Coronavirus replication does not require the autophagy gene ATG5

被引:172
作者
Zhao, Zijiang
Thackrayl, Larissa B.
Miller, Brian C.
Lynnl, Leresa M.
Becker, Michelle M.
Ward, Eric
Mizushima, Noboru N.
Denison, Mark R.
Virgin, Herbert W., IV
机构
[1] Washington Univ, Dept Pathol & Immunol, Sch Med, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA
[3] Tokyo Med & Dent Univ, Dept Physiol & Cell Biol, Tokyo, Japan
[4] Japan Sci & Technol Agcy, Solut Oriented Res Sci & Technol, Kawaguchi, Japan
[5] Vanderbilt Univ, Sch Med, Dept Pediat, Nashville, TN 37212 USA
关键词
autophagy; coronavirus; macrophage; fibroblast; murine hepatitis virus;
D O I
10.4161/auto.4782
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Macroautophagy (herein autophagy) is a cellular process, requiring ATG5, by which cells deliver double membrane-bound packets containing cytoplasm or cytoplasmic organelles to the lysosome. This process has been reported in some cases to be antiviral, while in other cases it has been reported to be required for efficient viral replication or release. A role for autophagy in RNA virus replication has been an attractive hypothesis because of the association of RNA virus replication with complex membrane rearrangements in the cytoplasm that can generate opposed double membranes. In this study we demonstrate that ATG5 is not required for murine hepatitis virus (MHV) replication in either bone marrow derived macrophages (BMM phi) lacking ATG5 by virtue of Crerecombinase mediated gene deletion or primary low passage murine ATG5(-/-) embryonic fibroblasts (pMEFs). We conclude that neither ATG5 nor an intact autophagic pathway are required for MHV replication or release.
引用
收藏
页码:581 / 585
页数:5
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