John Libbey Eurotext



Hepatitis E virus: from the infected organism to the cellular response Volume 22, issue 5, Septembre-Octobre 2018


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1 Inserm U1043/CNRS U5282,
Centre de physiopathologie Toulouse-Purpan,
Équipe « infection virale : persistance, réponse de l’hôte et physiopathologie »,
CHU Purpan, BP3028,
31024 Toulouse cedex 3, France
2 CHU de Toulouse,
Hôpital Purpan,
Laboratoire de virologie,
Institut fédératif de biologie de Purpan,
330 avenue de Grande-Bretagne,
31300 Toulouse, France
3 Université Paul-Sabatier,
118 Route de Narbonne
31330 Toulouse, France
4 CHU de Toulouse,
Hôpital Rangueil,
Service de néphrologie-hypertension artérielle-dialyse-transplantation,
1 avenue du Pr Jean Poulhès,
31400 Toulouse, France
* Tirés à part

Hepatitis E virus (HEV) presents a worldwide distribution. In developing countries, hepatitis E, related to HEV1 and HEV2, is a waterborne disease. In developed countries, hepatitis E is a zoonotic disease due to HEV3 and HEV4. It is mainly transmitted through meat consumption from animal reservoirs such as pig, boar, deer and rabbit. New clinical forms include neurological manifestations that are now clearly associated with HEV3 infection. Recent studies showed that ORF1 polyprotein was able to disrupt the innate immune response. It was also shown that ORF2 protein exists at least in two forms: a free, glycosylated form and a non-glycosylated form, which assembles to form the capsid. Lastly, it was shown that ORF3 protein, involved in the virus egress, acts as a viroporin. New culture systems and animal models have been developed recently, and will be very helpful to complete our understanding of HEV life cycle and pathogenesis.

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