Shi Wen, Jin Mengyun, Chen Hao, Wu Zongxue, Yuan Liuyang, Liang Si, Wang Xiaohan, Memon Fareed Uddin, Eldemery Fatma, Si Hongbin, Ou Changbo
College of Animal Science and Technology, Guangxi University, Nanning, China.
QYH Biotech Ltd., Beijing, China.
Front Microbiol. 2023 Aug 7;14:1247377. doi: 10.3389/fmicb.2023.1247377. eCollection 2023.
Viral diseases are the most common problems threatening human health, livestock, and poultry industries worldwide. Viral infection is a complex and competitive dynamic biological process between a virus and a host/target cell. During viral infection, inflammasomes play important roles in the host and confer defense mechanisms against the virus. Inflammasomes are polymeric protein complexes and are considered important components of the innate immune system. These immune factors recognize the signals of cell damage or pathogenic microbial infection after activation by the canonical pathway or non-canonical pathway and transmit signals to the immune system to initiate the inflammatory responses. However, some viruses inhibit the activation of the inflammasomes in order to replicate and proliferate in the host. In recent years, the role of inflammasome activation and/or inhibition during viral infection has been increasingly recognized. Therefore, in this review, we describe the biological properties of the inflammasome associated with viral infection, discuss the potential mechanisms that activate and/or inhibit NLRP1, NLRP3, and AIM2 inflammasomes by different viruses, and summarize the reciprocal regulatory effects of viral infection on the NLRP3 inflammasome in order to explore the relationship between viral infection and inflammasomes. This review will pave the way for future studies on the activation mechanisms of inflammasomes and provide novel insights for the development of antiviral therapies.
病毒性疾病是全球范围内威胁人类健康、畜牧业和家禽业的最常见问题。病毒感染是病毒与宿主/靶细胞之间复杂且具有竞争性的动态生物学过程。在病毒感染期间,炎性小体在宿主中发挥重要作用,并赋予针对病毒的防御机制。炎性小体是聚合蛋白复合物,被认为是先天免疫系统的重要组成部分。这些免疫因子在通过经典途径或非经典途径激活后识别细胞损伤或病原微生物感染的信号,并将信号传递给免疫系统以引发炎症反应。然而,一些病毒为了在宿主体内复制和增殖而抑制炎性小体的激活。近年来,炎性小体激活和/或抑制在病毒感染过程中的作用越来越受到认可。因此,在本综述中,我们描述了与病毒感染相关的炎性小体的生物学特性,讨论了不同病毒激活和/或抑制NLRP1、NLRP3和AIM2炎性小体的潜在机制,并总结了病毒感染对NLRP3炎性小体的相互调节作用,以探索病毒感染与炎性小体之间的关系。本综述将为未来炎性小体激活机制的研究铺平道路,并为抗病毒治疗的发展提供新的见解。