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1: J Antimicrob Chemother. 2008 Sep;62(3):451-5. Epub 2008 Jun 13.
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HIV-1-infected patients from the French National Observatory experiencing virological failure while receiving enfuvirtide.

Descamps D, Assoumou L, Masquelier B, Marcelin AG, Saidi S, Tamalet C, Cottalorda J, Plantier JC, Montes B, Izopet J, Peytavin G, Yerly S, Schneider V, Delaugerre C, Ferré V, Ruffault A, Pallier C, Morand-Joubert L, Chaix ML, Calvez V, Brun-Vézinet F, Costagliola D; ANRS AC-11 Resistance Study Group.

AP-HP, Groupe Hospitalier Bichat-Claude Bernard, Laboratoire de Virologie, Paris F-75018, France. diane.descamps@bch.aphp.fr

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.

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PMID: 18552344 [PubMed - indexed for MEDLINE]