ArticleNature immunology2013
RNA-mediated interference and reverse transcription control the persistence of RNA viruses in the insect model Drosophila.
Article in Nature immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
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Who cites it
136 citing papers in PubMed, 255 citations in OpenAlex.
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- In vivo Dicer-2 interactome during viral infection reveals novel pro and antiviral factors in Drosophila melanogaster.PLoS pathogens · 2025Article
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- Dissecting the dynamics of virus-derived DNA of dengue virus 2 (DENV-2) in Aedes mosquitoes.PloS one · 2025Article
- DsRNA as pathogen-associated molecular pattern in innate immunity and multiple functions of the RNAi machinery complicate the use of RNAi in pest control.Frontiers in insect science · 2025Review
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- Mosquito transgenerational antiviral immunity is mediated by vertical transfer of virus DNA sequences and RNAi.iScience · 2024Article
- In-depth transcriptomic analysis of Anopheles gambiae hemocytes uncovers novel genes and the oenocytoid developmental lineage.BMC genomics · 2024Article
- Evolutionary genomics of three agricultural pest moths reveals rapid evolution of host adaptation and immune-related genes.GigaScience · 2024Article
- Characterization of Viral Interference inPathogens (Basel, Switzerland) · 2023Article
- Review
- Article
76 more citing papers are in PubMed but not listed here.
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10 authors at 3 institutions in 1 country.
Funding
Abstract
How persistent viral infections are established and maintained is widely debated and remains poorly understood. We found here that the persistence of RNA viruses in Drosophila melanogaster was achieved through the combined action of cellular reverse-transcriptase activity and the RNA-mediated interference (RNAi) pathway. Fragments of diverse RNA viruses were reverse-transcribed early during infection, which resulted in DNA forms embedded in retrotransposon sequences. Those virus-retrotransposon DNA chimeras produced transcripts processed by the RNAi machinery, which in turn inhibited viral replication. Conversely, inhibition of reverse transcription hindered the appearance of chimeric DNA and prevented persistence. Our results identify a cooperative function for retrotransposons and antiviral RNAi in the control of lethal acute infection for the establishment of viral persistence.
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