Hepatitis E Virus Entry

被引：34

作者：

Yin, Xin ^{[1
,3
]}

Feng, Zongdi ^{[1
,2
]}

机构：

[1] Nationwide Childrens Hosp, Res Inst, Ctr Vaccines & Immun, Columbus, OH 43205 USA

[2] Ohio State Univ, Coll Med, Dept Pediat, Columbus, OH 43210 USA

[3] Sanford Burnham Prebys Med Discovery Inst, Infect & Inflammatory Dis Ctr, Immun & Pathogenesis Program, La Jolla, CA 92037 USA

来源：

VIRUSES-BASEL | 2019年 / 11卷 / 10期

关键词：

quasienveloped virus; receptor; lysosomal acid lipase; NPC1; RIBAVIRIN TREATMENT FAILURE; ENTERS LIVER-CELLS; ORF3; PROTEIN; VIRAL-HEPATITIS; CULTURED-CELLS; HEV; INFECTION; PATHOGENESIS; REPLICATION; INTERACTS;

D O I：

10.3390/v11100883

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

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.

引用

页数：10

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