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Review
. 2021 Oct 25:12:757238.
doi: 10.3389/fmicb.2021.757238. eCollection 2021.

Inhibition of PKR by Viruses

Affiliations
Review

Inhibition of PKR by Viruses

Teresa Cesaro et al. Front Microbiol. .

Abstract

Cells respond to viral infections through sensors that detect non-self-molecules, and through effectors, which can have direct antiviral activities or adapt cell physiology to limit viral infection and propagation. Eukaryotic translation initiation factor 2 alpha kinase 2, better known as PKR, acts as both a sensor and an effector in the response to viral infections. After sensing double-stranded RNA molecules in infected cells, PKR self-activates and majorly exerts its antiviral function by blocking the translation machinery and inducing apoptosis. The antiviral potency of PKR is emphasized by the number of strategies developed by viruses to antagonize the PKR pathway. In this review, we present an update on the diversity of such strategies, which range from preventing double-stranded RNA recognition upstream from PKR activation, to activating eIF2B downstream from PKR targets.

Keywords: double-stranded RNA; innate immunity; innate immunity evasion; integrated stress response; mRNA translation; viral proteins.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
PKR activation pathway and viral countermeasures. Steps of the PKR activation pathway are framed in gray. Viral evasion mechanisms are presented in yellow frames. See Table 1 for a list of viral products involved in evasion of PKR activity.

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