A Novel lncRNA SAAL Suppresses IAV Replication by Promoting Innate Responses

文献类型： 外文期刊

第一作者： Liu, Qingzheng

作者： Liu, Qingzheng;Zhao, Lingcai;Huang, Nan;Ping, Jihui;Liu, Qingzheng;Yang, Hongjun;Liu, Qingzheng;Yang, Hongjun

作者机构：

关键词： influenza A virus; long noncoding RNAs; SAAL; Serpina3i; IFN-beta; ISGs

期刊名称：MICROORGANISMS （ 影响因子：4.926； 五年影响因子：5.143 ）

ISSN：

年卷期： 2022 年 10 卷 12 期

页码：

收录情况： SCI

摘要： Influenza A virus (IAV) infection has traditionally been a serious problem in animal husbandry and human public health security. Recently, many studies identified that long noncoding RNAs play an important role in the antiviral immune response after the infection of the influenza virus. However, there are still lots of IAV-related lncRNAs that have not been well-characterized. Using RNA sequencing analysis, we identified a lncRNA, named Serpina3i Activation Associated lncRNA (SAAL), which can be significantly upregulated in mice after IAV infection. In this study, we found that overexpression of SAAL inhibited the replication of A/WSN/33(WSN). SAAL upregulated Serpina3i with or without WSN infection. Overexpression of Serpina3i reduced influenza virus infection. Meanwhile, knockdown of Serpina3i enhanced the replication of WSN. Furthermore, knockdown of Serpina3i abolished the SAAL-mediated decrease in WSN infection. Overexpression of SAAL or Serpina3i positively regulated the transcription of interferon beta (IFN-beta) and several critical ISGs after WSN infection. In conclusion, we found that the novel lncRNA SAAL is a critical anti-influenza regulator by upregulating the mRNA level of Serpina3i.

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