Occult hepatitis B infection (OBI) is defined as the presence of hepatitis B virus (HBV) DNA in the liver or serum in the absence of detectable HBV surface antigen (HBsAg). OBI poses a risk for the development of cirrhosis and hepatocellular carcinoma. The prevalence of OBI in Kenya is unknown, thus a study was undertaken to determine the prevalence and molecular characterization of OBI in Kenyan populations at high risk of HBV infection. Sera from two Nairobi cohorts, 99 male sex workers, primarily having sex with men (MSM-SW), and 13 non-MSM men having HIV-positive partners, as well as 65 HBsAg-negative patients presenting with jaundice at Kenyan medical facilities, were tested for HBV serological markers, including HBV DNA by real-time PCR. Positive DNA samples were sequenced and MSM-SW patients were further tested for hepatitis C virus (HCV) infection. Of the 166 HBsAg-negative samples tested, 31 (18.7%; 95% confidence interval [CI] 13.5-25.3) were HBV DNA positive (i.e., occult), the majority (20/31; 64.5%) of which were HBV core protein antibody positive. HCV infection was not observed in the MSM-SW participants, although the prevalence of HBsAg positivity was 10.1% (10/99; 95% CI 5.6-17.6). HBV genotype A was predominant among study cases, including both HBsAg-positive and OBI participants, although the data suggests a non-African network transmission source among MSM-SW. The high prevalence of HBV infection among MSM-SW in Kenya suggests that screening programmes be instituted among high-risk cohorts to facilitate preventative measures, such as vaccination, and establish entry to treatment and linkage to care.
In chronic hepatitis B (CHB), hepatitis D virus (HDV) superinfection can lead to acute liver failure. The incidence of HDV superinfection is unknown, but is often detected in immigrants from HDV endemic countries. In this report, we characterize long-term clinical and virological outcomes in a hepatitis B virus (HBV) infected carrier before and after HDV superinfection, acquired from their spouse having HBV/HDV co-infection. A 38 year-old Mongolian male with CHB on anti-HBV therapy developed acute liver failure following HDV superinfection. Although he recovered, avoiding the need for liver transplant, HDV serological and molecular markers of infection persisted for the subsequent 16-month follow-up period, suggesting the development of CHB/HDV co-infection. The source of his HDV was from his wife of 10 years, a 34-year old Mongolian female known to have inactive CHB/HDV co-infection but who was not on anti-HBV therapy. Phylogenetic analysis of the complete HDV genome from the couple showed >99% similarity, with post-transmission longitudinal sequence revealing specific nucleotide substitutions between both spouse’s HDV genome sequences. This study highlights the ongoing risk of HDV superinfection due to long-term co-habitation or sexual transmission in CHB patients. The fact that transmission occurred after almost a decade of marriage may be due to host immune or environmental factors that created a more favorable condition for transmission.
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