<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>6(8)</volume><submitter>Ghosn J</submitter><pubmed_abstract>Our objective was to analyze the evolution of resistance mutations (RM) and viral tropism of multi-drug-resistant (MDR) strains detected at primary HIV-1 infection (PHI). MDR HIV strain was defined as the presence of genotypic resistance to at least 1 antiretroviral of the 3 classes. Tropism determinations (CCR5 or CXCR4) were performed on baseline plasma HIV-RNA and/or PBMC-HIV-DNA samples, then during follow-up using population-based sequencing of V3 loop and phenotypic tests. Clonal analysis was performed at baseline for env, RT and protease genes, and for HIV-DNA env gene during follow-up. Five patients were eligible. At baseline, RT, protease and env clones from HIV-RNA and HIV-DNA were highly homogenous for each patient; genotypic tropism was R5 in 3 (A,B,C) and X4 in 2 patients (D,E</pubmed_abstract><journal>PloS one</journal><pagination>e23301</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3160852</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>X4 tropic multi-drug resistant quasi-species detected at the time of primary HIV-1 infection remain exclusive or at least dominant far from PHI.</pubmed_title><pmcid>PMC3160852</pmcid><pubmed_authors>Ravaux I</pubmed_authors><pubmed_authors>Abraham B</pubmed_authors><pubmed_authors>Rannou MT</pubmed_authors><pubmed_authors>Leboucher B</pubmed_authors><pubmed_authors>Merrien D</pubmed_authors><pubmed_authors>Chambrin V</pubmed_authors><pubmed_authors>Drogoul MP</pubmed_authors><pubmed_authors>Massip P</pubmed_authors><pubmed_authors>Zucman D</pubmed_authors><pubmed_authors>Beck-Wirth G</pubmed_authors><pubmed_authors>Touam F</pubmed_authors><pubmed_authors>Levy Y</pubmed_authors><pubmed_authors>Lascoux C</pubmed_authors><pubmed_authors>Leport C</pubmed_authors><pubmed_authors>Quinsat DT</pubmed_authors><pubmed_authors>David F</pubmed_authors><pubmed_authors>Morlat P</pubmed_authors><pubmed_authors>Galanaud P</pubmed_authors><pubmed_authors>Saada M</pubmed_authors><pubmed_authors>Drenou B</pubmed_authors><pubmed_authors>Granier F</pubmed_authors><pubmed_authors>Hussonnois C</pubmed_authors><pubmed_authors>Zeng A</pubmed_authors><pubmed_authors>Genet C</pubmed_authors><pubmed_authors>Choutet P</pubmed_authors><pubmed_authors>Rouzioux C</pubmed_authors><pubmed_authors>Koffi K</pubmed_authors><pubmed_authors>Genet P</pubmed_authors><pubmed_authors>Colasante U</pubmed_authors><pubmed_authors>Buisson M</pubmed_authors><pubmed_authors>Therby A</pubmed_authors><pubmed_authors>Chakvetadze C</pubmed_authors><pubmed_authors>Cheret A</pubmed_authors><pubmed_authors>Lepeu A</pubmed_authors><pubmed_authors>Herson S</pubmed_authors><pubmed_authors>Obadia M</pubmed_authors><pubmed_authors>Girard PM</pubmed_authors><pubmed_authors>Chevojon P</pubmed_authors><pubmed_authors>Boue F</pubmed_authors><pubmed_authors>Stein A</pubmed_authors><pubmed_authors>May T</pubmed_authors><pubmed_authors>Morelon S</pubmed_authors><pubmed_authors>Bonnet E</pubmed_authors><pubmed_authors>Bonnet F</pubmed_authors><pubmed_authors>Greder Belan A</pubmed_authors><pubmed_authors>Bergmann JF</pubmed_authors><pubmed_authors>Jacomet C</pubmed_authors><pubmed_authors>Audhuy B</pubmed_authors><pubmed_authors>Delfraissy JF</pubmed_authors><pubmed_authors>Debab Y</pubmed_authors><pubmed_authors>Tubiana R</pubmed_authors><pubmed_authors>Katlama C</pubmed_authors><pubmed_authors>Chemlal K</pubmed_authors><pubmed_authors>De Lacroix Szmania I</pubmed_authors><pubmed_authors>Gonzales Canali G</pubmed_authors><pubmed_authors>Sauser F</pubmed_authors><pubmed_authors>Phung 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J</pubmed_authors><pubmed_authors>Ragnaud JM</pubmed_authors><pubmed_authors>Jestin C</pubmed_authors><pubmed_authors>Izopet J</pubmed_authors><pubmed_authors>Grihon F</pubmed_authors><pubmed_authors>Caron F</pubmed_authors><pubmed_authors>Trepo C</pubmed_authors><pubmed_authors>Gastaut JA</pubmed_authors><pubmed_authors>Martha B</pubmed_authors><pubmed_authors>Slama B</pubmed_authors><pubmed_authors>Sohn C</pubmed_authors><pubmed_authors>Clavel C</pubmed_authors><pubmed_authors>Chaix ML</pubmed_authors><pubmed_authors>Picard O</pubmed_authors><pubmed_authors>Saint-Dizier F</pubmed_authors><pubmed_authors>Diab G</pubmed_authors><pubmed_authors>Bouvet E</pubmed_authors><pubmed_authors>Saraux JL</pubmed_authors><pubmed_authors>Weinbreck P</pubmed_authors><pubmed_authors>Poinsignon Y</pubmed_authors><pubmed_authors>Fior R</pubmed_authors><pubmed_authors>Rosenthal E</pubmed_authors><pubmed_authors>Deveau C</pubmed_authors><pubmed_authors>Raffenne L</pubmed_authors><pubmed_authors>Bastides F</pubmed_authors><pubmed_authors>Diemer M</pubmed_authors><pubmed_authors>Aumaitre H</pubmed_authors><pubmed_authors>Guillevin L</pubmed_authors><pubmed_authors>Sereni D</pubmed_authors><pubmed_authors>Bloch M</pubmed_authors><pubmed_authors>Campa P</pubmed_authors><pubmed_authors>Pialoux G</pubmed_authors><pubmed_authors>Galimand J</pubmed_authors><pubmed_authors>Chaillou S</pubmed_authors><pubmed_authors>Yeni P</pubmed_authors><pubmed_authors>Ghosn J</pubmed_authors><pubmed_authors>Lafeuillade A</pubmed_authors><pubmed_authors>Sordage M</pubmed_authors><pubmed_authors>El Alami N</pubmed_authors><pubmed_authors>Miodovski C</pubmed_authors></additional><is_claimable>false</is_claimable><name>X4 tropic multi-drug resistant quasi-species detected at the time of primary HIV-1 infection remain exclusive or at least dominant far from PHI.</name><description>Our objective was to analyze the evolution of resistance mutations (RM) and viral tropism of multi-drug-resistant (MDR) strains detected at primary HIV-1 infection (PHI). MDR HIV strain was defined as the presence of genotypic resistance to at least 1 antiretroviral of the 3 classes. Tropism determinations (CCR5 or CXCR4) were performed on baseline plasma HIV-RNA and/or PBMC-HIV-DNA samples, then during follow-up using population-based sequencing of V3 loop and phenotypic tests. Clonal analysis was performed at baseline for env, RT and protease genes, and for HIV-DNA env gene during follow-up. Five patients were eligible. At baseline, RT, protease and env clones from HIV-RNA and HIV-DNA were highly homogenous for each patient; genotypic tropism was R5 in 3 (A,B,C) and X4 in 2 patients (D,E</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011</publication><modification>2026-04-16T19:10:06.506Z</modification><creation>2026-04-07T14:18:13.551Z</creation></dates><accession>S-EPMC3160852</accession><cross_references><pubmed>21887243</pubmed><doi>10.1371/journal.pone.0023301</doi></cross_references></HashMap>