1. Departments of Microbiology and Immunology and
2. Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
3. Department of Biology, Harding University, Searcy, Arkansas 72149, USA
4. Department of Molecular Sciences, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA

Correspondence to: Marie Chow¹Khaled Machaca² Correspondence and requests for materials should be addressed to M.C. (Email: chowmarie@uams.edu) or K.M. (Email: kamachaca@uams.edu).

Abstract

RNA interference (RNAi) is an evolutionarily conserved sequence-specific post-transcriptional gene silencing mechanism that is well defined genetically in Caenorhabditis elegans^{1, 2, 3, 4}. 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.

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