Update on hepatitis E virology: Implications for clinical practice

Yannick Debing, Darius Moradpour, Johan Neyts, Jerome Gouttenoire*

*Corresponding author for this work

Research output: Contribution to journal(Systematic) Review article peer-review

Abstract

Hepatitis E virus (HEV) is a positive-strand RNA virus transmitted by the fecal-oral route. The 7.2 kb genome encodes three open reading frames (ORF) which are translated into (i) the ORF1 polyprotein, representing the viral replicase, (ii) the ORF2 protein, corresponding to the viral capsid, and (iii) the ORF3 protein, a small protein involved in particle secretion. Although HEV is a non-enveloped virus in bile and feces, it circulates in the bloodstream wrapped in cellular membranes. HEV genotypes 1 and 2 infect only humans and cause mainly waterborne outbreaks. HEV genotypes 3 and 4 are widely represented in the animal kingdom and are transmitted as a zoonosis mainly via contaminated meat. HEV infection is usually self-limited but may persist and cause chronic hepatitis in immunocompromised patients. Reduction of immunosuppressive treatment or antiviral therapy with ribavirin have proven effective in most patients with chronic hepatitis E but therapy failures have been reported. Alternative treatment options are needed, therefore. Infection with HEV may also cause a number of extrahepatic manifestations, especially neurologic complications. Progress in the understanding of the biology of HEV should contribute to improved control and treatment of HEV infection. (C) 2016 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
Original languageEnglish
Pages (from-to)200-212
Number of pages13
JournalJournal of Hepatology
Volume65
Issue number1
DOIs
Publication statusPublished - 1 Jul 2016

Keywords

  • Antivirals
  • Chronic hepatitis
  • Positive-strand RNA virus
  • Tissue tropism
  • Zoonotic infection
  • E VIRUS HEV
  • NON-B HEPATITIS
  • ORF3 PROTEIN
  • NON-A
  • RIBAVIRIN TREATMENT
  • C VIRUS
  • EXTRAHEPATIC MANIFESTATIONS
  • INTRACELLULAR MEMBRANE
  • INTERFERON INDUCTION
  • MACRO DOMAIN

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