In Vitro Phenotypic Susceptibility of Human Immunodeficiency Virus Type 2 Clinical Isolates to Protease Inhibitors

Laboratoire de Virologie, Service de Microbiologie, Hôpital Bichat-Claude Bernard, Paris, France.
Antimicrobial Agents and Chemotherapy (Impact Factor: 4.48). 05/2008; 52(4):1545-8. DOI: 10.1128/AAC.01284-07
Source: PubMed


We determine phenotypic susceptibility of human immunodeficiency virus type 2 (HIV-2) isolates to amprenavir, atazanavir,
darunavir, indinavir, lopinavir, nelfinavir, saquinavir, and tipranavir. Saquinavir, lopinavir, and darunavir are potent against
wild-type HIV-2 isolates and should be preferred as first-line options for HIV-2-infected patients. Other protease inhibitors
are less active against HIV-2 than against HIV-1.

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Available from: Antoine Bénard, Sep 25, 2015
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    • "HIV-1 and HIV-2 are genetically related and share several characteristics [18] [19] [20] [21] [22] [23], therefore, accurate diagnosis and differentiation of HIV-2 from HIV-1 infection is important due to the clinical implications of disease progression and for the institution of the appropriate treatment regimens [24] [25] [26] [27] [28] [29] [30]. Currently, no serological method is available to confirm HIV-2 infection due to the absence of an FDA-approved HIV-2 Western blot. "
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    ABSTRACT: Background Currently, no FDA-approved HIV-2 nucleic acid assay is commercially available in the United States, although several laboratories have developed in-house assays to confirm HIV-2 infections. A major limitation in the development of novel HIV-2 diagnostic assays is the lack of reference materials that can be used to evaluate, optimize, and monitor assay performance. Study design: Eleven viral stocks of HIV-2 isolates from various West African countries, including the Ivory Coast, Senegal, and Guinea-Bissau, were used to clone the entire LTR and pol regions from each virus. Results We successfully cloned, sequenced, and group classified 22 HIV-2 DNA plasmids including 11 full length LTR (∼849 bp) and 11 pol (∼2995 bp) sequences. There were eight HIV-2 group A and three group B in both the LTR and pol regions. Conclusions This reference panel provides a robust, quantifiable, renewable, and non-infectious set of reagents that can be used for the development and evaluation of new HIV-2 molecular diagnostic assays and quality assurance and quality control reagents for use in the clinical laboratories.
    Journal of Clinical Virology 10/2014; 61(2). DOI:10.1016/j.jcv.2014.06.028 · 3.02 Impact Factor
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    • "HIV-2 is naturally resistant to non-nucleosidic reverse transcriptase inhibitors, including those of second generation, and to the fusion inhibitor enfuvirtide (Witvrouw et al. 2004; Andries et al. 2004; Poveda et al. 2004). The sensitivity to some protease inhibitors is reduced: amprenavir and its prodrug are not active, and contradictory results were published for atazanavir and tipranavir (Desbois et al. 2008; Brower et al. 2008). Moreover, the genetic barrier to resistance is reduced for several NRTIs and PIs (Smith et al. 2009). "

    HIV Testing, 01/2012; , ISBN: 978-953-307-871-7
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    • "A more in-depth study (kinetic inhibition assays) has shown that LPV, SQV, TPV, and DRV exhibit the highest potency in this order and that atazanavir (ATV), NFV, and APV show the lowest potency, respectively [54]. The data on TPV are however controversial, with other studies showing several fold lower potency when compared to LPV, SQV, and DRV [55] [56]. Once protease inhibitor(PI- ) based ART starts, this background of minor mutations may result in rapid acquisition of a multi-PI resistance phenotype [45] [46]. "
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    ABSTRACT: HIV-2 contributes approximately a third to the prevalence of HIV in West Africa and is present in significant amounts in several low-income countries outside of West Africa with historical ties to Portugal. It complicates HIV diagnosis, requiring more expensive and technically demanding testing algorithms. Natural polymorphisms and patterns in the development of resistance to antiretrovirals are reviewed, along with their implications for antiretroviral therapy. Nonnucleoside reverse transcriptase inhibitors, crucial in standard first-line regimens for HIV-1 in many low-income settings, have no effect on HIV-2. Nucleoside analogues alone are not sufficiently potent enough to achieve durable virologic control. Some protease inhibitors, in particular those without ritonavir boosting, are not sufficiently effective against HIV-2. Following review of the available evidence and taking the structure and challenges of antiretroviral care in West Africa into consideration, the authors make recommendations and highlight the needs of special populations.
    AIDS research and treatment 02/2011; 2011(6):463704. DOI:10.1155/2011/463704
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