Key result
Viruses subvert host RNA binding proteins to reshape RNA fate and evade immune responses.
Why the study?
Viruses subvert host defenses to take control of cellular RNA binding proteins, but a comprehensive synthesis of how this host-viral interplay influences RBP functions and modulates RNA stability was needed.
This review summarizes the mechanisms by which viruses co-opt host RNA binding proteins to modulate host gene expression and evade immune responses.
Supports further investigation into RNA-binding proteins as antiviral targets; leaves open clinical translation pending targeted studies.
A defining feature of a productive infection is the co-opting of host cell resources for viral replication. Despite their repertoire of molecular functions, viruses subvert host defenses to take control of cellular factors such as RNA binding proteins (RBPs). RBPs are involved in virtually all steps of mRNA life forming ribonucleoprotein complexes (mRNPs) in a highly ordered and regulated process to control RNA fate and stability in the cell. Thus, the hallmark of this viral takeover is to reshape RNA fate in the cell to modulate host gene expression and evade immune responses. Here we provide an extensive review of work in this area, particularly how the host-viral interplay influences RBP functions to modulate the host cell. Overall, in this review, we highlight the myriad of ways RBPs can regulate RNA stability in either a pro-viral or antiviral manner by gathering novel insights gained from research studies in this field.
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Bermudez et al. (2023) conducted a review in Viral infection. RNA binding proteins (RBPs) was evaluated. Viruses subvert host RNA binding proteins to reshape RNA fate, modulate host gene expression, and evade immune responses in either a pro-viral or antiviral manner.
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