Why the study?
Many studies over the past decade have demonstrated that poly(A) binding proteins are manipulated by viruses to hijack cellular gene expression and evade host antiviral defenses.
Key points are not available for this paper at this time.
Design
Review
This review highlights the mechanisms by which viruses, including SARS-CoV-2, manipulate poly(A) binding proteins to subvert host translation machinery and evade antiviral defenses.
Viruses have evolved diverse strategies to hijack the cellular gene expression system for their replication. The poly(A) binding proteins (PABPs), a family of critical gene expression factors, are viruses' common targets. PABPs act not only as a translation factor but also as a key factor of mRNA metabolism. During viral infections, the activities of PABPs are manipulated by various viruses, subverting the host translation machinery or evading the cellular antiviral defense mechanism. Viruses harness PABPs by modifying their stability, complex formation with other translation initiation factors, or subcellular localization to promote viral mRNAs translation while shutting off or competing with host protein synthesis. For the past decade, many studies have demonstrated the PABPs' roles during viral infection. This review summarizes a comprehensive perspective of PABPs' roles during viral infection and how viruses evade host antiviral defense through the manipulations of PABPs.
No takes yet. Share an insight, caveat, or question.
Gao et al. (2022) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: