ArticleAntimicrobial agents and chemotherapy2012
In vitro phenotypic susceptibility of HIV-2 clinical isolates to CCR5 inhibitors.
Article in Antimicrobial agents and chemotherapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- A Trial of a Single-tablet Regimen of Elvitegravir, Cobicistat, Emtricitabine, and Tenofovir Disoproxil Fumarate for the Initial Treatment of Human Immunodeficiency Virus Type 2 Infection in a Resource-limited Setting: 48-Week Results From Senegal, West Africa.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2018Trial
- Antiretroviral Treatment of HIV-2 Infection: Available Drugs, Resistance Pathways, and Promising New Compounds.International journal of molecular sciences · 2023Review
- In vitro inhibitory effect of maraviroc on the association of the simian immunodeficiency virus envelope glycoprotein with CCR5.Virus genes · 2021Article
- Article
- Management of Virologic Failure and HIV Drug Resistance.Infectious disease clinics of North America · 2019Review
- A genotypic method for determining HIV-2 coreceptor usage enables epidemiological studies and clinical decision support.Retrovirology · 2016Article
- Maraviroc: a review of its use in HIV infection and beyond.Drug design, development and therapy · 2015Review
- Cenicriviroc, a Novel CCR5 (R5) and CCR2 Antagonist, Shows In Vitro Activity against R5 Tropic HIV-2 Clinical Isolates.PloS one · 2015Article
- Genotypic resistance profiles of HIV-2-treated patients in West Africa.AIDS (London, England) · 2014Article
- Chemokine receptor CCR5 antagonist maraviroc: medicinal chemistry and clinical applications.Current topics in medicinal chemistry · 2014Review
- Article
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Authors and funding
11 authors.
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Abstract
HIV-2 is naturally resistant to nonnucleoside reverse transcriptase inhibitors, to a fusion inhibitor, and to some of the protease inhibitors. Maraviroc is the first drug of the new anti-CCR5 drug class and is effective only on CCR5-tropic (R5) HIV-1. No previous studies concerning HIV-2 susceptibility to maraviroc have been reported yet. We developed a phenotypic maraviroc susceptibility test using a peripheral blood mononuclear cell (PBMC) model. We analyzed the maraviroc susceptibility of 13 R5 HIV-2, 2 X4R5 (dual) HIV-2, and 2 CXCR4-tropic (X4) HIV-2 clinical isolates. We also tested, with the same protocol, 1 X4 HIV-1 and 4 R5 HIV-1 clinical isolates. For the R5 HIV-2 clinical isolates, the 50% effective concentration (EC(50)) for maraviroc was 0.80 nM (interquartile range [IQR], 0.48 to 1.39 nM), similar to that observed for the R5 HIV-1 isolates. The median maximum percentage of inhibition in the R5 HIV-2 isolates was 93% (IQR, 84 to 98%), similar to that observed in the R5 HIV-1 isolates. As expected, both X4 HIV-1 and HIV-2 were highly resistant to maraviroc. Our study showed for the first time that maraviroc is active in vitro against R5 HIV-2. The new tools we developed will allow identification of HIV-2-infected patients eligible for CCR5 inhibitor use and management of virological failure when receiving a maraviroc-based regimen.
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