{"title":"抗病毒 RNA 干扰诱导的 RNA 和 DNA 病毒感染缺陷","authors":"Si Liu, Yanhong Han, Wan-Xiang Li, Shou-Wei Ding","doi":"10.1128/mmbr.00035-22","DOIUrl":null,"url":null,"abstract":"<p><p>Immune recognition of viral genome-derived double-stranded RNA (dsRNA) molecules and their subsequent processing into small interfering RNAs (siRNAs) in plants, invertebrates, and mammals trigger specific antiviral immunity known as antiviral RNA interference (RNAi). Immune sensing of viral dsRNA is sequence-independent, and most regions of viral RNAs are targeted by virus-derived siRNAs which extensively overlap in sequence. Thus, the high mutation rates of viruses do not drive immune escape from antiviral RNAi, in contrast to other mechanisms involving specific virus recognition by host immune proteins such as antibodies and resistance (R) proteins in mammals and plants, respectively. Instead, viruses actively suppress antiviral RNAi at various key steps with a group of proteins known as viral suppressors of RNAi (VSRs). Some VSRs are so effective in virus counter-defense that potent inhibition of virus infection by antiviral RNAi is undetectable unless the cognate VSR is rendered nonexpressing or nonfunctional. Since viral proteins are often multifunctional, resistance phenotypes of antiviral RNAi are accurately defined by those infection defects of VSR-deletion mutant viruses that are efficiently rescued by host deficiency in antiviral RNAi. Here, we review and discuss <i>in vivo</i> infection defects of VSR-deficient RNA and DNA viruses resulting from the actions of host antiviral RNAi in model systems.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0000,"publicationDate":"2023-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10304667/pdf/","citationCount":"0","resultStr":"{\"title\":\"Infection Defects of RNA and DNA Viruses Induced by Antiviral RNA Interference.\",\"authors\":\"Si Liu, Yanhong Han, Wan-Xiang Li, Shou-Wei Ding\",\"doi\":\"10.1128/mmbr.00035-22\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Immune recognition of viral genome-derived double-stranded RNA (dsRNA) molecules and their subsequent processing into small interfering RNAs (siRNAs) in plants, invertebrates, and mammals trigger specific antiviral immunity known as antiviral RNA interference (RNAi). Immune sensing of viral dsRNA is sequence-independent, and most regions of viral RNAs are targeted by virus-derived siRNAs which extensively overlap in sequence. Thus, the high mutation rates of viruses do not drive immune escape from antiviral RNAi, in contrast to other mechanisms involving specific virus recognition by host immune proteins such as antibodies and resistance (R) proteins in mammals and plants, respectively. Instead, viruses actively suppress antiviral RNAi at various key steps with a group of proteins known as viral suppressors of RNAi (VSRs). Some VSRs are so effective in virus counter-defense that potent inhibition of virus infection by antiviral RNAi is undetectable unless the cognate VSR is rendered nonexpressing or nonfunctional. Since viral proteins are often multifunctional, resistance phenotypes of antiviral RNAi are accurately defined by those infection defects of VSR-deletion mutant viruses that are efficiently rescued by host deficiency in antiviral RNAi. Here, we review and discuss <i>in vivo</i> infection defects of VSR-deficient RNA and DNA viruses resulting from the actions of host antiviral RNAi in model systems.</p>\",\"PeriodicalId\":18520,\"journal\":{\"name\":\"Microbiology and Molecular Biology Reviews\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":8.0000,\"publicationDate\":\"2023-06-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10304667/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Microbiology and Molecular Biology Reviews\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1128/mmbr.00035-22\",\"RegionNum\":1,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/4/13 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Microbiology and Molecular Biology Reviews","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1128/mmbr.00035-22","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/4/13 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
Infection Defects of RNA and DNA Viruses Induced by Antiviral RNA Interference.
Immune recognition of viral genome-derived double-stranded RNA (dsRNA) molecules and their subsequent processing into small interfering RNAs (siRNAs) in plants, invertebrates, and mammals trigger specific antiviral immunity known as antiviral RNA interference (RNAi). Immune sensing of viral dsRNA is sequence-independent, and most regions of viral RNAs are targeted by virus-derived siRNAs which extensively overlap in sequence. Thus, the high mutation rates of viruses do not drive immune escape from antiviral RNAi, in contrast to other mechanisms involving specific virus recognition by host immune proteins such as antibodies and resistance (R) proteins in mammals and plants, respectively. Instead, viruses actively suppress antiviral RNAi at various key steps with a group of proteins known as viral suppressors of RNAi (VSRs). Some VSRs are so effective in virus counter-defense that potent inhibition of virus infection by antiviral RNAi is undetectable unless the cognate VSR is rendered nonexpressing or nonfunctional. Since viral proteins are often multifunctional, resistance phenotypes of antiviral RNAi are accurately defined by those infection defects of VSR-deletion mutant viruses that are efficiently rescued by host deficiency in antiviral RNAi. Here, we review and discuss in vivo infection defects of VSR-deficient RNA and DNA viruses resulting from the actions of host antiviral RNAi in model systems.
期刊介绍:
Microbiology and Molecular Biology Reviews (MMBR), a journal that explores the significance and interrelationships of recent discoveries in various microbiology fields, publishes review articles that help both specialists and nonspecialists understand and apply the latest findings in their own research. MMBR covers a wide range of topics in microbiology, including microbial ecology, evolution, parasitology, biotechnology, and immunology. The journal caters to scientists with diverse interests in all areas of microbial science and encompasses viruses, bacteria, archaea, fungi, unicellular eukaryotes, and microbial parasites. MMBR primarily publishes authoritative and critical reviews that push the boundaries of knowledge, appealing to both specialists and generalists. The journal often includes descriptive figures and tables to enhance understanding. Indexed/Abstracted in various databases such as Agricola, BIOSIS Previews, CAB Abstracts, Cambridge Scientific Abstracts, Chemical Abstracts Service, Current Contents- Life Sciences, EMBASE, Food Science and Technology Abstracts, Illustrata, MEDLINE, Science Citation Index Expanded (Web of Science), Summon, and Scopus, among others.