Wu Qingfa team found a new mechanism of natural immunity mediated by long non-coding RNA.

RNAi is a conserved natural immune mechanism against virus. It has been proved that fungi, plants, invertebrates and mammals (including human beings) play a key role in antiviral activities.viruses usually encode RNA silencing suppressor (VSR) to inhibit the host's RNAi response in order to escape the host's immune response.on January 8, 2020, Professor Wu Qingfa, School of life, University of science and technology of China published an article lncrna sensing of a viral suppressor of RNAi activates non canonical innate immune signaling in the journal Cell Host microbe Drosophila, for the first time, reported that the host perceives the viral VSR through long noncoding RNA, and then activates a new nonclassical innate immune pathway.in this study, the naturally infected Drosophila C virus (DCV) was selected as the research object. The dcv-1a protein encoded by the virus protected the dsRNA from being cut into siRNA through its double stranded RNA binding domain, thus inhibiting the host's RNAi response.the researchers found that: 1) a new long non coding RNA vinr was identified in Drosophila melanogaster, and vinr was selectively upregulated in Drosophila cells infected with DCV virus or exogenous expression of dcv-1a.2) reducing / eliminating vinr level by RNAi or crispr-cas9 technology can increase the replication of DCV in cells, but it has no obvious effect on other viruses. It was found that vinr could escape from the RNA degradation environment and increase the half-life of vinr through the direct binding of vinr to dcv-1a cells, which resulted in the accumulation of vinr in DCV infected or dcv-1a expressing cells. (BR / >4) vinr does not affect the function of dcv-1a in inhibiting RNAi, and does not participate in the known antiviral immune pathways such as RNAi, JAK-STAT, dcr-2 / vago, sting / Nazo, etc., but vinr is necessary for DCV to induce the expression of antimicrobial peptide genes, which are known to be regulated by toll and IMD pathways. It was found that vinr could bind to cactin protein and stabilize the level of cactin protein by inhibiting ubiquitination of cactin protein. It was also found that vinr specifically inhibited DCV replication through cactin in Drosophila cells.6) it was found that cactin can regulate the expression of some antimicrobial peptide genes known to be regulated by toll and IMD pathways by binding with transcription factor deaf1 and universal transcription factor RNA polymerase II. The results showed that vinr knockout Drosophila was not only susceptible to DCV, but also more susceptible to gram-positive and Gram-negative bacteria.this work not only deepens the understanding of the complexity of host virus interaction mechanism, but also expands the understanding of the biological function of lncrna.lncrna vinr regulates immune gene expression. The work was completed by Professor Wu Qingfa, School of life, University of science and technology of China.Zhang Liqin, a postdoctoral student, and Xu Wen, a doctoral student, are the first authors of the paper, and Professor Wu Qingfa is the corresponding author of the paper.original link: plate maker: Ke