期刊
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
卷 45, 期 8, 页码 1546-1555出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2013.05.012
关键词
Mitochondrial antiviral signaling protein; Borna disease virus; Apoptosis; Mitochondria; Host cell defense
资金
- National Natural Science Foundation of China (NSFC) [J1103609, J0730858, 81202296]
- Doctor Innovation Foundation of Heilongjiang Province, China [YJSCX2011-323HLJ]
- National Health and Medical Research Council of Australia [606425]
- Victorian Government's Operational Infrastructure Support Program
- Longjiang Scholar award
- Heilongjiang Provincial Science and Technology Innovation Team in Higher Education Institutes for Infection and Immunity, Harbin Medical University
Viruses often have strategies for preventing host cell apoptosis, which antagonizes viral replication. Borna disease virus (BDV) is a neurotropic RNA virus that establishes a non-cytolytic persistent infection. Although BDV suppresses type I Interferon (IFN) through (TANK)-binding kinase 1 (TBK-1) associated BDV P protein, it is still unclear how BDV can survive in the host cell and establish a persistent infection. Recently, it has been recognized that mitochondria-mediated apoptosis through the mitochondrial antiviral signaling protein (MAVS) and the RIG-I-like receptor (RLR) signaling pathway is a crucial component of the innate immune response. In this work we show that BDV X protein colocalizes and interacts with MAVS in the mitochondria to block programmed cell death. BDV X protein-mediated inhibition of apoptosis was independent of type I IFN production and NF-kappa B activity. The reduction of BDV X expression with RNA interference (RNAi) or the mutation of BDV X enhanced MAVS-induced cell death. Collectively, our data provide novel insights into how BDV X protein inhibits antiviral-associated programmed cell death, through its action of MAVS function. Crown Copyright (c) 2013 Published by Elsevier Ltd. All rights reserved.
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