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The emergence of cytotoxic T-lymphocyte (CTL) escape mutations in human immunodeficiency virus type 1 (HIV-1) proteins has been anecdotally associated with progression to AIDS, but it has been difficult to determine whether viral mutation is the cause or the result of increased viral replication. Here we describe a perinatally HIV-infected child who maintained a plasma viral load of <400 copies/ml for almost a decade until a nonbinding escape mutation emerged within the immunodominant CTL epitope. The child subsequently experienced a reemergence of HIV-1 viremia accompanied by a marked increase in the number of CTL epitopes targeted. This temporal pattern suggests that CD8 escape can play a causal role in the loss of immune control.

Original publication

DOI

10.1128/JVI.78.16.8927-8930.2004

Type

Journal article

Journal

J Virol

Publication Date

08/2004

Volume

78

Pages

8927 - 8930

Keywords

Amino Acid Sequence, Child, Disease Progression, Epitopes, T-Lymphocyte, HIV Infections, HIV Long-Term Survivors, HIV-1, HLA-B27 Antigen, Humans, Immunodominant Epitopes, Molecular Sequence Data, Mutation, T-Lymphocytes, Cytotoxic, Viremia