titers (p<0.001) compared to HIV uninfected persons. In addition, compared to men, women were more likely not to have protective anti-HBs levels (11.5% vs. 25.1%, p=0.002). Seven (11.3%) of the 62 samples that did not have a positive antibody response for anti-HBs also tested positive for HBV surface antigen (HBsAg), all of whom were HIV-1 positive individuals. In conclusion, more than a quarter of HIV-infected individuals vaccinated against HBV did not have protective anti-HBs titers three years post-vaccination, some of whom acquired HBV infection. Regular testing for the immune response to HBV vaccination among HIV infected persons should be considered and reviewed regularly, and those with waning antibodies be offered booster doses. Additional research is needed to evaluate the impact of HBV booster doses in this population. In addition, those persons infected with HIV are at a higher risk of being infected with HBV and efforts should be made to vaccinate them.