Double-Stranded RNA Is Produced by Positive-Strand RNA Viruses and DNA Viruses but Not in Detectable Amounts by Negative-Strand RNA Viruses

Abstract

Double-stranded RNA (dsRNA) longer than 30 bp is a key activator of the innate immune response against viral infections. It is widely assumed that the generation of dsRNA during genome replication is a trait shared by all viruses. However, to our knowledge, no study exists in which the production of dsRNA by different viruses is systematically investigated. Here, we investigated the presence and localization of dsRNA in cells infected with a range of viruses, employing a dsRNA-specific antibody for immunofluorescence analysis. Our data revealed that, as predicted, significant amounts of dsRNA can be detected for viruses with a genome consisting of positive-strand RNA, dsRNA, or DNA. Surprisingly, however, no dsRNA signals were detected for negativestrand RNA viruses. Thus, dsRNA is indeed a general feature of most virus groups, but negative-strand RNA viruses appear to be an exception to that rule.

Citrus tristeza virus infection induces the accumulation of viral small RNAs (21–24-nt) mapping preferentially at the 3′-terminal region of the genomic RNA and affects the host small RNA profile

“…) and presum ably accum ulating in vivo at least transiently as reported for som e anim al viruses (Weber et al 2006)-are substrates for the citrus hom ologues of DCL2 and DCL4. The m od erate excess of (+) over (-) CTV sRN As basically results from the regions cod ing for p20 and p23 ( Fig.…”

Inactivation of the type I interferon pathway reveals long double‐stranded RNA‐mediated RNA interference in mammalian cells

“…However, the replication of IAV ΔNS1, like that of parental wild‐type IAV, was similar in Ago2 −/− Mavs −/− MEFs reconstituted to display an intact or a defective RNAi pathway (Appendix Fig S7D). Finally, because IAV is a negative‐sense ssRNA virus and may not produce sufficient amounts of dsRNA (Pichlmair et al , 2006; Weber et al , 2006), we also tested a (+)ssRNA picornavirus, EMCV. As a precaution, we chose an EMCV mutant lacking the L gene, which encodes an IFN antagonist (Hato et al , 2007) that could potentially act as a VSR.…”

“…Virus infection is often accompanied by generation of dsRNA or long base‐paired RNAs (Jacobs & Langland, 1996; Weber et al , 2006; Son et al , 2015). These can serve as substrates for Dicer to generate virus‐derived siRNAs (viRNAs) (Ding & Voinnet, 2007; Kemp & Imler, 2009; Swarts et al , 2014; tenOever, 2016) that are loaded onto RISC and target complementary viral RNA to block virus replication.…”

Synergistic activation of interferon‐β gene transcription by the viral FLICE inhibitory protein of Kaposi's sarcoma‐associated herpesvirus and type I IFN activators

“…As with most large DNA viruses, including pox-, adeno-and herpesviruses, viral gene transcription occurs on both DNA strands of the genome, producing easily detectable dsRNA molecules [20,21]. These RNA duplexes are therefore susceptible to be recognized by dsRNA-sensing molecules such as MDA-5 and TLR-3 [22][23][24][25].…”