Genotype specific pathogenicity of hepatitis E virus at the human maternal-fetal interface

Jordi Gouilly, Qian Chen, Johan Siewiera, Géraldine Cartron, Claude Levy, Martine Dubois, Reem Al-Daccak, Jacques Izopet, Nabila Jabrane-Ferrat () and Hicham El Costa ()
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Jordi Gouilly: Centre of Pathophysiology Toulouse Purpan, INSERM U1043, CNRS UMR5282, Toulouse III University
Qian Chen: Centre of Pathophysiology Toulouse Purpan, INSERM U1043, CNRS UMR5282, Toulouse III University
Johan Siewiera: University of California San Francisco, School of Medicine, Laboratory of Medicine
Géraldine Cartron: Service de Gynécologie-Obstétrique, Hôpital Paule de Viguier, Centre Hospitalier Universitaire
Claude Levy: Service de Gynécologie-Obstétrique, Clinique Sarrus-Teinturiers
Martine Dubois: Laboratoire de Virologie, Institute of Federative Biology, Centre Hospitalier Universitaire
Reem Al-Daccak: INSERM UMRS976, Université Paris Diderot, Hôpital Saint-Louis
Jacques Izopet: Centre of Pathophysiology Toulouse Purpan, INSERM U1043, CNRS UMR5282, Toulouse III University
Nabila Jabrane-Ferrat: Centre of Pathophysiology Toulouse Purpan, INSERM U1043, CNRS UMR5282, Toulouse III University
Hicham El Costa: Centre of Pathophysiology Toulouse Purpan, INSERM U1043, CNRS UMR5282, Toulouse III University

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract Hepatitis E virus (HEV) infection, particularly HEV genotype 1 (HEV-1), can result in fulminant hepatic failure and severe placental diseases, but mechanisms underlying genotype-specific pathogenicity are unclear and appropriate models are lacking. Here, we model HEV-1 infection ex vivo at the maternal-fetal interface using the decidua basalis and fetal placenta, and compare its effects to the less-pathogenic genotype 3 (HEV-3). We demonstrate that HEV-1 replicates more efficiently than HEV-3 both in tissue explants and stromal cells, produces more infectious progeny virions and causes severe tissue alterations. HEV-1 infection dysregulates the secretion of several soluble factors. These alterations to the cytokine microenvironment correlate with viral load and contribute to the tissue damage. Collectively, this study characterizes an ex vivo model for HEV infection and provides insights into HEV-1 pathogenesis during pregnancy that are linked to high viral replication, alteration of the local secretome and induction of tissue injuries.

Date: 2018
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DOI: 10.1038/s41467-018-07200-2

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