Francoise Brun-Vezinet
French Institute of Health and Medical Research
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Featured researches published by Francoise Brun-Vezinet.
Journal of Antimicrobial Chemotherapy | 2008
B. Roquebert; Florence Damond; G. Collin; Sophie Matheron; Gilles Peytavin; Antoine Bénard; P. Campa; Geneviève Chêne; Francoise Brun-Vezinet; Diane Descamps
OBJECTIVES We investigated the in vitro phenotypic susceptibility of HIV-2 isolates from integrase inhibitor (INI)-naive patients to INIs and its relation to HIV-2 integrase gene polymorphism. METHODS We determined the phenotypic susceptibility to raltegravir and elvitegravir of co-cultured isolates obtained from the HIV-2 ROD reference strain and from 14 clinical isolates. IC(50) values were compared with those for HIV-1 reference strains. HIV-2 integrase gene polymorphism was assessed in isolates from 52 INI-naive patients enrolled in the French HIV-2 cohort. RESULTS Median raltegravir and elvitegravir IC(50) values for the 14 clinical HIV-2 isolates were 2.4 and 0.7 nM, respectively, and were similar to those observed for HIV-2 ROD and HIV-1 reference strains. Overall, 38% of HIV-2 integrase amino acids were polymorphic. The catalytic triad DDE and the HHCC and RKK motifs were fully conserved, at the same genomic positions as described in HIV-1. In subtype B isolates, the total length of the integrase gene varied, owing to the presence of stop codons at positions 288, 294, 297 and 302. Fourteen of the positions associated with substitutions conferring INI resistance in HIV-1 were polymorphic in HIV-2. CONCLUSIONS Despite 40% heterogeneity between the HIV-1 and HIV-2 integrase genes, the phenotypic susceptibility of clinical HIV-2 isolates to INIs was similar to that of HIV-1. This new class of antiretroviral drugs thus represents a novel therapeutic possibility for HIV-2-infected patients who otherwise have few treatment options.
Journal of Antimicrobial Chemotherapy | 2008
Bernard Masquelier; K. L. Assoumou; Diane Descamps; Laurence Bocket; Jacqueline Cottalorda; Annick Ruffault; Anne-Geneviève Marcelin; Laurence Morand-Joubert; Catherine Tamalet; Charlotte Charpentier; Gilles Peytavin; Z. Antoun; Francoise Brun-Vezinet; Dominique Costagliola
BACKGROUND We developed clinically relevant genotypic scores for resistance to fosamprenavir/ritonavir in HIV-1 protease inhibitor (PI)-experienced patients. METHODS PI-experienced patients with virological failure receiving fosamprenavir/ritonavir as the sole PI for at least 3 months and with detectable fosamprenavir plasma levels were included. The impact of baseline protease mutations on virological response (VR, i.e. decrease in plasma HIV-1 RNA between baseline and month 3) was analysed using the Mann-Whitney test. Mutations with prevalence >10% and P value <0.10 were retained. The Jonckheere-Terpstra test was used to select the combination of mutations most strongly associated with VR. The association between score and VR was assessed by multivariate backward regression. RESULTS In the 73 patients included, the median baseline HIV-1 RNA was 4.6 log(10) copies/mL (range: 2.7-6.9) and the mean decrease at month 3 was -1.07 +/- 1.40 log(10) copies/mL. Ninety per cent of the patients were infected by HIV-1 subtype B variants. Two fosamprenavir/ritonavir mutation scores were constructed: score A (L10F/I/V + L33F + M36I + I54L/M/V/A/T/S + I62V + V82A/F/C/G + I84V + L90M) was based only on mutations associated with a worse VR, whereas score B (L10FIV + L33F + M36I + I54L/M/V/A/T/S + A71V - V77I - N88S + L90M) also took into account favourable mutations. Both scores were independent predictors of VR, however, co-administration of tenofovir was associated with a worse VR and the presence of the N88S protease mutation and co-administration of enfuvirtide with a better VR. CONCLUSIONS These clinically validated mutation scores should be of interest for the clinical management of PI-experienced patients. The fosamprenavir/ritonavir score A was introduced in the 2006 ANRS algorithm along with isolated mutations I50V and V32I + I47V.
Journal of Antimicrobial Chemotherapy | 2008
Diane Descamps; Lambert Assoumou; Bernard Masquelier; Anne-Geneviève Marcelin; Souhila Saidi; Catherine Tamalet; Jacqueline Cottalorda; Jean-Christophe Plantier; Brigitte Montes; Jacques Izopet; Gilles Peytavin; Sabine Yerly; Véronique Schneider; Constance Delaugerre; Virginie Ferré; Annick Ruffault; Coralie Pallier; Laurence Morand-Joubert; Marie-Laure Chaix; Vincent Calvez; Francoise Brun-Vezinet; Dominique Costagliola
OBJECTIVES We studied gp41 mutations associated with failing enfuvirtide salvage therapy. METHODS This multicentre study involved patients with HIV-1 plasma viral load (pVL) > 5000 copies/mL after at least 3 months of uninterrupted enfuvirtide therapy and with plasma samples available at inclusion (T0), at initial enfuvirtide failure (T1) and at last follow-up visit during continued failing enfuvirtide therapy (T2). The HR-1 and HR-2 domains of the gp41 gene were sequenced at T0, T1 and T2. RESULTS Ninety-nine patients were enrolled. At baseline, the median pVL and CD4 cell count were 5.1 log copies/mL and 72 cells/mm(3), respectively. Based on the ANRS Resistance Group algorithm, the proportion of patients harbouring viruses with enfuvirtide resistance mutations increased significantly between T0 and T1. In the HR-1 domain, the V38A/M, Q40H, N42T, N43D and L45M mutations wereselected (P < 0.02). In the HR-2 domain, no mutations were significantly selected during the follow-up. None of the mutations was associated with a CD4 cell count increment. CONCLUSIONS Mutations selected during failing enfuvirtide salvage therapy are mainly located in the HR-1 domain of the gp41 gene, between codons 38 and 45. No mutations were associated with an increase in the CD4 cell count.
International Journal of Cancer | 1988
Eric Delaporte; Alain Dupont; Martine Peeters; Richard Josse; Marcel Merlin; Dirk Schrijvers; Bernard Hamono; Léonard Bedjabaga; Henri Cheringou; Franck Boyer; Francoise Brun-Vezinet; Bernard Larouze
Archive | 2004
Jean-Noel Telles; Francoise Brun-Vezinet; Diane Descamps
Archive | 2006
Diane Descamps; Francoise Brun-Vezinet
Archive | 2014
Francoise Brun-Vezinet; Sophie Matheron; Diane Descamps
Archive | 2000
Francoise Brun-Vezinet; Diane Descamps; Jean-Noil Telles
Archive | 2000
Francoise Brun-Vezinet; Diane Descamps; Jean-No L Telles
Archive | 2000
Francoise Brun-Vezinet; Diane Descamps; Jean-No L Telles