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.