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The contribution of virologic and host factors to CD4 cell depletion associated with human immunodeficiency virus (HIV) type 1 was evaluated in children drawn from a larger efficacy trial of 2 doses of didanosine (ddI) monotherapy (Pediatric AIDS Clinical Trials Group 144). Thirty children, half with stable CD4 cell counts (non-progressors) and half with a marked decline in CD4 cells (progressors), were studied during 60-72 weeks of ddI therapy. The children were matched for age and CD4 cell counts at study entry. Three viral parameters, syncytium-inducing phenotype, higher virus load, and mutation in HIV-1 pol encoding the T69D/N mutation, were associated with disease progression. Disease progression was not associated with mutations in the reverse-transcriptase gene previously associated with resistance to ddI (L74V, K65R, or M184V). The selection of the T69D/N mutation in children with HIV-1 disease progression during ddI therapy suggests that this mutation confers a fitness advantage to the virus that may include resistance to ddI.

the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases

T69D/N<i>pol</i>Mutation, Human Immunodeficiency Virus Type 1 RNA Levels, and Syncytium‐Inducing Phenotype Are Associated with CD4 Cell Depletion during Didanosine Therapy

T69D/NpolMutation, Human Immunodeficiency Virus Type 1 RNA Levels, and Syncytium‐Inducing Phenotype Are Associated with CD4 Cell Depletion during Didanosine Therapy