Achieving a more robust antiviral RNAi via subverting a viral virulence protein
Achieving a more robust antiviral RNAi via subverting a viral virulence protein
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DOI:
10.1016/j.molp.2022.09.020
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发表时间:
2022-09
期刊:
影响因子:
27.5
通讯作者:
Liyuan You;Ruize Zhang;Z. Fu
中科院分区:
文献类型:
--
作者:
Liyuan You;Ruize Zhang;Z. Fu
As submicroscopic organisms with small genomes, viruses can only replicate inside living cells. In fact, viruses can infect all forms of life, from animals and plants to microorganisms including fungi, bacteria, and archaea. Besides well-known human diseases such as human acquired immune deficiency syndrome, common cold, influenza, hepatitis, and coronavirus disease 2019, viral pathogens also cause more than $30 billion crop yield losses annually worldwide (Chauhan et al., 2019).RNA interference (RNAi), which is conserved in plants, nematodes, fungi, vertebrates, and invertebrates, has been proven to play a major role in host defense against viral pathogens. RNAi is also known as post-transcriptional gene silencing, cosuppression, or quelling. Gene silencing was first discovered in plants (Lindbo and Dougherty, 2005). Dicer or Dicer-like proteins process viral RNAs into small RNAs, which then guide Argonautecontaining RNAi-induced silencing complex (RISC) to the targets in viral RNAs through Watson-Crick base pairing, resulting in viral repression (Wilson and Doudna, 2013). Host-adapted viral pathogens, however, developed suppressor of RNAi (VSR), which antagonizes antiviral RNAi. For example, the nucleocapsid protein from SARS-CoV-1/2 suppresses the production of viralderived small interfering RNAs (vsiRNAs) through doublestranded RNA sequestration (Li and Ding, 2022). On the other hand, the HC-Pro VSR of potyviruses binds vsiRNAs and inhibits their loading onto Argonaute proteins (Valli et al., 2018).