Hepatitis B Virus Genetic Diversity and Surface Antigen Mutations among Voluntary Blood Donors in Kenya

Abstract

Hepatitis B virus belongs to Hepadnaviridae family and replicates by reverse transcription of the viral RNA. Nucleotide variation within the virus has led to its classification into ten genotypes (A-J). The reverse transcription step within its life cycle is prone to introduction of errors and accounts for the current existence of mutants, recombinants, and quasi species of HBV. As a consequence, mutations may render blood donations false negative for hepatitis B surface antigen (HBsAg) upon serological testing. In Kenya, data on escape mutations of HBsAg is limited. This study aimed at determining HBV genetic diversity and surface antigen mutations among voluntary blood donors in Kenya. A total of 301 blood samples were collected from the Regional Blood Transfusion Centres (RBTCs) and tested for HBsAg using the Enzyme-Linked Immunosorbent Assay (ELISA) and nested PCR. The amplified products were sequenced, the generated HBV sequences analysed for S gene mutations and the genetic diversity of HBV was determined. All the statistical analyses were performed using SPSS version 19.0. Out of the 301 samples tested by PCR for the HBV DNA, two samples 2/301 (0.66 %) were identified were identified as occult HBV infection. The cases were confirmed by sequencing. All strains were genotype A, with A1 (94.20%) predominated, A2 (1.45%) and A3 (4.35%) sub genotypes. The amino acid substitutions Q101H, T118A, K122R, K133E, M133I, T143M, C149R, E164G and V184A were detected in ORF S with T143M and K122R as the most prevalent mutations. The present study revealed the predominance of genotype A, with A1, A2 and A3 sub genotypes among Kenyan voluntary blood donors. In addition, surface antigen mutations were detected. Different HBV genotypes have been associated with disease chronicity and development of Hepatocellular Carcinoma (HCC) and response to treatment. Surface antigen mutants evade the immune surveillance leading to false negative diagnosis for HBsAg in blood donations. This could lead to increased HBV transmission in the general population. Therefore, there is need for continuous surveillance of HBV genotypes and mutations with clinical significance in the population.