Abstract
Enteroviral replication reorganizes the cellular membrane. Upon infection, viral proteins and hijacked host factors generate unique structures called replication organelles (ROs) to replicate their viral genomes. ROs promote efficient viral genome replication, coordinate the steps of the viral replication cycle, and protect viral RNA from host immune responses. More recent researches have focused on the ultrastructure structures, formation mechanism, and functions in the virus life cycle of ROs. Dynamic model of enterovirus ROs structure is proposed, and the secretory pathway, the autophagy pathway, and lipid metabolism are found to be associated in the formation of ROs. With deeper understanding of ROs, some compounds have been found to show inhibitory effects on viral replication by targeting key proteins in the process of ROs formation. Here, we review the recent findings concerning the role, morphology, biogenesis, formation mechanism, and inhibitors of enterovirus ROs.
Highlights
Enteroviruses, members of the Picornaviridae family Enterovirus genus, include poliovirus (PV), enterovirus (EV), coxsackievirus (CV), and human rhinovirus (HRV), which can cause poliomyelitis, meningitis, hand-foot-and-mouth disease, respiratory disease, and so on (Tapparel et al, 2013)
Sac1, which converts phosphatidylinositol 4-phosphate (PI4P) to PI on ER membrane, and PI transfer protein beta (PITP-b), which transports PI to the replication organelles (ROs), where PI is phosphorylated by phosphatidylinositol 4-kinase beta (PI4KB) to PI4P, are vital for completing the cycle (Mesmin et al, 2013; Roulin et al, 2014; Nchoutmboube et al, 2015; van der Schaar et al, 2016a; Figure 4)
We summarized the current knowledge of enterovirus ROs, including their function, morphology, biogenesis, and generation mechanism
Summary
Enteroviruses, members of the Picornaviridae family Enterovirus genus, include poliovirus (PV), enterovirus (EV), coxsackievirus (CV), and human rhinovirus (HRV), which can cause poliomyelitis, meningitis, hand-foot-and-mouth disease, respiratory disease, and so on (Tapparel et al, 2013). Researches on PV and CVB3 infection elucidated that there is a link between viral proteins, dsRNA, and both SMTs and DMVs. In the exponential phase of vRNA replication, the structure of ROs mainly forms SMTs, suggesting that the early and mid-term SMTs are related to the onset and most dense rates of RNA synthesis.
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