Abstract

BackgroundViral hepatitis is a major concern worldwide, with hepatitis A (HAV) and E (HEV) viruses showing sporadic outbreaks while hepatitis B (HBV) and C (HCV) viruses are associated with chronic hepatitis, cirrhosis and hepatocellular carcinoma. The present study determined the proportion, geographic distribution and molecular characterization of hepatitis viruses among patients seeking medical services at hospitals throughout Kenya.MethodsPatients presenting with jaundice at four selected hospitals were recruited (n = 389). Sera were tested for the presence of antibody to hepatitis viruses A through E, and HBV surface antigen (HBsAg). Nucleic acid from anti-HAV IgM antibody and HBsAg positive samples was extracted, amplified and sequenced.ResultsChronic HBV infection was the leading cause of morbidity among patients with symptoms of liver disease seeking medical help. Incident HCV, HEV and HDV infection were not detected among the patients in this study, while the proportion of acute HAV was low; HAV IgM positivity was observed in 6.3 % of patients and sequencing revealed that all cases belonged to genotype 1B. HCV seropositivity upon initial screening was 3.9 % but none were confirmed positive by a supplementary immunoblot assay. There was no serological evidence of HDV and acute HEV infection (anti-HEV IgM). HBsAg was found in 50.6 % of the patients and 2.3 % were positive for IgM antibody to the core protein, indicating probable acute infection. HBV genotype A was predominant (90.3 %) followed by D (9.7 %) among HBV DNA positive specimens. Full genome analysis showed HBV/D isolates having similarity to both D4 and D6 subgenotypes and D/E recombinant reference sequences. Two recombinant sequences demonstrated > 4 % nucleotide divergence from other previously known D/E recombinants.ConclusionsHBV is highly prevalent among patients seeking care for symptoms consistent with hepatitis, compared to the general population. Molecular characterization of HBV isolates indicated recombinant strains that may give rise to new circulating variants. There is a need to document the prevalence, clinical manifestation and distribution of the variants observed. HAV genotype 1B, prevalent in Africa, was observed; however, the absence of HCV, HDV and acute HEV in this study does not rule out their presence in Kenya.

Highlights

  • Viral hepatitis is a major concern worldwide, with hepatitis A (HAV) and E (HEV) viruses showing sporadic outbreaks while hepatitis B (HBV) and C (HCV) viruses are associated with chronic hepatitis, cirrhosis and hepatocellular carcinoma

  • Kenya is a large country at the geographical junction of the distribution of the three Hepatitis B virus (HBV) genotypes A, D and E; little is known about the molecular diversity of HBV in Kenya apart from analysis of the basal core promoter/ precore (BCP/PC) and partial hepatitis B virus pre-surface/surface genomic region (preS2/S) regions [6, 7, 14]

  • Screening for Hepatitis C virus (HCV) antibody was conducted on 388 samples, while 385, 382, and 332 samples were screened for HEV, Hepatitis A virus (HAV) and HBV, respectively, as sample volumes became exhausted

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Summary

Introduction

Viral hepatitis is a major concern worldwide, with hepatitis A (HAV) and E (HEV) viruses showing sporadic outbreaks while hepatitis B (HBV) and C (HCV) viruses are associated with chronic hepatitis, cirrhosis and hepatocellular carcinoma. Hepatitis A and E viruses (HAV, HEV) are often asymptomatic but can result in acute disease often characterized by jaundice. They are transmitted primarily through a fecal oral route and are common in areas with sanitation challenges. HBV genotype E (HBV/E) is confined to West, Central and North Eastern Africa [5, 13]. It has low genetic diversity with no identified subgenotypes but it is often associated with recombinant variants including genotypes D and A. Kenya is a large country at the geographical junction of the distribution of the three HBV genotypes A, D and E; little is known about the molecular diversity of HBV in Kenya apart from analysis of the basal core promoter/ precore (BCP/PC) and partial preS2/S regions [6, 7, 14]

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