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Virology. 2019 Oct;536:119-124. doi: 10.1016/j.virol.2019.07.025. Epub 2019 Jul 30.

Integrin α3 is involved in non-enveloped hepatitis E virus infection.

Author information

1
Department of Virology II, National Institute of Infectious Diseases, Gakuen 4-7-1, Musashi-murayama, Tokyo, 208-0011, Japan.
2
Department of Virology I, National Institute of Infectious Diseases, Gakuen 4-7-1, Musashi-murayama, Tokyo, 208-0011, Japan.
3
Department of Quality Assurance and Radiological Protection, National Institute of Infectious Diseases, Gakuen 4-7-1, Musashi-murayama, Tokyo, 208-0011, Japan. Electronic address: kishii@nih.go.jp.

Abstract

Hepatitis E virus (HEV) causes acute and fulminant hepatitis worldwide. Although enveloped (e) and non-enveloped (ne) forms of HEV have been discovered, host factors involved in infection, including receptors, remain to be elucidated. Here, we identified integrin α3 (encoded by ITGA3), a protein that binds and responds to the extracellular matrix, as an essential host factor for HEV infection. Integrin α3 expression was lower in four HEV-non-permissive cell subclones than in an HEV-permissive subclone. ITGA3 knockout cells lost HEV permissibility, suggesting that integrin α3 is critical for HEV infection. Stable expression of integrin α3 in an HEV-non-permissive subclone provided permissibility only to infection by neHEV; expression of integrin α3 lacking the ectodomain did not. Direct interaction between neHEV and the integrin α3 ectodomain was confirmed by co-precipitation using a soluble integrin α3-Fc. These results strongly suggest that integrin α3 is a key molecule for cellular attachment and entry of neHEV.

KEYWORDS:

Hepatitis E virus (HEV); Integrin α3; Non-enveloped HEV; Receptor

PMID:
31421623
DOI:
10.1016/j.virol.2019.07.025
[Indexed for MEDLINE]
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