RNAi and retroviruses: are they in RISC?

Abstract

RNA interference (RNAi) is a potent cellular system against viruses in various organisms. Although common traits are observed in plants, insects, and nematodes, the situation observed in mammals appears more complex. In mammalian somatic cells, RNAi is implicated in endonucleolytic cleavage mediated by artificially delivered small interfering RNAs (siRNAs) as well as in translation repression mediated by microRNAs (miRNAs). Because siRNAs and miRNAs recognize viral mRNAs, RNAi inherently limits virus production and participates in antiviral defense. However, several observations made in the cases of hepatitis C virus and retroviruses (including the human immunodeficiency virus and the primate foamy virus) bring evidence that this relationship is much more complex and that certain components of the RNAi effector complex [called the RNA-induced silencing complex (RISC)], such as AGO2, are also required for viral replication. Here, we summarize recent discoveries that have revealed this dual implication in virus biology. We further discuss their potential implications for the functions of RNAi-related proteins, with special emphasis on retrotransposition and genome stability.

Filovirus Strategies to Escape Antiviral Responses

“…The related miRNA and RNAi pathways serve as cellular antiviral defense systems aside from their roles in normal cellular functions (Umbach and Cullen 2009;Haasnoot and Berkhout 2011;Vasselon et al 2013). Three EBOV proteins, VP30, VP35, and VP40, each inhibit RNA interference (RNAi) in co-transfection experiments (Haasnoot et al 2007;Fabozzi et al 2011).…”