Abstract
Non-coding RNAs (ncRNAs) are a new type of regulators that play important roles in various cellular processes, including cell growth, differentiation, survival, and apoptosis. ncRNAs, including small non-coding RNAs (e.g., microRNAs, small interfering RNAs) and long non-coding RNAs (lncRNAs), are pervasively transcribed in human and mammalian cells. Recently, it has been recognized that these ncRNAs are critically implicated in the virus–host interaction as key regulators of transcription or post-transcription during viral infection. Influenza A virus (IAV) is still a major threat to human health. Hundreds of ncRNAs are differentially expressed in response to infection with IAV, such as infection by pandemic H1N1 and highly pathogenic avian strains. There is increasing evidence demonstrating functional involvement of these regulatory microRNAs, vault RNAs (vtRNAs) and lncRNAs in pathogenesis of influenza virus, including a variety of host immune responses. For example, it has been shown that ncRNAs regulate activation of pattern recognition receptor (PRR)-associated signaling and transcription factors (nuclear factor κ-light-chain-enhancer of activated B cells, NF-κB), as well as production of interferons (IFNs) and cytokines, and expression of critical IFN-stimulated genes (ISGs). The vital functions of IAV-regulated ncRNAs either to against defend viral invasion or to promote progeny viron production are summarized in this review. In addition, we also highlight the potentials of ncRNAs as therapeutic targets and diagnostic biomarkers.
Highlights
One of the most important discoveries contributed by transcriptome projects ENCODE and GENCODE is the finding that more than 85% of human genome are transcribed to RNA, but less than 3% of genome encode proteins, and most transcripts of human genome are non-coding RNAs without protein-coding capacity [1,2]
We summarize the roles of ncRNAs, including microRNAs, long non-coding RNAs (lncRNAs) and vault RNAs (vtRNAs), in the influenza virus pathogenesis
It was observed that during the early stage of Influenza A virus (IAV) infection, the virus induces the downregulation of miR-548an and subsequently increases the abundance of non-structural-1A binding protein (NS1ABP), a host protein that mediates the inhibition of apoptosis and facilitates the virus replication [60,63]
Summary
One of the most important discoveries contributed by transcriptome projects ENCODE and GENCODE is the finding that more than 85% of human genome are transcribed to RNA, but less than 3% of genome encode proteins, and most transcripts of human genome are non-coding RNAs (ncRNAs) without protein-coding capacity [1,2]. The number of human long non-coding RNA genes (lncRNAs, >200 nt) is 15,767, in addition to 14,650 pseudogenes. Series cascades of transcription and activation in innate immune response are triggered, including the PRR-dependent signaling pathways, production of IFNs and other cytokines, and expression of antiviral ISGs [14]. These proteins inhibit virus replication in the infected cells, and recruit dendritic cells and macrophages to virus infected tissues, and further stimulate the immune response mediated by T cells and B cells [15]. The mechanisms underlying involvement of these ncRNAs in the virus infection will be discussed
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