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Li Y.,Key Laboratory of Pathogenic Biology Heilongjiang Higher Education Institutions | Li Y.,State Province Key Laboratories of Biomedicine Pharmaceutics of China | Song W.,Key Laboratory of Pathogenic Biology Heilongjiang Higher Education Institutions | Song W.,State Province Key Laboratories of Biomedicine Pharmaceutics of China | And 12 more authors.
International Journal of Biochemistry and Cell Biology | Year: 2013

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 infec-tion. 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 com-ponent 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- κB 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 © 2013 Published by Elsevier Ltd. All rights reserved. Source

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