MAVS-mediated host cell defense is inhibited by Borna disease virus

Yujun Li, Wuqi Song, Jing Wu, Qingmeng Zhang, Junming He, Aimei Li, Jun Qian, Aixia Zhai, Yunlong Hu, Wenping Kao, Lanlan Wei, Feng-Min Zhang, Dakang Xu

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13 Citations (Scopus)


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-?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.
Original languageEnglish
Pages (from-to)1546 - 1555
Number of pages10
JournalInternational Journal of Biochemistry & Cell Biology
Issue number8
Publication statusPublished - 2013

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