Dicer-2-Dependent Generation of Viral DNA from Defective Genomes of RNA Viruses Modulates Antiviral Immunity in Insects
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 mos...
Gespeichert in:
Veröffentlicht in: | Cell host & microbe 2018-03, Vol.23 (3), p.353-365.e8 |
---|---|
Hauptverfasser: | , , , , , , , , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 365.e8 |
---|---|
container_issue | 3 |
container_start_page | 353 |
container_title | Cell host & microbe |
container_volume | 23 |
creator | Poirier, Enzo Z. Goic, Bertsy Tomé-Poderti, Lorena Frangeul, Lionel Boussier, Jérémy Gausson, Valérie Blanc, Hervé Vallet, Thomas Loyd, Hyelee Levi, Laura I. Lanciano, Sophie Baron, Chloé Merkling, Sarah H. Lambrechts, Louis Mirouze, Marie Carpenter, Susan Vignuzzi, Marco Saleh, Maria-Carla |
description | 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.
[Display omitted]
•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
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. |
doi_str_mv | 10.1016/j.chom.2018.02.001 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5857290</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1931312818300878</els_id><sourcerecordid>2010839223</sourcerecordid><originalsourceid>FETCH-LOGICAL-c559t-bd606bb56e004bb9e223c9584c305034f8191fc5a0a3477b4d9f44fe540061783</originalsourceid><addsrcrecordid>eNp9kUFv1DAQhSMEoqXwBzigHLkkjJ04iSWEtOpCu9ICEgKuluNMWK8Se7GTrfrvmXRLBRw4eSx_79nPL0leMsgZsOrNPjc7P-YcWJMDzwHYo-ScyaLMKqjk47uZZQXjzVnyLMY9gBBQs6fJGZcCCtbAeXKztgZDxrM1HtB16Kb0Ch0GPVnvUt-n323QQ7r-tEr74Md0jT2ayR5xwfyIcWG-0Clxc6TtR9_Ng55oWjni7tSbcZydnW5T69KNi2QQnydPej1EfHG_XiTfPrz_enmdbT9fbS5X28wIIaes7ShK24oKAcq2lch5YaRoSlMARSj7hknWG6FBF2Vdt2Un-7LsUZQAFaub4iJ5d_I9zO2InaGA9CJ1CHbU4VZ5bdXfJ87u1A9_VKIRNZdABtnJYPeP7Hq1VQcdJ5yDAiYFFwU7MuJf318Y_M8Z46RGGw0Og3bo56ioLWgKSTkI5SfUBB9jwP7Bn4FaGlZ7tTS8aBoFXFHDJHr1Z6AHye9KCXh7ApC-9WgxqGgsOoOdDfTzqvP2f_6_AEQMt14</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2010839223</pqid></control><display><type>article</type><title>Dicer-2-Dependent Generation of Viral DNA from Defective Genomes of RNA Viruses Modulates Antiviral Immunity in Insects</title><source>MEDLINE</source><source>Cell Press Free Archives</source><source>Elsevier ScienceDirect Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Poirier, Enzo Z. ; Goic, Bertsy ; Tomé-Poderti, Lorena ; Frangeul, Lionel ; Boussier, Jérémy ; Gausson, Valérie ; Blanc, Hervé ; Vallet, Thomas ; Loyd, Hyelee ; Levi, Laura I. ; Lanciano, Sophie ; Baron, Chloé ; Merkling, Sarah H. ; Lambrechts, Louis ; Mirouze, Marie ; Carpenter, Susan ; Vignuzzi, Marco ; Saleh, Maria-Carla</creator><creatorcontrib>Poirier, Enzo Z. ; Goic, Bertsy ; Tomé-Poderti, Lorena ; Frangeul, Lionel ; Boussier, Jérémy ; Gausson, Valérie ; Blanc, Hervé ; Vallet, Thomas ; Loyd, Hyelee ; Levi, Laura I. ; Lanciano, Sophie ; Baron, Chloé ; Merkling, Sarah H. ; Lambrechts, Louis ; Mirouze, Marie ; Carpenter, Susan ; Vignuzzi, Marco ; Saleh, Maria-Carla</creatorcontrib><description>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.
[Display omitted]
•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
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.</description><identifier>ISSN: 1931-3128</identifier><identifier>ISSN: 1934-6069</identifier><identifier>EISSN: 1934-6069</identifier><identifier>DOI: 10.1016/j.chom.2018.02.001</identifier><identifier>PMID: 29503180</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Antiviral Agents ; arbovirus ; Arboviruses ; Arboviruses - immunology ; Arboviruses - pathogenicity ; Biochemistry, Molecular Biology ; circular viral DNA ; Culicidae ; Culicidae - immunology ; DEAD-box RNA Helicases ; DEAD-box RNA Helicases - metabolism ; defective viral genomes ; Dicer-2 ; DNA, Viral ; DNA, Viral - metabolism ; Drosophila ; Drosophila - immunology ; Drosophila Proteins ; Drosophila Proteins - genetics ; Drosophila Proteins - metabolism ; Genes, Viral ; Genes, Viral - genetics ; Genome, Viral ; Genomics ; Host-Pathogen Interactions ; Host-Pathogen Interactions - genetics ; Host-Pathogen Interactions - immunology ; Immunology ; insect ; Life Sciences ; Microbiology and Parasitology ; Molecular biology ; persistence ; Point Mutation ; Ribonuclease III ; Ribonuclease III - genetics ; Ribonuclease III - metabolism ; RNA Helicases ; RNA Helicases - genetics ; RNA Helicases - metabolism ; RNA Interference ; RNA Interference - immunology ; RNA virus ; RNA Virus Infections ; RNA Viruses ; RNA Viruses - genetics ; RNA Viruses - immunology ; RNA Viruses - pathogenicity ; RNA, Small Interfering ; RNA, Small Interfering - genetics ; RNA, Viral ; RNA, Viral - metabolism ; RNAi ; Viral Load ; Virology ; Virus Replication</subject><ispartof>Cell host & microbe, 2018-03, Vol.23 (3), p.353-365.e8</ispartof><rights>2018 The Author(s)</rights><rights>Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.</rights><rights>Attribution - NonCommercial - ShareAlike</rights><rights>2018 The Author(s) 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559t-bd606bb56e004bb9e223c9584c305034f8191fc5a0a3477b4d9f44fe540061783</citedby><cites>FETCH-LOGICAL-c559t-bd606bb56e004bb9e223c9584c305034f8191fc5a0a3477b4d9f44fe540061783</cites><orcidid>0000-0001-8593-4117 ; 0000-0002-2249-377X ; 0000-0002-6823-4474 ; 0000-0001-5958-2138 ; 0000-0002-0992-8775 ; 0000-0002-9727-3448 ; 0000-0002-0514-1270</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1931312818300878$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29503180$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://pasteur.hal.science/pasteur-01952531$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Poirier, Enzo Z.</creatorcontrib><creatorcontrib>Goic, Bertsy</creatorcontrib><creatorcontrib>Tomé-Poderti, Lorena</creatorcontrib><creatorcontrib>Frangeul, Lionel</creatorcontrib><creatorcontrib>Boussier, Jérémy</creatorcontrib><creatorcontrib>Gausson, Valérie</creatorcontrib><creatorcontrib>Blanc, Hervé</creatorcontrib><creatorcontrib>Vallet, Thomas</creatorcontrib><creatorcontrib>Loyd, Hyelee</creatorcontrib><creatorcontrib>Levi, Laura I.</creatorcontrib><creatorcontrib>Lanciano, Sophie</creatorcontrib><creatorcontrib>Baron, Chloé</creatorcontrib><creatorcontrib>Merkling, Sarah H.</creatorcontrib><creatorcontrib>Lambrechts, Louis</creatorcontrib><creatorcontrib>Mirouze, Marie</creatorcontrib><creatorcontrib>Carpenter, Susan</creatorcontrib><creatorcontrib>Vignuzzi, Marco</creatorcontrib><creatorcontrib>Saleh, Maria-Carla</creatorcontrib><title>Dicer-2-Dependent Generation of Viral DNA from Defective Genomes of RNA Viruses Modulates Antiviral Immunity in Insects</title><title>Cell host & microbe</title><addtitle>Cell Host Microbe</addtitle><description>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.
[Display omitted]
•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
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.</description><subject>Animals</subject><subject>Antiviral Agents</subject><subject>arbovirus</subject><subject>Arboviruses</subject><subject>Arboviruses - immunology</subject><subject>Arboviruses - pathogenicity</subject><subject>Biochemistry, Molecular Biology</subject><subject>circular viral DNA</subject><subject>Culicidae</subject><subject>Culicidae - immunology</subject><subject>DEAD-box RNA Helicases</subject><subject>DEAD-box RNA Helicases - metabolism</subject><subject>defective viral genomes</subject><subject>Dicer-2</subject><subject>DNA, Viral</subject><subject>DNA, Viral - metabolism</subject><subject>Drosophila</subject><subject>Drosophila - immunology</subject><subject>Drosophila Proteins</subject><subject>Drosophila Proteins - genetics</subject><subject>Drosophila Proteins - metabolism</subject><subject>Genes, Viral</subject><subject>Genes, Viral - genetics</subject><subject>Genome, Viral</subject><subject>Genomics</subject><subject>Host-Pathogen Interactions</subject><subject>Host-Pathogen Interactions - genetics</subject><subject>Host-Pathogen Interactions - immunology</subject><subject>Immunology</subject><subject>insect</subject><subject>Life Sciences</subject><subject>Microbiology and Parasitology</subject><subject>Molecular biology</subject><subject>persistence</subject><subject>Point Mutation</subject><subject>Ribonuclease III</subject><subject>Ribonuclease III - genetics</subject><subject>Ribonuclease III - metabolism</subject><subject>RNA Helicases</subject><subject>RNA Helicases - genetics</subject><subject>RNA Helicases - metabolism</subject><subject>RNA Interference</subject><subject>RNA Interference - immunology</subject><subject>RNA virus</subject><subject>RNA Virus Infections</subject><subject>RNA Viruses</subject><subject>RNA Viruses - genetics</subject><subject>RNA Viruses - immunology</subject><subject>RNA Viruses - pathogenicity</subject><subject>RNA, Small Interfering</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA, Viral</subject><subject>RNA, Viral - metabolism</subject><subject>RNAi</subject><subject>Viral Load</subject><subject>Virology</subject><subject>Virus Replication</subject><issn>1931-3128</issn><issn>1934-6069</issn><issn>1934-6069</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUFv1DAQhSMEoqXwBzigHLkkjJ04iSWEtOpCu9ICEgKuluNMWK8Se7GTrfrvmXRLBRw4eSx_79nPL0leMsgZsOrNPjc7P-YcWJMDzwHYo-ScyaLMKqjk47uZZQXjzVnyLMY9gBBQs6fJGZcCCtbAeXKztgZDxrM1HtB16Kb0Ch0GPVnvUt-n323QQ7r-tEr74Md0jT2ayR5xwfyIcWG-0Clxc6TtR9_Ng55oWjni7tSbcZydnW5T69KNi2QQnydPej1EfHG_XiTfPrz_enmdbT9fbS5X28wIIaes7ShK24oKAcq2lch5YaRoSlMARSj7hknWG6FBF2Vdt2Un-7LsUZQAFaub4iJ5d_I9zO2InaGA9CJ1CHbU4VZ5bdXfJ87u1A9_VKIRNZdABtnJYPeP7Hq1VQcdJ5yDAiYFFwU7MuJf318Y_M8Z46RGGw0Og3bo56ioLWgKSTkI5SfUBB9jwP7Bn4FaGlZ7tTS8aBoFXFHDJHr1Z6AHye9KCXh7ApC-9WgxqGgsOoOdDfTzqvP2f_6_AEQMt14</recordid><startdate>20180314</startdate><enddate>20180314</enddate><creator>Poirier, Enzo Z.</creator><creator>Goic, Bertsy</creator><creator>Tomé-Poderti, Lorena</creator><creator>Frangeul, Lionel</creator><creator>Boussier, Jérémy</creator><creator>Gausson, Valérie</creator><creator>Blanc, Hervé</creator><creator>Vallet, Thomas</creator><creator>Loyd, Hyelee</creator><creator>Levi, Laura I.</creator><creator>Lanciano, Sophie</creator><creator>Baron, Chloé</creator><creator>Merkling, Sarah H.</creator><creator>Lambrechts, Louis</creator><creator>Mirouze, Marie</creator><creator>Carpenter, Susan</creator><creator>Vignuzzi, Marco</creator><creator>Saleh, Maria-Carla</creator><general>Elsevier Inc</general><general>Elsevier</general><general>Cell Press</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8593-4117</orcidid><orcidid>https://orcid.org/0000-0002-2249-377X</orcidid><orcidid>https://orcid.org/0000-0002-6823-4474</orcidid><orcidid>https://orcid.org/0000-0001-5958-2138</orcidid><orcidid>https://orcid.org/0000-0002-0992-8775</orcidid><orcidid>https://orcid.org/0000-0002-9727-3448</orcidid><orcidid>https://orcid.org/0000-0002-0514-1270</orcidid></search><sort><creationdate>20180314</creationdate><title>Dicer-2-Dependent Generation of Viral DNA from Defective Genomes of RNA Viruses Modulates Antiviral Immunity in Insects</title><author>Poirier, Enzo Z. ; Goic, Bertsy ; Tomé-Poderti, Lorena ; Frangeul, Lionel ; Boussier, Jérémy ; Gausson, Valérie ; Blanc, Hervé ; Vallet, Thomas ; Loyd, Hyelee ; Levi, Laura I. ; Lanciano, Sophie ; Baron, Chloé ; Merkling, Sarah H. ; Lambrechts, Louis ; Mirouze, Marie ; Carpenter, Susan ; Vignuzzi, Marco ; Saleh, Maria-Carla</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c559t-bd606bb56e004bb9e223c9584c305034f8191fc5a0a3477b4d9f44fe540061783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Antiviral Agents</topic><topic>arbovirus</topic><topic>Arboviruses</topic><topic>Arboviruses - immunology</topic><topic>Arboviruses - pathogenicity</topic><topic>Biochemistry, Molecular Biology</topic><topic>circular viral DNA</topic><topic>Culicidae</topic><topic>Culicidae - immunology</topic><topic>DEAD-box RNA Helicases</topic><topic>DEAD-box RNA Helicases - metabolism</topic><topic>defective viral genomes</topic><topic>Dicer-2</topic><topic>DNA, Viral</topic><topic>DNA, Viral - metabolism</topic><topic>Drosophila</topic><topic>Drosophila - immunology</topic><topic>Drosophila Proteins</topic><topic>Drosophila Proteins - genetics</topic><topic>Drosophila Proteins - metabolism</topic><topic>Genes, Viral</topic><topic>Genes, Viral - genetics</topic><topic>Genome, Viral</topic><topic>Genomics</topic><topic>Host-Pathogen Interactions</topic><topic>Host-Pathogen Interactions - genetics</topic><topic>Host-Pathogen Interactions - immunology</topic><topic>Immunology</topic><topic>insect</topic><topic>Life Sciences</topic><topic>Microbiology and Parasitology</topic><topic>Molecular biology</topic><topic>persistence</topic><topic>Point Mutation</topic><topic>Ribonuclease III</topic><topic>Ribonuclease III - genetics</topic><topic>Ribonuclease III - metabolism</topic><topic>RNA Helicases</topic><topic>RNA Helicases - genetics</topic><topic>RNA Helicases - metabolism</topic><topic>RNA Interference</topic><topic>RNA Interference - immunology</topic><topic>RNA virus</topic><topic>RNA Virus Infections</topic><topic>RNA Viruses</topic><topic>RNA Viruses - genetics</topic><topic>RNA Viruses - immunology</topic><topic>RNA Viruses - pathogenicity</topic><topic>RNA, Small Interfering</topic><topic>RNA, Small Interfering - genetics</topic><topic>RNA, Viral</topic><topic>RNA, Viral - metabolism</topic><topic>RNAi</topic><topic>Viral Load</topic><topic>Virology</topic><topic>Virus Replication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Poirier, Enzo Z.</creatorcontrib><creatorcontrib>Goic, Bertsy</creatorcontrib><creatorcontrib>Tomé-Poderti, Lorena</creatorcontrib><creatorcontrib>Frangeul, Lionel</creatorcontrib><creatorcontrib>Boussier, Jérémy</creatorcontrib><creatorcontrib>Gausson, Valérie</creatorcontrib><creatorcontrib>Blanc, Hervé</creatorcontrib><creatorcontrib>Vallet, Thomas</creatorcontrib><creatorcontrib>Loyd, Hyelee</creatorcontrib><creatorcontrib>Levi, Laura I.</creatorcontrib><creatorcontrib>Lanciano, Sophie</creatorcontrib><creatorcontrib>Baron, Chloé</creatorcontrib><creatorcontrib>Merkling, Sarah H.</creatorcontrib><creatorcontrib>Lambrechts, Louis</creatorcontrib><creatorcontrib>Mirouze, Marie</creatorcontrib><creatorcontrib>Carpenter, Susan</creatorcontrib><creatorcontrib>Vignuzzi, Marco</creatorcontrib><creatorcontrib>Saleh, Maria-Carla</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell host & microbe</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Poirier, Enzo Z.</au><au>Goic, Bertsy</au><au>Tomé-Poderti, Lorena</au><au>Frangeul, Lionel</au><au>Boussier, Jérémy</au><au>Gausson, Valérie</au><au>Blanc, Hervé</au><au>Vallet, Thomas</au><au>Loyd, Hyelee</au><au>Levi, Laura I.</au><au>Lanciano, Sophie</au><au>Baron, Chloé</au><au>Merkling, Sarah H.</au><au>Lambrechts, Louis</au><au>Mirouze, Marie</au><au>Carpenter, Susan</au><au>Vignuzzi, Marco</au><au>Saleh, Maria-Carla</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dicer-2-Dependent Generation of Viral DNA from Defective Genomes of RNA Viruses Modulates Antiviral Immunity in Insects</atitle><jtitle>Cell host & microbe</jtitle><addtitle>Cell Host Microbe</addtitle><date>2018-03-14</date><risdate>2018</risdate><volume>23</volume><issue>3</issue><spage>353</spage><epage>365.e8</epage><pages>353-365.e8</pages><issn>1931-3128</issn><issn>1934-6069</issn><eissn>1934-6069</eissn><abstract>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.
[Display omitted]
•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
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.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>29503180</pmid><doi>10.1016/j.chom.2018.02.001</doi><orcidid>https://orcid.org/0000-0001-8593-4117</orcidid><orcidid>https://orcid.org/0000-0002-2249-377X</orcidid><orcidid>https://orcid.org/0000-0002-6823-4474</orcidid><orcidid>https://orcid.org/0000-0001-5958-2138</orcidid><orcidid>https://orcid.org/0000-0002-0992-8775</orcidid><orcidid>https://orcid.org/0000-0002-9727-3448</orcidid><orcidid>https://orcid.org/0000-0002-0514-1270</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1931-3128 |
ispartof | Cell host & microbe, 2018-03, Vol.23 (3), p.353-365.e8 |
issn | 1931-3128 1934-6069 1934-6069 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5857290 |
source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
subjects | Animals Antiviral Agents arbovirus Arboviruses Arboviruses - immunology Arboviruses - pathogenicity Biochemistry, Molecular Biology circular viral DNA Culicidae Culicidae - immunology DEAD-box RNA Helicases DEAD-box RNA Helicases - metabolism defective viral genomes Dicer-2 DNA, Viral DNA, Viral - metabolism Drosophila Drosophila - immunology Drosophila Proteins Drosophila Proteins - genetics Drosophila Proteins - metabolism Genes, Viral Genes, Viral - genetics Genome, Viral Genomics Host-Pathogen Interactions Host-Pathogen Interactions - genetics Host-Pathogen Interactions - immunology Immunology insect Life Sciences Microbiology and Parasitology Molecular biology persistence Point Mutation Ribonuclease III Ribonuclease III - genetics Ribonuclease III - metabolism RNA Helicases RNA Helicases - genetics RNA Helicases - metabolism RNA Interference RNA Interference - immunology RNA virus RNA Virus Infections RNA Viruses RNA Viruses - genetics RNA Viruses - immunology RNA Viruses - pathogenicity RNA, Small Interfering RNA, Small Interfering - genetics RNA, Viral RNA, Viral - metabolism RNAi Viral Load Virology Virus Replication |
title | Dicer-2-Dependent Generation of Viral DNA from Defective Genomes of RNA Viruses Modulates Antiviral Immunity in Insects |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T18%3A56%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Dicer-2-Dependent%20Generation%20of%20Viral%20DNA%20from%20Defective%20Genomes%20of%20RNA%20Viruses%20Modulates%20Antiviral%20Immunity%20in%20Insects&rft.jtitle=Cell%20host%20&%20microbe&rft.au=Poirier,%20Enzo%20Z.&rft.date=2018-03-14&rft.volume=23&rft.issue=3&rft.spage=353&rft.epage=365.e8&rft.pages=353-365.e8&rft.issn=1931-3128&rft.eissn=1934-6069&rft_id=info:doi/10.1016/j.chom.2018.02.001&rft_dat=%3Cproquest_pubme%3E2010839223%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2010839223&rft_id=info:pmid/29503180&rft_els_id=S1931312818300878&rfr_iscdi=true |