Details

Autor(en) / Beteiligte

• 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

Titel

Newcastle Disease Virus V Protein Inhibits Cell Apoptosis and Promotes Viral Replication by Targeting CacyBP/SIP

Ist Teil von

• Frontiers in cellular and infection microbiology, 2018-09, Vol.8, p.304-304

Ort / Verlag

Switzerland: Frontiers Media S.A

Erscheinungsjahr

2018

Quelle

MEDLINE

Beschreibungen/Notizen

• 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.