Journal
EBIOMEDICINE
Volume 11, Issue -, Pages 31-42Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ebiom.2016.07.039
Keywords
Hepatitis E virus; HEV infection; HEV mutation; HEV variability; HEV treatment failure; HEV replication
Funding
- European Association for the Study of the Liver (EASL) through the Andrew K. Burroughs fellowship
- China Scholarship Council (CSC), Beijing, China
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Hepatitis E virus (HEV) infection is a major cause of acute hepatitis and affects more than 20 million individuals, with three million symptomatic cases and 56,000 recognized HEV-related deaths worldwide. HEV is endemic in developing countries and is gaining importance in developed countries, due to increased number of autochthone cases. Although HEV replication is controlled by the host immune system, viral factors (especially specific viral genotypes and mutants) can modulate HEV replication, infection and pathogenesis. Limited knowledge exists on the contribution of HEV genome variants towards pathogenesis, susceptibility and to therapeutic response. Nonsynonymous substitutions can modulate viral proteins structurally and thus dysregulate virus-host interactions. This review aims to compile knowledge and discuss recent advances on the casual role of HEV heterogeneity and its variants on viral morphogenesis, pathogenesis, clinical outcome and antiviral resistance. (C) 2016 The Authors. Published by Elsevier B.V.
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