Cesaro Teresa, Michiels Thomas
de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
Front Microbiol. 2021 Oct 25;12:757238. doi: 10.3389/fmicb.2021.757238. eCollection 2021.
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.
细胞通过检测非自身分子的传感器以及具有直接抗病毒活性或调节细胞生理以限制病毒感染和传播的效应器来应对病毒感染。真核翻译起始因子2α激酶2，更广为人知的是PKR，在对病毒感染的反应中既充当传感器又充当效应器。在检测到受感染细胞中的双链RNA分子后，PKR自我激活，主要通过阻断翻译机制和诱导细胞凋亡来发挥其抗病毒功能。病毒为对抗PKR途径而开发的多种策略凸显了PKR的抗病毒效力。在这篇综述中，我们介绍了这些策略的多样性的最新情况，这些策略从PKR激活上游的双链RNA识别的阻止，到PKR靶点下游的eIF2B激活不等。
