Antiretroviral Drug Resistance in HIV‐2: Three Amino Acid Changes Are Sufficient for Classwide Nucleoside Analogue Resistance | Zendy

Robert A. Smith | Zendy; Donovan J. Anderson | Zendy; Crystal L. Pyrak | Zendy; Bradley D. Preston | Zendy; Geoffrey S. Gottlieb | Zendy

Open Access

Antiretroviral Drug Resistance in HIV‐2: Three Amino Acid Changes Are Sufficient for Classwide Nucleoside Analogue Resistance

Author(s) -

Robert A. Smith,

Donovan J. Anderson,

Crystal L. Pyrak,

Bradley D. Preston,

Geoffrey S. Gottlieb

Publication year - 2009

Publication title -

the journal of infectious diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.69

H-Index - 252

eISSN - 1537-6613

pISSN - 0022-1899

DOI - 10.1086/597802

Subject(s) - antiretroviral drug , drug resistance , hiv drug resistance , human immunodeficiency virus (hiv) , nucleoside , nucleoside analogue , virology , didanosine , medicine , biology , antiretroviral therapy , viral load , genetics

Genotypic surveys suggest that human immunodeficiency virus type 1 (HIV-1) and HIV-2 evolve different sets of mutations in response to nucleoside reverse-transcriptase inhibitors (NRTIs). We used site-directed mutagenesis, culture-based phenotyping, and cell-free assays to determine the resistance profiles conferred by specific amino acid replacements in HIV-2 reverse transcriptase. Although thymidine analogue mutations had no effect on zidovudine sensitivity, the addition of Q151M together with K65R or M184V was sufficient for high-level resistance to both lamivudine and zidovudine in HIV-2, and the combination of K65R, Q151M, and M184V conferred classwide NRTI resistance. These data suggest that current NRTI-based regimens are suboptimal for treating HIV-2 infection.

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