Abstract
In vitro, the reverse transcriptase mutation K65R can simultaneously reduce drug susceptibility, replicative capacity and restrict HIV-1 replication. Here, we assessed the effect of tenofovir discontinuation for a patient receiving antiretroviral therapy whose HIV-1 had a dominant K65R/M184V genotype. Although limited by the single-case nature, the data support a hypothesis that there is no HIV viral RNA or CD4+ T-cell count benefit of taking tenofovir for experienced patients with genotypic evidence of K65R/M184V.
MeSH terms
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Adenine / administration & dosage
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Adenine / analogs & derivatives*
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Adenine / pharmacology
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Adenine / therapeutic use
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Adult
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Anti-HIV Agents* / administration & dosage
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Anti-HIV Agents* / pharmacology
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CD4 Lymphocyte Count
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Drug Administration Schedule
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Drug Resistance, Viral*
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Drug Therapy, Combination
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Genotype
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HIV Infections* / drug therapy
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HIV Infections* / immunology
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HIV Infections* / virology
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HIV Reverse Transcriptase / genetics*
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HIV-1 / drug effects*
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HIV-1 / enzymology
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HIV-1 / genetics
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Humans
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Lamivudine* / administration & dosage
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Lamivudine* / therapeutic use
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Male
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Mutation*
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Organophosphonates* / administration & dosage
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Organophosphonates* / pharmacology
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Organophosphonates* / therapeutic use
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RNA, Viral / blood
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Reverse Transcriptase Inhibitors* / administration & dosage
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Reverse Transcriptase Inhibitors* / pharmacology
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Tenofovir
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Treatment Outcome
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Viremia / drug therapy
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Viremia / immunology
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Viremia / virology
Substances
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Anti-HIV Agents
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Organophosphonates
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RNA, Viral
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Reverse Transcriptase Inhibitors
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Lamivudine
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Tenofovir
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reverse transcriptase, Human immunodeficiency virus 1
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HIV Reverse Transcriptase
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Adenine