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Primary genotypic resistance of HIV-1 to CCR5 antagonists in CCR5 antagonist treatment-naive patients

Cathia Soulié, Isabelle Malet, Sidonie Lambert-Niclot, Roland Tubiana, Monique Thévenin, Anne Simon, Robert L. Murphy, Christine Katlama, Vincent Cálvez, Anne‐Geneviève Marcelin

Open publisher page 27 citations

Abstract

Resistance to CCR5 antagonists can be driven by mutations in gp120. Sequences from 323 anti-CCR5 naive patients were analyzed for the presence of previously described in-vivo or in-vitro resistance mutations to CCR5 antagonists located in the V3 loop of gp120. The V3 loop region was rather polymorphic, and 7.3% of patients showed viruses with combinations of mutations in V3 loop previously described to be involved in maraviroc resistance, a licensed CCR5 antagonist.

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What this paper is about

Resistance to CCR5 antagonists can be driven by mutations in gp120. Sequences from 323 anti-CCR5 naive patients were analyzed for the presence of previously described in-vivo or in-vitro resistance mutations to CCR5 antagonists located in the V3 loop of gp120. The V3 loop region was rather polymorphic, and 7.3% of patients showed viruses with combinations of mutations in V3 loop previously described to be involved in maraviroc resistance, a licensed CCR5 antagonist.

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OpenAlex reports 27 citations for this work. Citation counts describe recorded attention and do not establish research quality.

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Available abstract

Resistance to CCR5 antagonists can be driven by mutations in gp120. Sequences from 323 anti-CCR5 naive patients were analyzed for the presence of previously described in-vivo or in-vitro resistance mutations to CCR5 antagonists located in the V3 loop of gp120. The V3 loop region was rather polymorphic, and 7.3% of patients showed viruses with combinations of mutations in V3 loop previously described to be involved in maraviroc resistance, a licensed CCR5 antagonist.

Key concepts: CCR5 receptor antagonist, Maraviroc, V3 loop, Antagonist, Biology, Genotype, Mutation, In vivo

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