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HIV-1 Dynamics and Coreceptor Usage in Maraviroc-Treated Patients with Ongoing Replication
Author(s) -
Patricia RecordonPinson,
Stéphanie Raymond,
Pantxika Bellecave,
AnneGeneviève Marcelin,
Cathia Soulié,
D. Descamps,
Vincent Cálvez,
P. Richard Harrigan,
Hervé Fleury,
Jacques Izopet,
Bernard Masquelier
Publication year - 2012
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.02159-12
Subject(s) - maraviroc , viral quasispecies , v3 loop , tropism , ccr5 receptor antagonist , biology , virology , mutation , viral replication , population , selection (genetic algorithm) , viral evolution , human immunodeficiency virus (hiv) , tissue tropism , genetics , virus , medicine , gene , chemokine , rna , chemokine receptor , artificial intelligence , hepatitis c virus , immune system , environmental health , computer science , peptide sequence
There is evidence that HIV-1 evolution under maraviroc (MVC) pressure can lead to the selection of either X4-tropic variants and/or R5-tropic, MVC-resistant isolates. However, the viral dynamics of HIV-1 variants in patients with virological failure (VF) on MVC-containing regimens remain poorly studied. Here, we investigated the V3 loop evolution of HIV-1 on MVC in relation to coreceptor usage and the nature of HIV-1 quasispecies before MVC therapy using bulk population sequences and ultradeep sequencing. The majority of patients had no detectable minority X4 variant at baseline. The evolution of tropism was followed up until VF and showed three possibilities for viral evolution in these patients: emergence of preexisting X4 variants, de novo selection of R5 variants presenting V3 loop mutations, or replication of R5 variants without selection of known mutations.

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