溶解循环
先天免疫系统
延迟(音频)
小RNA
病毒学
生物
免疫
刺
免疫学
计算机科学
基因
遗传学
病毒
免疫系统
工程类
电信
航空航天工程
作者
Kimberly Paulsen,Rosenna Chan,Lauren A. Gay,Zhe Ma
出处
期刊:Cell Reports
[Cell Press]
日期:2025-05-24
卷期号:44 (6): 115741-115741
标识
DOI:10.1016/j.celrep.2025.115741
摘要
Kaposi sarcoma-associated herpesvirus (KSHV) employs various strategies to evade host immune surveillance and maintain lifelong latency. The cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) DNA sensing pathway is a key innate immunity pathway that detects viral DNA and restricts KSHV lytic replication upon reactivation from latency. Here, we identify three KSHV microRNAs (miRNAs), miR-K12-6-3p, miR-K12-7-3p, and miR-K12-11-3p, that directly bind to STING1 mRNA to repress its translation and inhibit downstream immune signaling. Exogenous delivery of these KSHV miRNAs led to decreased STING expression and attenuated cGAS/STING signaling in response to STING agonist stimulation. Conversely, genetic deletion of these KSHV miRNAs rescued STING and interferon-stimulated gene expression in latent KSHV cell lines, delaying KSHV lytic reactivation and reducing KSHV lytic gene expression. These findings shed light on the immune evasion strategy of KSHV miRNA-mediated STING repression, representing the discovery of viral miRNAs that target STING.
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