甲型流感病毒诱使自噬蛋白 LC3 聚集到出芽位点。

Influenza A virus lures autophagic protein LC3 to budding sites.

机构信息

Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, 8057 Zürich, Switzerland.

出版信息

Cell Host Microbe. 2014 Feb 12;15(2):130-1. doi: 10.1016/j.chom.2014.01.014.

DOI:10.1016/j.chom.2014.01.014

Abstract

Autophagy, a cellular degradation pathway, can restrict or assist viral replication. In this issue of Cell Host & Microbe, Beale et al. (2014) report that the influenza virus matrix protein 2 binds to the essential autophagy protein LC3 to presumably transport LC3-conjugated membranes to the cell surface for budding of stable viruses.

摘要

自噬是一种细胞降解途径，可以限制或协助病毒复制。在本期《细胞宿主与微生物》中，Beale 等人（2014）报告称，流感病毒基质蛋白 2 与必需的自噬蛋白 LC3 结合，可能将 LC3 连接的膜转运到细胞表面，用于稳定病毒的出芽。