State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, 130062, Changchun, Jilin Province, China.
College of Basic Medical Sciences, Jilin University, 130021, Changchun, Jilin Province, China.
Vet Res. 2024 Sep 27;55(1):121. doi: 10.1186/s13567-024-01379-7.
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.
甲型流感病毒（IAV）由于其潜在的人畜共患病性，对动物和人类的健康产生重大影响。越来越多的证据表明，宿主的长非编码 RNA（lncRNA）在 IAV 感染期间调节宿主-病毒相互作用中发挥着关键作用。然而，许多与 IAV 感染相关的 lncRNA 尚未得到很好的描述。在本研究中，我们鉴定了 LINC01197 作为一种抗病毒宿主因子。IAV 感染后，LINC01197 的表达显著上调，这受 NF-κB 通路的调控。功能分析显示，LINC01197 的过表达抑制了 IAV 的复制和病毒生成，而 LINC01197 的敲低则促进了 IAV 的复制。在机制上，LINC01197 直接与多聚（A）结合蛋白细胞质 1（PABPC1）相互作用，从而将其隔离并限制其功能。这项工作表明，LINC01197 作为一种蛋白诱饵，抑制 IAV 的复制，在控制 IAV 复制中发挥关键作用。
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