Problem hepatitis viruses: the mutants.

Abstract

Genetic variations in the known human hepatitis viruses are probably the result (a) of high viral replication rates and poor or absent proofreading ability intrinsic to RNA viruses (HAV, HCV, HDV, HEV) and (b) to a DNA virus (HBV) that uses a reverse-transcription mechanism for genomic replication. Nucleotide substitutions, deletions, duplications, insertions, and rearrangements resulting in amino acid changes may have no consequences, may impair replication, change host susceptibility, or may lead to escape from immune attack. Genetic diversity has been identified in each of the known hepatitis viruses. The importance of mutant viruses in pathogenicity, immunity, natural history, clinical outcomes, vaccine production, and responsiveness to treatment has emerged as an area for intensive study.