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Identification of a small protein encoded by PCBP1-AS1 that promotes replication of influenza virus via inducing enhancement of autophagy

ABSTRACT: Many annotated long noncoding RNAs (lncRNAs) contain small open reading frames (sORFs), some of which have been demonstrated to encode small proteins or micropeptides with fundamental biological importance. However, the small proteins or micropeptides encoded by lncRNAs and their functions in viral infection remain largely unexplored. Here, we identified and characterized a small 110-amino acid protein named ORF6 encoded by the putative lncRNA PCBP1-AS1. Interestingly, both PCBP1-AS1 and ORF6 were significantly upregulated by influenza virus infection. Furthermore, we observed that they were markedly induced by type I interferon treatment. Overexpression of PCBP1-AS1 or ORF6 enhanced influenza virus replication. Conversely, knockdown of PCBP1-AS1 or knockout of ORF6 inhibited the viral production. In addition, loss-of-function experiment demonstrated that ORF6 is essential for PCBP1-AS1 to facilitate influenza virus replication. Importantly, the overexpression of ORF6 induced enhancement of autophagy by increasing the expression of ATG7, a gene encoding an essential effector enzyme for canonical autophagy. These findings reveal a lncRNA-derived small protein that is exploited by influenza virus, and provide new insights into the virus-host regulatory network.

ORGANISM(S): Homo sapiens

PROVIDER: GSE253139 | GEO | 2024/08/03

REPOSITORIES: GEO

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A small protein encoded by lncRNA PCBP1-AS1 promotes the replication of influenza virus via regulating the expression of proviral effectors (Ribo-Seq)

Project description:Many annotated long noncoding RNAs (lncRNAs) contain small open reading frames (sORFs), some of which have been demonstrated to encode small proteins or micropeptides with fundamental biological importance. While the small proteins or micropeptides hidden in lncRNA are gradually being revealed, their functions in influenza virus infection remain largely unexplored. Here, we identified and characterized a small 110-amino acid protein named PAESP that is encoded by the putative lncRNA PCBP1-AS1. We found that both PCBP1-AS1 and PAESP were upregulated by influenza virus infection as well as type I interferon treatment. Overexpression of PCBP1-AS1 or PAESP enhanced influenza virus replication. Conversely, knockdown of PCBP1-AS1 or knockout of PAESP inhibited viral production. In addition, loss-of-function experiment demonstrated that PAESP is essential for PCBP1-AS1 to facilitate influenza virus replication. More importantly, the overexpression of PAESP increases the mRNA level of several genes such as IFIT2 and IFIT3, which have been proved to be retasked by influenza virus from canonical antiviral factors into proviral effectors. Interestingly, when IFIT2 or IFIT3 expression was knocked down in PAESP-overexpressed cells, the virus titers significantly decreased compared to control cells. These findings reveal a novel lncRNA-derived small protein that is exploited by influenza virus and provide new insights into the virus-host regulatory network.

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