Abstract
Outbreaks of influenza, caused by the influenza A virus (IAV), occur almost every year in various regions worldwide, seriously endangering human health. Studies have shown that host non-coding RNA is an important regulator of host–virus interactions in the process of IAV infection. In this paper, we comprehensively analyzed the research progress on host non-coding RNAs with regard to the regulation of IAV replication. According to the regulation mode of host non-coding RNAs, the signal pathways involved, and the specific target genes, we found that a large number of host non-coding RNAs directly targeted the PB1 and PB2 proteins of IAV. Nonstructural protein 1 and other key genes regulate the replication of IAV and indirectly participate in the regulation of the retinoic acid-induced gene I-like receptor signaling pathway, toll-like receptor signaling pathway, Janus kinase signal transducer and activator of transcription signaling pathway, and other major intracellular viral response signaling pathways to regulate the replication of IAV. Based on the above findings, we mapped the regulatory network of host non-coding RNAs in the innate immune response to the influenza virus. These findings will provide a more comprehensive understanding of the function and mechanism of host non-coding RNAs in the cellular anti-virus response as well as clues to the mechanism of cell–virus interactions and the discovery of antiviral drug targets.
Highlights
Publisher’s Note: MDPI stays neutralInfluenza viruses belong to the Orthomyxoviridae RNA virus family and is divided into genera A, B, C and D
Many different molecular signals are recruited to inhibit the replication of the influenza virus through a series of complex signal pathways, including pattern recognition receptors (PRRs)-dependent signal pathways, which can induce the production of interferon (IFN) and inflammatory factors, as well as the expression of antiviral IFN-stimulated genes with regard to jurisdictional claims in published maps and institutional affiliations
toll-like receptors (TLRs) a: ncRNAs target key genes; b : ncRNA mediated regulation of influenza virus replication; c : induced expression of ncRNA after influenza virus infection; d : sequences of miRNA binding site of target (50 -30 ); e : signaling pathways involved in regulation by ncRNA; f : target genes bound by ncRNAs
Summary
Influenza viruses belong to the Orthomyxoviridae RNA virus family and is divided into genera A, B, C and D. Viruses 2022, 14, 51 including PRR-dependent signal pathways, which can induce the production of interferon (IFN) and inflammatory factors, as well as the expression of antiviral IFN-stimulated genes (ISGs) [5,6,7,8] These proteins inhibit the replication of viruses in infected (ISGs) [5,6,7,8]. The natural immune response is the body’s first line of defense against viral infection and involves the activation of multiple antiviral signal pathways as well as the activation and expression of antiviral factors During this process, host noncoding RNAs are induced or inhibited by influenza virus infection, which mediates the activation of target genes, affects the expression of antiviral natural immune molecules, and indirectly regulates the replication and proliferation of influenza virus. The target gene sites in the natural immune response signaling pathway involved in the regulation of noncoding RNA are concentrated in the RLR signaling pathway, TLR-like receptor signaling pathway, JAK-STAT signal pathway, and NF-κB signaling pathway. (Dotted arrow is indirect effect; solid line is direct effect)
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