Rodrigues Tamara S, Zamboni Dario S
Department of Cell Biology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Immunol Rev. 2025 Mar;330(1):e70003. doi: 10.1111/imr.70003.
Respiratory viruses, including SARS-CoV-2, influenza, parainfluenza, rhinovirus, and respiratory syncytial virus (RSV), are pathogens responsible for lower respiratory tract infections, particularly in vulnerable populations such as children and the elderly. Upon infection, these viruses are recognized by pattern recognition receptors, leading to the activation of inflammasomes, which are essential for mediating inflammatory responses. This review discusses the mechanisms by which these RNA respiratory viruses activate inflammasomes, emphasizing the roles of various signaling pathways and components involved in this process. Additionally, we highlight the specific interactions between viral proteins and inflammasome sensors, elucidating how these viruses manipulate the host immune response to facilitate infection. Understanding the dynamics of inflammasome activation in response to respiratory viruses provides critical insights for developing immunomodulatory therapeutic strategies aimed at mitigating inflammation and improving outcomes in respiratory tract infections.
呼吸道病毒,包括严重急性呼吸综合征冠状病毒2(SARS-CoV-2)、流感病毒、副流感病毒、鼻病毒和呼吸道合胞病毒(RSV),是导致下呼吸道感染的病原体,尤其是在儿童和老年人等易感人群中。感染后,这些病毒被模式识别受体识别,导致炎性小体激活,这对于介导炎症反应至关重要。本综述讨论了这些RNA呼吸道病毒激活炎性小体的机制,强调了参与这一过程的各种信号通路和组分的作用。此外,我们突出了病毒蛋白与炎性小体传感器之间的特定相互作用,阐明了这些病毒如何操纵宿主免疫反应以促进感染。了解呼吸道病毒感染后炎性小体激活的动态变化,为制定旨在减轻炎症和改善呼吸道感染结局的免疫调节治疗策略提供了关键见解。