The role of human leukocyte antigen class I polymorphism in HIV/AIDS

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Purpose of review

Polymorphism at human leukocyte antigen class I loci accounts for a portion of the individual variability in susceptibility to, and evolution of, HIV-1 infection. Evaluation of the impact of class I polymorphism has improved, with refined techniques for genotyping, quantifying peptide binding characteristics of class I molecules, and measuring cytotoxic T lymphocyte responses.

Recent findings

Most class I alleles that are particularly advantageous or disadvantageous in controlling HIV/AIDS are human leukocyte antigen-B locus products. Some act more uniformly than others, across racial and viral subtype boundaries, and different alleles may exert their effects at different times during the course of infection. Disease progression may be retarded by alleles of less common supertypes. The virus mutates to escape host pressure exerted by class 1 programmed cytotoxic T lymphocytes, and may or may not revert to its earlier form, depending on the toll taken on its replication capacity.


Large virologically and immunologically well defined cohorts will be critical for increasingly comprehensive evaluation of the multiple small effects conferred by these highly polymorphic loci. Elucidating these effects at the population, clinical, cellular, and molecular levels poses a formidable challenge, but the reward could be vaccine constructs customized to the genetic profiles of individual populations, along with more effective individualized therapeutic intervention.

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