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MAVS-mediated host cell defense is inhibited by Borna disease virus #MMPMID23702035
Li Y; Song W; Wu J; Zhang Q; He J; Li A; Qian J; Zhai A; Hu Y; Kao W; Wei L; Zhang F; Xu D
Int J Biochem Cell Biol 2013[Aug]; 45 (8): 1546-55 PMID23702035show ga
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-kappaB 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.
|Adaptor Proteins, Signal Transducing/*metabolism[MESH]
Int+J+Biochem+Cell+Biol 2013 ; 45 (8): 1546-55
