Zika Virus Infection Induced Apoptosis by Modulating the Recruitment and Activation of Proapoptotic Protein Bax
Xiaodong Han, Jiuqiang Wang, Yang Yang, Shuxiang Qu, Fang Wan, Ziyi Zhang, Ruigang Wang, Guojing Li, Haolong Cong
Abstract
Since the large outbreaks that occurred in the Pacific Islands and Latin America in 2013, Zika virus has been confirmed a neuroteratogenic pathogen and causative agent of microcephaly and other developmental anomalies of the central nervous system in children born to infected mothers. As the widespread apoptosis throughout the whole brain, studies in animal models have reinforced the link between microcephaly caused by ZIKV infection and NPC apoptosis. Currently, the detailed mechanism of ZIKV infection-induced apoptosis still remains to be elucidated. Here, we firstly demonstrate that ZIKV infection activated the classic signs of mitochondrial apoptotic pathway by modulating the recruitment and activation of Bax. ZIKV NS4B represents a novel viral apoptotic protein that can modulate the recruitment and activation of Bax and trigger the apoptotic program. This is a new insight into understanding the interplay between apoptosis and ZIKV infection.