Extensive editing of a small fraction of human T-cell leukemia virus type 1 genomes by four APOBEC3 cytidine deaminases.

Renaud Mahieux (1) , Rodolphe Suspene (2) , Frédéric Delebecque (2) , Michel Henry (2) , Olivier Schwartz (3) , Simon Wain-Hobson (2) , Jean Pierre Vartanian (2)

1 Epidémiologie et Physiopathologie des Virus Oncogènes
2 Rétrovirologie Moléculaire
3 Virus et Immunité

In the absence of the human immunodeficiency virus type 1 (HIV-1) Vif protein, the host-cell cytidine deaminases APOBEC3F and -3G are co-packaged along with virion RNA. Upon infection of target cells, nascent single-stranded DNA can be edited extensively, invariably giving rise to defective genomes called G-->A hypermutants. Although human T-cell leukemia virus type 1 (HTLV-1) replicates in the same cell type as HIV-1, it was shown here that HTLV-1 is relatively resistant to the antiviral effects mediated by human APOBEC3B, -3C, -3F and -3G. Nonetheless, a small percentage of genomes (0.1

Domaines: Virologie

Renaud Mahieux, Rodolphe Suspene, Frédéric Delebecque, Michel Henry, Olivier Schwartz, et al.. Extensive editing of a small fraction of human T-cell leukemia virus type 1 genomes by four APOBEC3 cytidine deaminases.. Journal of General Virology, 2005, 86 (Pt 9), pp.2489-94. ⟨10.1099/vir.0.80973-0⟩. ⟨pasteur-00013751⟩