Abstract
Enteroviruses such as poliovirus (PV) and coxsackievirus B3 (CVB3) have evolved several parallel strategies to regulate cellular gene expression and stress responses to ensure efficient expression of the viral genome. Enteroviruses utilize their encoded proteinases to take over the cellular translation apparatus and direct ribosomes to viral mRNAs. In addition, viral proteinases are used to control and repress the two main types of cytoplasmic RNA granules, stress granules (SGs) and processing bodies (P-bodies, PBs), which are stress-responsive dynamic structures involved in repression of gene expression. This review discusses these processes and the current understanding of the underlying mechanisms with respect to enterovirus infections. In addition, the review discusses accumulating data suggesting linkage exists between RNA granule formation and innate immune sensing and activation.
Highlights
The enterovirus genome is a functional mRNA that must be expressed as the first step of the infectious cycle; it is of no surprise that enteroviruses exert rapid and dominant control over the cellular translation apparatus
Since the cellular translation apparatus quickly responds to stress and altered environmental conditions, it is important for the virus to strongly regulate multiple aspects of the translation apparatus to promote its own gene expression, but to restrict those cell responses that activate innate immunity and may limit access to metabolites and components needed by the virus
We have shown that stress granules (SGs) induced by G3BP1 overexpression are antiviral against multiple enteroviruses [64,75]
Summary
The enterovirus genome is a functional mRNA that must be expressed as the first step of the infectious cycle; it is of no surprise that enteroviruses exert rapid and dominant control over the cellular translation apparatus. The final initiation factor cleaved by cleavage of PABP is shared by caliciviruses, which translate cap-independently, but do not induce enterovirus proteinases, eIF5B, is cleaved by 3Cpro [14]. This cleavage plays no significant role in the cleavage of eIF4G during infection [13]. The final initiation factor cleaved by enterovirus proteinases, initial host translation shutoff, but rather reshapes the translation apparatus so viral RNA can achieve eIF5B, is cleaved by 3Cpro [14] This cleavage plays no significant role in the initial host translation eIF2-independent translation as will be discussed below. Shutoff, but rather reshapes the translation apparatus so viral RNA can achieve eIF2-independent translation as will be discussed
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