[Programmed cell death in paramyxovirus infection].

Q2 Medicine
Ye Liu, Yilong Wang, Zhixu He, Zhengyan Zhao
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引用次数: 0

Abstract

Paramyxoviruses are important respiratory pathogens with substantial clinical relevance in pediatric infectious diseases. During infection, multiple forms of programmed cell death (PCD) may be induced, and this plays pivotal roles in viral replication, dissemination, and host immune responses, thereby profoundly influencing the viral life cycle and disease progression. On one hand, PCD facilitates the clearance of infected cells, restricts viral spread, and activates host immune defenses, thereby enhancing antiviral immunity. On the other hand, excessive or dysregulated cell death may lead to tissue damage and immune imbalance, creating a microenvironment conducive to viral replication and exacerbating disease severity. For instance, apoptosis-mediated by both extrinsic and intrinsic pathways-contributes to infection control but may also be hijacked by viruses to promote dissemination. Pyroptosis, driven by inflammasome activation, triggers lytic cell death and the release of pro-inflammatory cytokines. Necroptosis, mediated by the RIPK1-RIPK3-MLKL signaling axis, and pyroptosis both amplify innate immune responses but may concurrently induce inflammatory dysregulation. Immunogenic cell death (ICD), characterized by the release of damage-associated molecular patterns and neoantigens, activates antigen-specific immune responses and holds therapeutic potential for antiviral and antitumor interventions. Emerging evidence suggests that ferroptosis, through the modulation of iron metabolism and associated transporters, may also participate in viral replication and infected cell clearance. This review comprehensively summarizes the roles of apoptosis, pyroptosis, necroptosis, ICD, and ferroptosis in paramyxovirus infection, aiming to deepen the understanding of paramyxovirus pathogenesis and to provide insights for developing novel antiviral strategies.

程序性细胞死亡在副粘病毒感染中的作用。
副粘病毒是一种重要的呼吸道病原体,在儿科传染病中具有重要的临床意义。在感染过程中,它们诱导多种形式的程序性细胞死亡(PCD),在病毒复制、传播和宿主免疫应答中起关键作用,从而深刻影响病毒的生命周期和疾病进展。PCD一方面促进被感染细胞的清除,限制病毒的传播,激活宿主免疫防御,从而增强抗病毒免疫。另一方面,过度或失调的细胞死亡可能导致组织损伤和免疫失衡,创造有利于病毒复制的微环境,加剧疾病严重程度。例如,由内在和外在途径介导的细胞凋亡有助于控制感染,但也可能被病毒劫持以促进传播。由炎性小体激活驱动的焦亡,引发溶解性细胞死亡和促炎细胞因子的释放。由RIPK1-RIPK3-MLKL信号轴介导的坏死下垂和焦下垂都能增强先天免疫反应,但可能同时诱导炎症失调。免疫原性细胞死亡(ICD)以损伤相关分子模式(DAMPs)和新抗原的释放为特征,激活抗原特异性免疫反应,具有抗病毒和抗肿瘤干预的治疗潜力。新出现的证据表明,铁死亡通过铁代谢和相关转运体的调节,也可能参与病毒复制和感染细胞的清除。本文综述了细胞凋亡、焦亡、坏死、ICD和铁亡在副粘病毒感染中的作用,旨在加深对副粘病毒发病机制的理解,并为开发新的抗病毒策略提供见解,特别是在儿科人群中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
67
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