Departement of Biochemistry, University of Lausanne, Epalinges 1066, Switzerland.
Departement of Biochemistry, University of Lausanne, Epalinges 1066, Switzerland.
Curr Opin Virol. 2021 Feb;46:59-64. doi: 10.1016/j.coviro.2020.10.001. Epub 2020 Nov 8.
The innate immune system has evolved mechanisms to keep the viral infection under control and repair damaged tissues. Several pathways can identify the presence of pathogenic components, such as viral nucleic acids and viral proteins. Also, the innate immune system can detect cellular and tissue perturbations caused by infections. Inflammasomes are cellular pieces of machinery that can detect a pathogen's presence and its possible impact on cellular integrity. Thereby several inflammasomes, including the NLRP3 inflammasome and the AIM2 inflammasome, contribute to antiviral innate immunity. Inflammation driven by inflammasomes promotes immune defenses and initiate repair mechanisms. However, its overactivation may trigger acute inflammatory responses that may harm the host. This pathologic activation could contribute to the hyperinflammatory response observed in patients infected with viruses, including influenza, SARS, and possibly SARS-CoV2.
先天免疫系统已经进化出了多种机制来控制病毒感染和修复受损组织。有几种途径可以识别病原体成分的存在，如病毒核酸和病毒蛋白。此外，先天免疫系统还可以检测感染引起的细胞和组织紊乱。炎性小体是一种可以检测病原体存在及其对细胞完整性可能产生的影响的细胞机器。几种炎性小体，包括 NLRP3 炎性小体和 AIM2 炎性小体，有助于抗病毒先天免疫。炎性小体驱动的炎症促进了免疫防御和启动修复机制。然而，其过度激活可能会引发急性炎症反应，从而损害宿主。这种病理性激活可能导致感染病毒（包括流感、SARS 甚至 SARS-CoV2）的患者中观察到的过度炎症反应。
