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      Dicer-2-Dependent Generation of Viral DNA from Defective Genomes of RNA Viruses Modulates Antiviral Immunity in Insects

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          Summary

          The RNAi pathway confers antiviral immunity in insects. Virus-specific siRNA responses are amplified via the reverse transcription of viral RNA to viral DNA (vDNA). The nature, biogenesis, and regulation of vDNA are unclear. We find that vDNA produced during RNA virus infection of Drosophila and mosquitoes is present in both linear and circular forms. Circular vDNA (cvDNA) is sufficient to produce siRNAs that confer partially protective immunity when challenged with a cognate virus. cvDNAs bear homology to defective viral genomes (DVGs), and DVGs serve as templates for vDNA and cvDNA synthesis. Accordingly, DVGs promote the amplification of vDNA-mediated antiviral RNAi responses in infected Drosophila. Furthermore, vDNA synthesis is regulated by the DExD/H helicase domain of Dicer-2 in a mechanism distinct from its role in siRNA generation. We suggest that, analogous to mammalian RIG-I-like receptors, Dicer-2 functions like a pattern recognition receptor for DVGs to modulate antiviral immunity in insects.

          Graphical Abstract

          Highlights

          • •

            Circular viral DNAs (vDNAs) produced during RNA virus infection are a source of siRNAs

          • •

            Defective viral genomes (DVG) serve as templates for vDNA synthesis

          • •

            The helicase domain of Dicer-2 modulates vDNA production and virus persistence

          • •

            DVGs serve to amplify siRNA-mediated antiviral immunity in insects

          Abstract

          Poirier et al. show that during RNA virus infection of insects, circular viral DNA is produced, regulated by Dicer-2 helicase domain. The main template for viral DNA is defective viral genomes, which appear to be key viral products modulating the host immune response and the establishment of viral persistence.

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          Argonaute2 is the catalytic engine of mammalian RNAi.

          Jidong Liu, Michelle A Carmell, Fabiola V Rivas … (2004)
          Gene silencing through RNA interference (RNAi) is carried out by RISC, the RNA-induced silencing complex. RISC contains two signature components, small interfering RNAs (siRNAs) and Argonaute family proteins. Here, we show that the multiple Argonaute proteins present in mammals are both biologically and biochemically distinct, with a single mammalian family member, Argonaute2, being responsible for messenger RNA cleavage activity. This protein is essential for mouse development, and cells lacking Argonaute2 are unable to mount an experimental response to siRNAs. Mutations within a cryptic ribonuclease H domain within Argonaute2, as identified by comparison with the structure of an archeal Argonaute protein, inactivate RISC. Thus, our evidence supports a model in which Argonaute contributes "Slicer" activity to RISC, providing the catalytic engine for RNAi.
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            Distinct roles for Drosophila Dicer-1 and Dicer-2 in the siRNA/miRNA silencing pathways.

            Young Lee, Kenji S Nakahara, John W. Pham … (2004)
            The RNase III enzyme Dicer processes RNA into siRNAs and miRNAs, which direct a RNA-induced silencing complex (RISC) to cleave mRNA or block its translation (RNAi). We have characterized mutations in the Drosophila dicer-1 and dicer-2 genes. Mutation in dicer-1 blocks processing of miRNA precursors, whereas dicer-2 mutants are defective for processing siRNA precursors. It has been recently found that Drosophila Dicer-1 and Dicer-2 are also components of siRNA-dependent RISC (siRISC). We find that Dicer-1 and Dicer-2 are required for siRNA-directed mRNA cleavage, though the RNase III activity of Dicer-2 is not required. Dicer-1 and Dicer-2 facilitate distinct steps in the assembly of siRISC. However, Dicer-1 but not Dicer-2 is essential for miRISC-directed translation repression. Thus, siRISCs and miRISCs are different with respect to Dicers in Drosophila.
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              Why do RNA viruses recombine?

              Etienne Simon-Loriere, Edward C. Holmes (2011)
              Key Points RNA viruses are able to undergo two forms of recombination: RNA recombination, which (in principle) can occur in any type of RNA virus, and reassortment, which is restricted to those viruses with segmented genomes. Rates of RNA recombination vary markedly among RNA viruses. Some viruses, particularly those with negative-sense single-stranded genomes, exhibit such low rates of recombination that they are effectively clonal. By contrast, some positive-sense single-stranded RNA viruses and some retroviruses such as HIV exhibit high rates of recombination that can exceed the rates of mutation when measured per nucleotide. Although recombination is often argued to represent a form of sexual reproduction, there is little evidence that recombination in RNA viruses evolved as a way of creating advantageous genotypes or removing deleterious mutations. In particular, there is no association between recombination frequency and the burden of a deleterious mutation. Similarly, there is little evidence that recombination could have been selected as a form of genetic repair. The strongest association for rates of recombination in RNA viruses is with genome structure. Hence, negative-sense single-stranded RNA viruses may recombine at low rates because of the restrictive association of genomic RNA in a ribonucleoprotein complex, as well as a lack of substrates for template switching, whereas some retroviruses recombine rapidly because their virions contain two genome copies and template switching between these copies is an inevitable part of the viral replication cycle. We therefore hypothesize that recombination in RNA viruses is a mechanistic by-product of the processivity of the viral polymerase that is used in replication, and that it varies with genome structure.
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                Author and article information

                Contributors
                Marco Vignuzzi
                Maria-Carla Saleh
                Journal
                Journal ID (nlm-ta): Cell Host Microbe
                Journal ID (iso-abbrev): Cell Host Microbe
                Title: Cell Host & Microbe
                Publisher: Cell Press
                ISSN (Print): 1931-3128
                ISSN (Electronic): 1934-6069
                Publication date PMC-release: 14 March 2018
                Publication date (Print): 14 March 2018
                Volume: 23
                Issue: 3
                Pages: 353-365.e8
                Affiliations
                [1 ]Institut Pasteur, Viruses and RNA Interference, Centre National de la Recherche Scientifique UMR 3569, 75015 Paris, France
                [2 ]Institut Pasteur, Viral Populations and Pathogenesis, Centre National de la Recherche Scientifique UMR 3569, 75015 Paris, France
                [3 ]University of Paris Diderot, Sorbonne Paris Cité, Cellule Pasteur, 75013 Paris, France
                [4 ]Institut Pasteur, Immunobiology of Dendritic Cells, Institut National de la Santé et de la Recherche Médicale, U1223, 75015 Paris, France
                [5 ]Department of Animal Science, Iowa State University, Ames, IA 50010, USA
                [6 ]Institut de Recherche pour le Développement, DIADE, Université de Montpellier, Université de Perpignan, LGDP, 66860 Perpignan, France
                [7 ]Institut Pasteur, Insect-Virus Interactions, Centre National de la Recherche Scientifique URA 3012, 75015 Paris, France
                Author notes
                [∗ ]Corresponding author marco.vignuzzi@ 123456pasteur.fr
                [∗∗ ]Corresponding author carla.saleh@ 123456pasteur.fr
                [8]

                These authors contributed equally

                [9]

                Lead Contact

                Article
                Publisher ID: S1931-3128(18)30087-8
                DOI: 10.1016/j.chom.2018.02.001
                PMC ID: 5857290
                PubMed ID: 29503180
                SO-VID: dc77a8eb-09a7-4336-a26f-1eb785dcf36d
                Copyright © © 2018 The Author(s)
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 17 May 2017
                Date revision received : 8 November 2017
                Date accepted : 7 February 2018
                Categories
                Subject: Article

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: rna virus,arbovirus,insect,persistence,rnai,dicer-2,circular viral dna,defective viral genomes
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: rna virus, arbovirus, insect, persistence, rnai, dicer-2, circular viral dna, defective viral genomes

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