Journal
JOURNAL OF VIROLOGY
Volume 78, Issue 16, Pages 8927-8930Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.78.16.8927-8930.2004
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Funding
- NIAID NIH HHS [AI46995, R01 AI028568, K23 AI052078, AI52078, R01 AI046995, R37 AI028568, AI28568] Funding Source: Medline
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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.
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