AUTHOR=Chu Zhili, Wang Caiying, Tang Qiuxia, Shi Xiaolei, Gao Xiaolong, Ma Jiangang, Lu Kejia, Han Qingsong, Jia Yanqing, Wang Xiangwei, Adam Fathalrhman Eisa Addoma, Liu Haijin, Xiao Sa, Wang Xinglong, Yang Zengqi TITLE=Newcastle Disease Virus V Protein Inhibits Cell Apoptosis and Promotes Viral Replication by Targeting CacyBP/SIP JOURNAL=Frontiers in Cellular and Infection Microbiology VOLUME=8 YEAR=2018 URL=https://www.frontiersin.org/articles/10.3389/fcimb.2018.00304 DOI=10.3389/fcimb.2018.00304 ISSN=2235-2988 ABSTRACT=Newcastle disease virus (NDV) has been classified by the World Organization for Animal Health (OIE) as a notable disease-causing virus, and this virus has the ability to infect a wide range of birds. V protein is a non-structural protein of NDV. V protein has been reported to inhibit cell apoptosis (Park et al., 2003a) and promote viral replication (Huang et al., 2003), however, the mechanisms of action of V protein have not been elucidated. In the present study, a yeast two-hybrid screen was performed, and V protein was found to interact with the CacyBP/SIP protein. The results of co-immunoprecipitation and immuno-colocalization assays confirmed the interaction between V protein and CacyBP/SIP. The results of quantitative-PCR and viral plaque assays showed that overexpression of CacyBP/SIP inhibited viral replication in DF-1 cells. Overexpression of CacyBP/SIP in DF-1 cells induced caspase3-dependent apoptosis. The effect of knocking down CacyBP/SIP by siRNA was the opposite of that observed upon overexpression. Moreover, it is known that NDV induces cell apoptosis via multiple caspase-dependent pathways. Furthermore, V protein inhibited cell apoptosis and downregulated CacyBP/SIP expression in DF-1 cells. Taken together, the findings of the current study indicate that V protein interacts with CacyBP/SIP, thereby regulating cell apoptosis and viral replication.