LINC01197 可作为 PABPC1 诱饵抑制甲型流感病毒的复制。

IF 3.7 1区农林科学 Q1 VETERINARY SCIENCES

Veterinary Research Pub Date : 2024-09-27 DOI:10.1186/s13567-024-01379-7

Yihe Wang, Ning Shi, Hansi Zhang, Jinna Luo, Hongjian Yan, Huiyan Hou, Zhenhong Guan, Lili Zhao, Ming Duan

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引用次数: 0

摘要

甲型流感病毒（IAV）具有人畜共患病的潜能，对动物和人类健康产生了重大影响。越来越多的证据表明，在 IAV 感染过程中，宿主的长非编码 RNA（lncRNA）在调节宿主与病毒的相互作用方面发挥着至关重要的作用。然而，许多与 IAV 感染相关的 lncRNA 还没有得到很好的表征。在本研究中，我们发现 LINC01197 是一种抗病毒宿主因子。LINC01197 在 IAV 感染后明显上调，而这是由 NF-κB 通路控制的。功能分析显示，过表达 LINC01197 可抑制 IAV 复制和病毒产生，而敲除 LINC01197 则可促进 IAV 复制。从机理上讲，LINC01197 直接与细胞质多聚（A）结合蛋白 1（PABPC1）相互作用，进而封存并限制其功能。这项工作表明，LINC01197 可作为蛋白诱饵，抑制 IAV 复制，在控制 IAV 复制中发挥关键作用。

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LINC01197 inhibits influenza A virus replication by serving as a PABPC1 decoy.

Influenza A viruses (IAVs) significantly impact animal and human health due to their zoonotic potential. A growing body of evidence indicates that the host's long noncoding RNAs (lncRNAs) play crucial roles in regulating host-virus interactions during IAV infection. However, numerous lncRNAs associated with IAV infection have not been well characterised. Here, in this study, we identify the LINC01197 as an antiviral host factor. LINC01197 was significantly upregulated after IAV infection, which is controlled by the NF-κB pathway. Functional analysis revealed that overexpression of LINC01197 inhibited IAV replication and virus production, while knockdown of LINC01197 facilitated IAV replication. Mechanistically, LINC01197 directly interacts with poly(A) binding protein cytoplasmic 1 (PABPC1), which in turn sequesters and restricts its functions. This work shows that LINC01197 acts as a protein decoy, suppressing IAV replication and playing a key role in controlling IAV replication.

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来源期刊

Veterinary Research 农林科学-兽医学

CiteScore

7.00

自引率

4.50%

发文量

审稿时长

3 months

期刊介绍： Veterinary Research is an open access journal that publishes high quality and novel research and review articles focusing on all aspects of infectious diseases and host-pathogen interaction in animals.