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ICP4-induced miR-101 attenuates HSV-1 replication.

Authors :
Wang X
Diao C
Yang X
Yang Z
Liu M
Li X
Tang H
Source :
Scientific reports [Sci Rep] 2016 Mar 17; Vol. 6, pp. 23205. Date of Electronic Publication: 2016 Mar 17.
Publication Year :
2016

Abstract

Hepes simplex Virus type 1 (HSV-1) is an enveloped DNA virus that can cause lytic and latent infection. miRNAs post-transcriptionally regulate gene expression, and our previous work has indicated that HSV-1 infection induces miR-101 expression in HeLa cells. The present study demonstrates that HSV-1-induced miR-101 is mainly derived from its precursor hsa-mir-101-2, and the HSV-1 immediate early gene ICP4 (infected-cell polypeptide 4) directly binds to the hsa-mir-101-2 promoter to activate its expression. RNA-binding protein G-rich sequence factor 1 (GRSF1) was identified as a new target of miR-101; GRSF1 binds to HSV-1 p40 mRNA and enhances its expression, facilitating viral proliferation. Together, ICP4 induces miR-101 expression, which downregulates GRSF1 expression and attenuates the replication of HSV-1. This allows host cells to maintain a permissive environment for viral replication by preventing lytic cell death. These findings indicate that HSV-1 early gene expression modulates host miRNAs to regulate molecular defense mechanisms. This study provides novel insight into host-virus interactions in HSV-1 infection and may contribute to the development of antiviral therapeutics.

Details

Language :
English
ISSN :
2045-2322
Volume :
6
Database :
MEDLINE
Journal :
Scientific reports
Publication Type :
Academic Journal
Accession number :
26984403
Full Text :
https://doi.org/10.1038/srep23205