| Autor: |
Ko NL; Epidemiology and Physiopathology of Oncogenic Viruses, Institut Pasteur, CNRS URA 3015, 28 rue du Dr Roux, 75724 Paris cedex 15, France., Birlouez E; Molecular Retrovirology Unit, Institut Pasteur, CNRS URA 3015, 28 rue du Dr Roux, 75724 Paris cedex 15, France., Wain-Hobson S; Molecular Retrovirology Unit, Institut Pasteur, CNRS URA 3015, 28 rue du Dr Roux, 75724 Paris cedex 15, France., Mahieux R; Retroviral Oncogenesis, U758 Human virology, ENS Lyon, UMS3444/US8 Biosciences Gerland-Lyon Sud, 46 allée d'Italie, 69007 Lyon, France.; Epidemiology and Physiopathology of Oncogenic Viruses, Institut Pasteur, CNRS URA 3015, 28 rue du Dr Roux, 75724 Paris cedex 15, France., Vartanian JP; Molecular Retrovirology Unit, Institut Pasteur, CNRS URA 3015, 28 rue du Dr Roux, 75724 Paris cedex 15, France. |
| Abstrakt: |
RNA editing mediated by adenosine deaminases acting on RNA (ADARs) converts adenosine (A) to inosine (I) residues in dsRNA templates. While ADAR-1-mediated editing was essentially described for RNA viruses, the present work addresses the issue for two δ-retroviruses, human T-cell leukemia virus type 2 and simian T-cell leukemia virus type 3 (HTLV-2 and STLV-3). We examined whether ADAR-1 could edit HTLV-2 and STLV-3 virus genomes in cell culture and in vivo. Using a highly sensitive PCR-based method, referred to as 3DI-PCR, we showed that ADAR-1 could hypermutate adenosine residues in HTLV-2. STLV-3 hypermutation was obtained without using 3DI-PCR, suggesting a higher mutation frequency for this virus. Detailed analysis of the dinucleotide editing context showed preferences for 5' ArA and 5' UrA. In conclusion, the present observations demonstrate that ADAR-1 massively edits HTLV-2 and STLV-3 retroviruses in vitro, but probably remains a rare phenomenon in vivo. |
