期刊
CLINICAL INFECTIOUS DISEASES
卷 49, 期 6, 页码 956-964出版社
OXFORD UNIV PRESS INC
DOI: 10.1086/605503
关键词
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资金
- Canadian Institutes of Health Research
- South African Department of Science and Technology/National Research Foundation Research Chair in Systems Biology of HIV/AIDS
- Bill and Melinda Gates Foundation
- International AIDS Vaccine Initiative
- South African AIDS Vaccine Initiative
- Center for AIDS Research at Harvard University
- National Institutes of Health [R01-AI067073, N01-AI-15422, R01-AI46995]
- Wellcome Trust
- National Cancer Institute and National Institutes of Health [HHSN261200800001E]
- Intramural Research Program
Background. The extent to which immunologic and clinical biomarkers influence human immunodeficiency virus type 1 (HIV-1) infection outcomes remains incompletely characterized, particularly for non-B subtypes. On the basis of data supporting in vitro HIV-1 protein-specific CD8 T lymphocyte responses as correlates of immune control in cross-sectional studies, we assessed the relationship of these responses, along with established HIV-1 biomarkers, with rates of CD4 cell count decrease in individuals infected with HIV-1 subtype C. Methods. Bivariate and multivariate mixed-effects models were used to assess the relationship of baseline CD4 cell count, plasma viral load, human leukocyte antigen (HLA) class I alleles, and HIV-1 protein-specific CD8 T cell responses with the rate of CD4 cell count decrease in a longitudinal population-based cohort of 300 therapy-naive, chronically infected adults with baseline CD4 cell counts >200 cells/mm(3) and plasma viral loads > 500 copies/mL over a median of 25 months of follow-up. Results. In bivariate analyses, baseline CD4 cell count, plasma viral load, and possession of a protective HLA allele correlated significantly with the rate of CD4 cell count decrease. No relationship was observed between HIV-1 protein - specific CD8 T cell responses and CD4 cell count decrease. Results from multivariate models incorporating baseline CD4 cell counts (201-350 vs >350 cells/mm(3)), plasma viral load (<= 100,000 vs >100,000 copies/mL), and HLA (protective vs not protective) yielded the ability to discriminate CD4 cell count decreases over a 10- fold range. The fastest decrease was observed among individuals with CD4 cell counts >350 cells/mm(3) and plasma viral loads >100,000 copies/mL with no protective HLA alleles (-59 cells/mm(3) per year), whereas the slowest decrease was observed among individuals with CD4 cell counts 201-350 cells/mm(3), plasma viral loads <= 100,000 copies/ mL, and a protective HLA allele (-6 cells/mm(3) per year). Conclusions. The combination of plasma viral load and HLA class I type, but not in vitro HIV-1 protein specific CD8 T cell responses, differentiates rates of CD4 cell count decrease in patients with chronic subtype-C infection better than either marker alone.
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