• Yannick Debing, Anett Gisa, Kai Dallmeier, Sven Pischke, Birgit Bremer, Michael Manns, Heiner Wedemeyer, Pothakamuri Venkata Suneetha, and Johan Neyts.
• Rega Institute for Medical Research, Department of Microbiology and Immunology, University of Leuven, Leuven, Belgium.
• Gastroenterology. 2014 Nov 1; 147 (5): 1008-11.e7; quiz e15-6.

AbstractWe analyzed blood samples collected from 15 patients with chronic hepatitis E who were recipients of solid-organ transplants. All patients cleared the hepatitis E virus (HEV) except for 2 (nonresponders); 1 patient died. A G1634R mutation in viral polymerase was detected in the HEV RNA of the nonresponders; this mutation did not provide the virus with resistance to ribavirin in vitro. However, the mutant form of a subgenomic replicon of genotype 3 HEV replicated more efficiently in vitro than HEV without this mutation, and the same was true for infectious virus, including in competition assays. Similar results were obtained for genotype 1 HEV. The G1634R mutation therefore appears to increase the replicative capacity of HEV in the human liver and hence reduce the efficacy of ribavirin.Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.

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