J
Joëlle Boretto
Researcher at Centre national de la recherche scientifique
Publications - 17
Citations - 959
Joëlle Boretto is an academic researcher from Centre national de la recherche scientifique. The author has contributed to research in topics: Reverse transcriptase & DNA. The author has an hindex of 14, co-authored 17 publications receiving 943 citations. Previous affiliations of Joëlle Boretto include Aix-Marseille University & University of Provence.
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Journal ArticleDOI
Mechanistic basis for reduced viral and enzymatic fitness of HIV-1 reverse transcriptase containing both K65R and M184V mutations.
Jerome Deval,Kirsten L. White,Michael D. Miller,Neil Parkin,Jérôme Courcambeck,Philippe Halfon,Boulbaba Selmi,Joëlle Boretto,Bruno Canard +8 more
TL;DR: The molecular mechanisms by which a virus resistant to lamivudine with the M184V reverse transcriptase mutation shows increased susceptibility to tenofovir and can suppress the effects of the ten ofovir resistance mutation K65R are reported, defining at the molecular level how nucleoside-resistant viruses can be driven to reduced viral fitness.
Journal ArticleDOI
The Molecular Mechanism of Multidrug Resistance by the Q151M Human Immunodeficiency Virus Type 1 Reverse Transcriptase and Its Suppression Using α-Boranophosphate Nucleotide Analogues
Jerome Deval,Boulbaba Selmi,Joëlle Boretto,Marie-Pierre Egloff,Catherine Guerreiro,Simon Sarfati,Bruno Canard +6 more
TL;DR: The general capacity of such analogues to circumvent multidrug resistance when RT-mediated nucleotide resistance originates from the selective decrease of the catalytic rate constant k pol is highlighted.
Journal ArticleDOI
HIV-1-associated uracil DNA glycosylase activity controls dUTP misincorporation in viral DNA and is essential to the HIV-1 life cycle.
Stéphane Priet,Nathalie Gros,Jean-Marc Navarro,Joëlle Boretto,Bruno Canard,Gilles Quérat,Joséphine Sire +6 more
TL;DR: HIV-1 prevents incorporation of dUTP in viral cDNA by UNG2-mediated uracil excision followed by a dNTP-dependent, reverse transcriptase-mediated endonucleolytic cleavage and finally by strand-displacement polymerization.
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A loss of viral replicative capacity correlates with altered DNA polymerization kinetics by the human immunodeficiency virus reverse transcriptase bearing the K65R and L74V dideoxynucleoside resistance substitutions.
Jerome Deval,Jean-Marc Navarro,Boulbaba Selmi,Jérôme Courcambeck,Joëlle Boretto,Philippe Halfon,Sarah Garrido-Urbani,Joséphine Sire,Bruno Canard +8 more
TL;DR: It is shown that recombinant viruses carrying K65R and L74V display the same resistance level to ddI relative to wild type, which explains why the two mutations do not combine in the clinic and might give a mechanism for a decreased viral fitness at the molecular level.
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General catalytic deficiency of hepatitis C virus RNA polymerase with an S282T mutation and mutually exclusive resistance towards 2'-modified nucleotide analogues.
TL;DR: The determination of the molecular mechanism by which the S282T mutation confers resistance to 2′-modified nucleotide analogues suggests not only that “2′-conformer” analogues target distinct steps in RNA synthesis but also that these analogues have interesting potential in combination therapies.