Immunological response of Hepatitis B Virus Surface Antigen in HBV Mono and HBV/HDV Co-infection

Abstract

Hepatitis B virus (HBV) can evolve under selection pressure exerted by drugs and host immunity, resulting in the accumulation of escape mutations that can affect the drug or the immune activity. Hepatitis B virus polymerase lacks proofreading ability and is, therefore, error prone which results in the incorporation of mismatch bases causes mutations in the Hepatitis B virus genome. Factors, which might contribute to a high Hepatitis B virus mutation rate, are drugs, host immune system and co infection. Hepatitis Delta Virus (HDV) co-infection is also known to exert selection pressure on Hepatitis B virus. This further leads to selective amplification of certain mutations, especially in genes that are required for hepatitis delta virus pathogenesis, such as Hepatitis B virus surface antigen. Some of these mutations affected the generation of proteasomal sites, binding of Hepatitis B virus surface antigen epitopes to major histocompatibility I and II ligands, and subsequent generation of B- and T-cell epitopes. Information and data from 2010 to 2020 were retrieved from search engines like PubMed, Medline, Google Scholar and Web of Science through original papers and reviews. This review focuses on mutations that the Hepatitis B virus selectively amplifies in presence of Hepatitis D virus co-infection and its effect on epitope generation.

Keywords:  Hepatitis B Virus; Hepatitis D Virus; Co Infection; Epitopes; Hepatitis B Virus Surface Antigen.