%0 Online Multimedia %A Yu, Jinghua %A Zhang, Liying %A Ren, Peiyou %A Zhong, Ting %A Li, Zhaolong %A Wang, Zengyan %A Li, Jingliang %A Liu, Xin %A Zhao, Ke %A Zhang, Wenyan %A Yu, Xiao-Fang %D 2015 %T Enterovirus 71 mediates cell cycle arrest in S phase through non-structural protein 3D %U https://tandf.figshare.com/articles/presentation/Enterovirus_71_mediates_cell_cycle_arrest_in_S_phase_through_non_structural_protein_3D/1301974 %R 10.6084/m9.figshare.1301974.v4 %2 https://ndownloader.figshare.com/files/1881252 %K cell cycle arrest %K enterovirus 71 (EV71) %K polymerase 3D %K viral replication %X

Many viruses disrupt the host cell cycle to facilitate their own growth. We assessed the mechanism and function of enterovirus 71 (EV71), a primary causative agent for recent hand, foot, and mouth disease outbreaks, in manipulating cell cycle progression. Our results suggest that EV71 infection induces S-phase arrest in diverse cell types by preventing the cell cycle transition from the S phase into the G2/M phase. Similar results were observed for an alternate picornavirus, Coxsackievirus A16. Synchronization in S phase, but not G0/G1 phase or G2/M phase, promotes viral replication. Consistent with its ability to arrest cells in S phase, the expression of cyclin A2, CDK 2, cyclin E1, and cyclin B1 was regulated by EV71 through increasing transcription of cyclin E1, promoting proteasome-mediated degradation of cyclin A2 and regulating the phosphorylation of CDK 2. Finally, a non-structural protein of EV71, the RNA-dependent RNA polymerase 3D, was demonstrated to mediate S-phase cell cycle arrest. These findings suggest that EV71 induces S-phase cell cycle arrest in infected cells via non-structural protein 3D, which may provide favorable conditions for virus production.

%I Taylor & Francis