Correction: The p17 nonstructural protein of avian reovirus triggers autophagy enhancing virus replication via activation of phosphatase and tensin deleted on chromosome 10 (PTEN) and AMP-activated protein kinase (AMPK), as well as dsRNA-dependent protein kinase (PKR)/eIF2 α signaling pathways.

I., Pei; Huang, Wei-Ru; Lai, I.H.; Cheng, Ching‐Yu; Liu, Hung-Jen

doi:10.1074/jbc.aac119.010041

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Mechanisms Of Pkr Inhibition By Viruses1

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2021

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“…Activation of PKR : in contrast to other viral proteins, p17 from ARV was shown to subvert the innate immune response by triggering PKR. In this case, activation of PKR contributed to triggering autophagy, which was found to increase virus replication ( Chi et al, 2013 , 2019 ). Other viruses take advantage of some extent of PKR activation.…”

Section: Mechanisms Of Pkr Inhibition By Virusesmentioning

confidence: 99%

Inhibition of PKR by Viruses

Cesaro

Michiels

2021

Front. Microbiol.

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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.

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Section: Mechanisms Of Pkr Inhibition By Virusesmentioning

confidence: 99%