Evidence for rapid disappearance of initially expanded HIV-specific CD8(+) T cell clones during primary HIV infection

被引:175
作者
Pantaleo, G
Soudeyns, H
Demarest, JF
Vaccarezza, M
Graziosi, C
Paolucci, S
Daucher, M
Cohen, OJ
Denis, F
Biddison, WE
Sekaly, RP
Fauci, AS
机构
[1] NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892
[2] NINCDS,NEUROIMMUNOL BRANCH,NIH,BETHESDA,MD 20892
[3] INST RECH CLIN MONTREAL,IMMUNOL LAB,MONTREAL,PQ H2W 1R7,CANADA
[4] UNIV MONTREAL,DEPT MICROBIOL & IMMUNOL,MONTREAL,PQ H3C 3J7,CANADA
[5] MCGILL UNIV,DEPT MICROBIOL & IMMUNOL,MONTREAL,PQ H3A 2B4,CANADA
关键词
D O I
10.1073/pnas.94.18.9848
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Down-regulation of the initial burst of viremia during primary HIV infection is thought to be mediated predominantly by HIV-specific cytotoxic T lymphocytes, and the appearance of this response is associated with major perturbations of the T cell receptor repertoire. Changes in the T cell receptor repertoire of virus-specific cytotoxic T lymphocytes were analyzed in patients with primary infection to understand the failure of the cellular immune response to control viral spread and replication. This analysis demonstrated that a significant number of HIV-specific T cell clones involved in the primary immune response rapidly disappeared. The disappearance was not the result of mutations in the virus epitopes recognized by these clones. Evidence is provided that phenomena such as high-dose tolerance or clonal exhaustion might be involved in the disappearance of these monoclonally expanded HIV-specific cytotoxic T cell clones, These findings should provide insights into how HIV, and possibly other viruses, elude the host immune response during primary infection.
引用
收藏
页码:9848 / 9853
页数:6
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