Orchestrated efforts on host network hijacking: Processes governing virus replication

Dai, Xiaofeng; Hakizimana, Olivier; Zhang, Xuanhao; Kaushik, Aman Chandra; Zhang, Jianying

Many IFN response genes are suppressed during viral invasion (Figure 3 ). Nearly all classes of viruses encode proteins targeting PKR, e.g. DNA viruses such as vaccinia virus (VACV) [78] , adenovirus (ADV) [79] , herpes simplex virus (HSV) [80] , Epstein-barr virus (EBV) [81] , and RNA viruses such as influenza A [82] , Ebola virus (EV) [83] , HCV [84] , rotavirus [85] . Viruses such as HSV-1/2 block RNase L activation by replacing its activators with weak homologues, i.e. the homologue of cellular 2ʹ-5ʹ oligoadenylate [86] . PML nuclear bodies are also IFN-responsive genes typically targeted by viruses including HSV-1, ADV, EBV, HPV, HCV, and rabies virus (RABV). Specifically, ICP0 from HSV-1 degrades PML nuclear bodies [87] ; HCV prevents cell apoptosis by co-localizing its core proteins with PML and TP53 [88] ; RABV subverts the localization of PML nuclear bodies from the nucleus to cytosol via binding between its P protein and PML [89] . Viruses have also evolved ways to suppress cellular restriction factors, e.g. HIV viral protein VIF degrades APOBECs (incorporable into virions during viral assembly) [90] and VACV E3L protein inhibits ADAR-1 activity (that catalyzes Carbon 6 deamination of adenosine to inosine in double-stranded RNA viruses) [91] .