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Journal of Virology, November 1999, p. 9153-9160, Vol. 73, No. 11
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Longitudinal Phenotypic Analysis of Human Immunodeficiency Virus Type 1-Specific Cytotoxic T Lymphocytes: Correlation with Disease Progression

Graham S. Ogg,1,* Stefan Kostense,2 Michel R. Klein,2,dagger Suzanne Jurriaans,3 Dörte Hamann,2 Andrew J. McMichael,1 and Frank Miedema2,3

MRC Human Immunology Unit, Institute of Molecular Medicine, Oxford OX3 9DS, United Kingdom,1 and Department of Clinical Viro-Immunology, CLB & Laboratory for Clinical and Experimental Immunology,2 and Department of Human Retrovirology,3 Academic Medical Center, Amsterdam, The Netherlands

Received 23 February 1999/Accepted 23 July 1999

Few studies have examined longitudinal changes in human immunodeficiency virus type 1 (HIV)-specific cytotoxic T lymphocytes (CTL). To more closely define the natural history of HIV-specific CTL, we used HLA-peptide tetrameric complexes to study the longitudinal CD8+ T-cell response evolution in 16 A*0201-positive untreated individuals followed clinically for up to 14 years. As early as 1 to 2 years after seroconversion, we found a significant association between high frequencies of A*0201-restricted p17Gag/Pol tetramer-binding cells and slower disease progression (P < 0.01). We observed that responses could remain stable over many months, but any longitudinal changes that occurred were typically accompanied by reciprocal changes in RNA viral load. Phenotypic analysis with markers CD45RO, CD45RA, and CD27 identified distinct subsets of antigen-specific cells and the preferential loss of CD27+ CD45RO+ cells during periods of rapid decline in the frequency of tetramer-binding cells. In addition we were unable to confirm previous studies showing a consistent selective loss of HIV-specific cells in the context of sustained Epstein-Barr virus-specific cell frequencies. Overall, these data support a role of HIV-specific CTL in the control of disease progression and suggest that the ultimate loss of such CTL may be preferentially from the CD27+ CD45RO+ subset.

* Corresponding author. Mailing address: MRC Human Immunology Unit, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom. Phone: 01865-222334. Fax: 01865-222502. E-mail: gogg{at}worf.molbiol.ox.ac.uk.

dagger Present address: TB Research Programme, Medical Research Council Laboratories, Banjul, The Gambia.

Journal of Virology, November 1999, p. 9153-9160, Vol. 73, No. 11
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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