Abstract
BackgroundHost shutoff refers to the widespread downregulation of host gene expression and has emerged as a key process that facilitates the reallocation of cellular resources for viral replication and evasion of host antiviral immune responses.Main bodyThe Herpesviridae family uses a number of proteins that are responsible for host shutoff by directly targeting messenger RNA (mRNA), including virion host shutoff (VHS) protein and the immediate-early regulatory protein ICP27 of herpes simplex virus types 1 (HSV-1) and the SOX (shutoff and exonuclease) protein and its homologs in Gammaherpesvirinae subfamilies, although these proteins are not homologous. In this review, we highlight evidence that host shutoff is promoted by the VHS, ICP27 and SOX-like proteins and that they also contribute to immune evasion.ConclusionsFurther studies regarding the host shutoff proteins will not only contribute to provide new insights into the viral replication, expression and host immune evasion process, but also provide new molecular targets for the development of antiviral drugs and therapies.
Highlights
Main text messenger RNA (mRNA) processingHSV infection leads to suppression of cellular protein synthesis through at least two distinct inhibitory pathways
The success of herpesviruses is due in part to their use of host shutoff mechanisms to ensure the efficient translation of viral mRNAs while constraining host protein expression
The herpes simplex virus types 1 (HSV-1) virion host shutoff (VHS) protein induces mRNA degradation, it promotes dsRNA degradation. These results suggest that VHS homologs in other alphaherpesviruses may have another function in addition to RNase activity, which should be further explored in future studies
Summary
Herpesviridae family members are among the most ubiquitous and successful viruses known and are thought to have coevolved with their hosts. The HSV-1 VHS protein induces mRNA degradation, it promotes dsRNA degradation These results suggest that VHS homologs in other alphaherpesviruses may have another function in addition to RNase activity, which should be further explored in future studies. The SRE in the IL-6 mRNA 3’UTR can effectively escape viral endonucleases, and this region contains AREs. The mechanisms associated with this process are undoubtedly complicated, and the role of viral endonucleases in the fate of AU-rich mRNAs is worth further study. The mechanisms associated with this process are undoubtedly complicated, and the role of viral endonucleases in the fate of AU-rich mRNAs is worth further study It is unclear whether SOX/muSOX proteins need host or viral proteins to target transcripts.
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