RNAi is a natural antiviral immune path in mammals.

In a June 21 paper published in the international academic journal Immunity, scientists showed that RNA interference (RNAi), which was previously only recognized as an antiviral immune role in fungi, plants and invertebrates, could do the same in mammals.
this work was carried out by the Zhouxi Researcher Group of Wuhan Virus Research Institute of the Chinese Academy of Sciences and the Qin Chengfeng Research Group of the Institute of Microbiology Epidemiology of the Academy of Military Medical Sciences.
international peer evaluation, this work improves the understanding of antiviral immune mechanisms in mammals and provides a theoretical basis for the design of antiviral drugs or immunotherapy research.
RNA interference (RNAi) is a highly conservative post-transcriptional gene silencing mechanism in ethon organisms.
Scientists have long found that when viruses invade fungi, plants, and invertebrates, the double-stranded RNA produced by viral RNA replication is identified and cut into small interfering RNA (siRNAs) by the host RNAi path, and that siRNAs derived from these viruses are loaded into RISC, an RNA-silent complex downstream of the RNAi path, to mediate the degradation of congener virus RNA for antiviral purposes.
although RNAi is also conservative in mammals and is widely used in life sciences and technology research, it remains unclear whether RNAi also plays an antiviral immune role in mammals.
in this study, the researchers used human body cells and mice infected with human enterovirus type 71 (EV71) as models and found that EV71 unstructured protein 3A inhibited the production of small interfering RNAs by binding to the virus's double-stranded RNA.
this feature is called "VSR."
vsR defective EV71 virus stimulates RNAi reactions in cells and mice, producing large amounts of virus siRNA, which eventually degrades the RNA of the same virus.
researchers found that in normal human cells and mice, vsR defective virus replication was significantly inhibited, while in cells with missing RNAi pathpes, replication of mutant viruses was significantly saved.
, the researchers also demonstrated that RNAi's antiviral role in mammals does not depend on interferon reactions. The
researchers noted that the study found that viral infections at the human cellular and animal levels could produce antiviral-functional siRNAs, confirming that RNAi is a natural antiviral immune path in mammals, and also revealed a specific mechanism for human viruses to escape RNAi's natural immunity.
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