circRNAcircVAMP3通过干扰NP和NS1蛋白来限制甲型流感病毒的复制。

IF 6.7 1区 医学 Q1 Immunology and Microbiology
PLoS Pathogens Pub Date : 2023-08-21 eCollection Date: 2023-08-01 DOI:10.1371/journal.ppat.1011577
Jie Min, Yucen Li, Xinda Li, Mingge Wang, Huizi Li, Yuhai Bi, Ping Xu, Wenjun Liu, Xin Ye, Jing Li
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引用次数: 0

摘要

环状核糖核酸(circRNAs)参与各种生物学作用,包括病毒感染和抗病毒免疫反应。为了鉴定甲型流感病毒(IAV)感染相关的circRNA,我们比较了感染IAV后A549细胞的circRNA谱。我们发现,在IAV感染或干扰素(IFN)刺激后,circVAMP3显著上调。此外,IAV和IFN-β诱导了QKI-5的表达,从而促进了circVAMP3的生物发生。circVAMP3的过表达抑制了IAV的复制,而circVAMP3敲低促进了病毒的复制,这表明circVAMP3限制了IAV复制。我们验证了circVAMP3对小鼠病毒感染的影响,并发现circVAMP3在体内限制了IAV的复制和发病机制。我们还发现circVAMP3作为病毒蛋白核蛋白(NP)和非结构蛋白1(NS1)的诱饵发挥作用。从机制上讲,circVAMP3通过减少NP与聚合酶碱性1、聚合酶碱性2或vRNA的相互作用来干扰病毒核糖核蛋白复合物的活性,并通过减轻NS1对RIG-I或TRIM25的抑制作用来恢复IFN-β的激活。我们的研究为circRNAs在直接抑制病毒复制和恢复对IAV感染的先天免疫方面的作用提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The circRNA circVAMP3 restricts influenza A virus replication by interfering with NP and NS1 proteins.

The circRNA circVAMP3 restricts influenza A virus replication by interfering with NP and NS1 proteins.

The circRNA circVAMP3 restricts influenza A virus replication by interfering with NP and NS1 proteins.

The circRNA circVAMP3 restricts influenza A virus replication by interfering with NP and NS1 proteins.

Circular RNAs (circRNAs) are involved in various biological roles, including viral infection and antiviral immune responses. To identify influenza A virus (IAV) infection-related circRNAs, we compared the circRNA profiles of A549 cells upon IAV infection. We found that circVAMP3 is substantially upregulated after IAV infection or interferon (IFN) stimulation. Furthermore, IAV and IFN-β induced the expression of QKI-5, which promoted the biogenesis of circVAMP3. Overexpression of circVAMP3 inhibited IAV replication, while circVAMP3 knockdown promoted viral replication, suggesting that circVAMP3 restricts IAV replication. We verified the effect of circVAMP3 on viral infection in mice and found that circVAMP3 restricted IAV replication and pathogenesis in vivo. We also found that circVAMP3 functions as a decoy to the viral proteins nucleoprotein (NP) and nonstructural protein 1 (NS1). Mechanistically, circVAMP3 interfered with viral ribonucleoprotein complex activity by reducing the interaction of NP with polymerase basic 1, polymerase basic 2, or vRNA and restored the activation of IFN-β by alleviating the inhibitory effect of NS1 to RIG-I or TRIM25. Our study provides new insights into the roles of circRNAs, both in directly inhibiting virus replication and in restoring innate immunity against IAV infection.

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来源期刊
PLoS Pathogens
PLoS Pathogens 生物-病毒学
CiteScore
11.40
自引率
3.00%
发文量
598
审稿时长
2 months
期刊介绍: Bacteria, fungi, parasites, prions and viruses cause a plethora of diseases that have important medical, agricultural, and economic consequences. Moreover, the study of microbes continues to provide novel insights into such fundamental processes as the molecular basis of cellular and organismal function.
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