Bayat Mobina, Nahid-Samiei Rahil, Sadri Nahand Javid, Naghili Behrouz
Infectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Molecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Front Immunol. 2025 May 9;16:1567459. doi: 10.3389/fimmu.2025.1567459. eCollection 2025.
Interferons (IFNs) are indispensable innate antiviral cytokines that orchestrate the vertebrate immune response against viral incursions. Nearly every cell possesses the remarkable ability to release IFNs upon detecting viral threats, triggering a robust signaling cascade that alerts neighboring cells and halts viral propagation via paracrine communication. The intricate influence of IFNs is mediated by an extensive network of proteins activated through the Jak-STAT pathways, facilitating the swift transcription of over 300 interferon-stimulated genes (ISGs) that fortify cellular defenses against replication. However, the cunning nature of viruses has led to the evolution of sophisticated evasion strategies, notably through the manipulation of host microRNAs (miRNAs) that disrupt vital components of the IFN signaling machinery. This review delves into the intricate interplay between viral infections and both host- and viral-derived miRNAs, exploring their potent roles in modulating RIG-I-like receptors, Toll-like receptors, IFN receptors, and the JAK/STAT pathway, ultimately shaping the landscape of antiviral immunity.
干扰素(IFNs)是不可或缺的先天性抗病毒细胞因子,可协调脊椎动物针对病毒入侵的免疫反应。几乎每个细胞都具有在检测到病毒威胁时释放干扰素的非凡能力,触发强大的信号级联反应,通过旁分泌通讯提醒邻近细胞并阻止病毒传播。干扰素的复杂影响由通过Jak-STAT途径激活的广泛蛋白质网络介导,促进300多个干扰素刺激基因(ISG)的快速转录,这些基因增强了细胞对复制的防御能力。然而,病毒的狡猾本性导致了复杂逃避策略的演变,特别是通过操纵宿主微小RNA(miRNA)来破坏干扰素信号传导机制的重要组成部分。本综述深入探讨了病毒感染与宿主和病毒来源的miRNA之间的复杂相互作用,探讨了它们在调节RIG-I样受体、Toll样受体、干扰素受体和JAK/STAT途径中的重要作用,最终塑造了抗病毒免疫的格局。