HIV-1-specific cellular immune responses among HIV-1-resistant sex workers

Citation
Kr. Fowke et al., HIV-1-specific cellular immune responses among HIV-1-resistant sex workers, IMM CELL B, 78(6), 2000, pp. 586-595
Citations number
58
Categorie Soggetti
Immunology
Journal title
IMMUNOLOGY AND CELL BIOLOGY
ISSN journal
08189641 → ACNP
Volume
78
Issue
6
Year of publication
2000
Pages
586 - 595
Database
ISI
SICI code
0818-9641(200012)78:6<586:HCIRAH>2.0.ZU;2-B
Abstract
The goal of the present study was to determine whether there were HIV-1 spe cific cellular immune responses among a subgroup of women within a cohort o f Nairobi prostitutes (n = 1800) who, despite their intense sexual exposure to HIV-1, are epidemiologically resistant to HIV-1 infection. Of the 80 wo men defined to be resistant, 24 were recruited for immunological evaluation . The HIV-1-specific T-helper responses were determined by IL-2 production following stimulation with HIV-1 envelope peptides and soluble gp120. Cytot oxic T lymphocyte responses were determined by lysis of autologous EBV-tran sformed B cell lines infected with control vaccinia virus or recombinant va ccinia viruses containing the HIV-1 structural genes env, gag and pol. Resi stant women had significantly increased HIV-1 specific T-helper responses, as determined by in vitro IL-2 production to HIV-1 envelope peptides and so luble glycoprotein 120, compared with low-risk seronegative and HIV-1-infec ted controls (P less than or equal to 0.01, Student's t-test). Seven of the 17 (41%) resistant women showed IL-2 stimulation indices greater than or e qual to 2.0. HIV-1-specific CTL responses were detected among 15/22 (68.2%) resistant women compared with 0/12 low-risk controls (Chi-squared test, P < 0.001). In the two resistant individuals tested, the CTL activity was med iated by CD8(+) effectors. Many HIV-1-resistant women show evidence of HIV- 1-specific T-helper and cytotoxic responses. These data support the suggest ion that HIV-1-specific T-cell responses contribute to protection against H IV-1 infection.