Journal
AIDS
Volume 14, Issue 8, Pages 951-958Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00002030-200005260-00006
Keywords
HIV; anemia; cytokines; immune activation; CD38; tumor necrosis factor; interleukin-6; b2-microglobulin; cell loss; immune deficiency
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Funding
- NHLBI NIH HHS [N01-HB-57116, N01-HB-57117, N01-HB-57115] Funding Source: Medline
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Objective: To model the relationships among HIV-1 replication, immune activation and CD4+ T-cell losses in HIV-1 infection. Methods: Cross-sectional analysis of baseline data from the Viral Activation by Transfusion Study. Comparisons of unadjusted and adjusted correlative analyses to establish models for mechanisms of cell loss in AIDS. Results: Using these analyses, significant correlations were found among plasma levels of tumor necrosis factor alpha (TNF alpha) and its type two receptor (TNFrII), interleukin-6 (IL-6), beta(2)-microglobulin, expression of CD38 and HLA-DR on CD8+ T lymphocytes and plasma levels of HIV-1 RNA. When correlations among these indices were adjusted for possible intermediary correlations, the relationship between HIV-1 RNA levels and all plasma markers of immune activation could be accounted for by the correlation between plasma HIV-1 RNA and plasma TNFrII levels. In addition, the negative correlations that both HIV-1 RNA levels and TNFrII levels had with CD4+ T-cell counts were partially accounted for by the correlations of HIV-1 RNA and TNFrII with CD38 expression on CD8+ T cells. In persons with advanced disease (CD4+ T cells < 50 x 10(6)/l) IL-6 levels were inversely correlated with CD4+ T-cell counts. Conclusions: This analysis is consistent with a model wherein HIV-1 replication induces TNF alpha expression that induces multiple other indices of immune activation. In this model, HIV-1 replication and TNF alpha expression induce CD4+ T-cell losses at least in part through mechanisms reflected in heightened CD38 expression. (C) 2000 Lippincott Williams & Wilkins.
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