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Viruses. 2019 Sep 20;11(10). pii: E883. doi: 10.3390/v11100883.

Hepatitis E Virus Entry.

Author information

1
Center for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, OH 43205, USA. xyin@sbpdiscovery.org.
2
Center for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, OH 43205, USA. zongdi.feng@nationwidechildrens.org.
3
Department of Pediatrics, The Ohio State University College of Medicine, Columbus, OH 43210, USA. zongdi.feng@nationwidechildrens.org.

Abstract

Hepatitis E virus (HEV) infection is a major cause of acute hepatitis worldwide. It is transmitted enterically but replicates in the liver. Recent studies indicate that HEV exists in two forms: naked, nonenveloped virions that are shed into feces to mediate inter-host transmission, and membrane-cloaked, quasienveloped virions that circulate in the bloodstream to mediate virus spread within a host. Both virion types are infectious, but differ in the way they infect cells. Elucidating the entry mechanism for both virion types is essential to understand HEV biology and pathogenesis, and is relevant to the development of treatments and preventions for HEV. This review summarizes the current understanding of the cell entry mechanism for these two HEV virion types.

KEYWORDS:

NPC1; lysosomal acid lipase; quasienveloped virus; receptor

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