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              <p>How persistent viral infections are established and maintained is widely debated and remains poorly understood. We found here that the persistence of RNA virus in Drosophila melanogaster was achieved through the combined action of cellular reverse-transcriptase activity and the RNA 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. The most well-characterized viral infections are those with human or economic effects. However, regardless of the organism under consideration, there are viruses able to infect that organism. Viral fossil registers highlight the long coevolutionary history between virus and</p>
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              <org type="consortium">We thank members of the Saleh, Antoniewski and Vignuzzi laboratories for discussions and technical support; M. Vignuzzi, J. Chandler and R. van Rij for critical reading of the manuscript; A. Schneemann (The Scripps Research Institute) for antibody to FHV; P. Vargas for assistance with flow cytometry; and A. Pelisson for advice on retrotransposition.</org>
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