RNA interference is an antiviral defence mechanism in Caenorhabditis elegans

• Published in: Nature 2005-08, Vol.436 (7053), p.1044-1047
• Main Authors: Chow, Marie, Machaca, Khaled, Wilkins, Courtney, Dishongh, Ryan, Moore, Steve C, Whitt, Michael A
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Caenorhabditis elegans; Caenorhabditis elegans - genetics; Caenorhabditis elegans - immunology; Caenorhabditis elegans - virology; Caenorhabditis elegans Proteins - genetics; Caenorhabditis elegans Proteins - metabolism; Cell culture; Cells, Cultured; Disease Models, Animal; Fundamental and applied biological sciences. Psychology; Genes; Humanities and Social Sciences; Infections; letter; Microbiology; multidisciplinary; Mutation - genetics; Pathogens; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains; Ribonucleic acid; RNA; RNA Interference; RNA, Small Interfering - genetics; RNA, Small Interfering - metabolism; RNA-Binding Proteins - genetics; RNA-Binding Proteins - metabolism; Science; Science (multidisciplinary); Substrate Specificity; Vesicular stomatitis Indiana virus - genetics; Vesicular stomatitis Indiana virus - growth & development; Vesicular stomatitis Indiana virus - immunology; Vesicular stomatitis virus; Virology; Viruses
• ISSN: 0028-0836; 1476-4687
• DOI: 10.1038/nature03957

RNA interference (RNAi) is an evolutionarily conserved sequence-specific post-transcriptional gene silencing mechanism that is well defined genetically in Caenorhabditis elegans. RNAi has been postulated to function as an adaptive antiviral immune mechanism in the worm, but there is no experimental evidence for this. Part of the limitation is that there are no known natural viral pathogens of C. elegans. Here we describe an infection model in C. elegans using the mammalian pathogen vesicular stomatitis virus (VSV) to study the role of RNAi in antiviral immunity. VSV infection is potentiated in cells derived from RNAi-defective worm mutants (rde-1; rde-4), leading to the production of infectious progeny virus, and is inhibited in mutants with an enhanced RNAi response (rrf-3; eri-1). Because the RNAi response occurs in the absence of exogenously added VSV small interfering RNAs, these results show that RNAi is activated during VSV infection and that RNAi is a genuine antiviral immune defence mechanism in the worm.