Human immunodeficiency virus genetic variation that can escape cytotoxic T cell recognition

In a longitudinal study of HIV seropositive patients, there were fluctuations in the specificity of cytotoxic T cells for the virus. This was matched by variability in proviral gag DNA epitope sequences in the lymphocytes of these patients. Some of these viral variants are not recognized by autologo...

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Bibliographic Details
Published in:Nature (London) 1991-12, Vol.354 (6353), p.453-459
Main Authors: Phillips, Rodney E, Rowland-Jones, Sarah, Nixon, Douglas F, Gotch, Frances M, Edwards, Jon P, Ogunlesi, Afolabi O, Elvin, John G, Rothbard, Jonathan A, Bangham, Charles R. M, Rizza, Charles R, McMichael, Andrew J
Format: Article
Language:English
Subjects:
Acquired immune deficiency syndrome
AIDS
AIDS/HIV
Amino Acid Sequence
Base Sequence
Biological and medical sciences
Epitopes - genetics
Epitopes - immunology
Fluctuations
Fundamental and applied biological sciences. Psychology
Genetic diversity
Genetic Variation - genetics
Genetic Variation - immunology
Hemophilia A - complications
HIV - genetics
HIV - immunology
HIV Core Protein p24 - genetics
HIV Core Protein p24 - immunology
HIV Infections - complications
HIV Infections - immunology
HIV Infections - microbiology
HIV Seropositivity - immunology
Humanities and Social Sciences
Humans
Longitudinal Studies
Lymphocytes
Medical research
Microbiology
Molecular Sequence Data
multidisciplinary
Mutation - genetics
Mutation - immunology
Peptide Fragments - immunology
Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains
Science
Science (multidisciplinary)
T-Lymphocytes, Cytotoxic - immunology
T-Lymphocytes, Cytotoxic - microbiology
Virology
Viruses
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Summary:In a longitudinal study of HIV seropositive patients, there were fluctuations in the specificity of cytotoxic T cells for the virus. This was matched by variability in proviral gag DNA epitope sequences in the lymphocytes of these patients. Some of these viral variants are not recognized by autologous T cells. Accumulation of such mutations in T-cell antigenic targets would provide a mechanism for immune escape.
ISSN:0028-0836
1476-4687
DOI:10.1038/354453a0