Relationship of Plasma HIV-RNA Levels and Levels of TNF-α and Immune Activation Products in HIV Infection

The goal of this study was to determine the relationship between plasma human immunodeficiency virus (HIV) load and cytokine expression. HIV-RNA plasma levels were determined in 34 HIV-seropositive (HIV+) asymptomatic subjects [range: 0.5 to 211 kiloequivalents (kEq)/ml HIV-RNA], by a modified branc...

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Bibliographic Details
Published in:Clinical immunology and immunopathology 1997-07, Vol.84 (1), p.36-45
Main Authors: Salazar-Gonzalez, Jesus F., Martinez-Maza, Otoniel, Aziz, Najib, Kolberg, Janice A., Yeghiazarian, Torange, Shen, Lu-Ping, Fahey, John L.
Format: Article
Language:English
Subjects:
AIDS/HIV
Biological and medical sciences
Biomarkers - blood
Cohort Studies
Cytokines - blood
HIV - genetics
HIV - immunology
HIV Infections - blood
HIV Infections - genetics
HIV Infections - immunology
Humans
Immunodeficiencies
Immunodeficiencies. Immunoglobulinopathies
Immunopathology
Lymphocyte Activation
Male
Medical sciences
Receptors, Tumor Necrosis Factor - blood
RNA, Messenger - blood
RNA, Viral - blood
Tumor Necrosis Factor-alpha - metabolism
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Summary:The goal of this study was to determine the relationship between plasma human immunodeficiency virus (HIV) load and cytokine expression. HIV-RNA plasma levels were determined in 34 HIV-seropositive (HIV+) asymptomatic subjects [range: 0.5 to 211 kiloequivalents (kEq)/ml HIV-RNA], by a modified branched-DNA (bDNA) assay. Plasma HIV-RNA levels were positively correlated with increased plasma levels of TNF-α, soluble TNF receptor type II, soluble IL-2 receptor, β2-microglobulin, and neopterin, but not with plasma IL-6 levels. In contrast, increased viral load and diminished CD4 counts correlated weakly. TNF-α mRNA levels, as determined by bDNA technology, were not significantly increased in peripheral blood mononuclear cells (PBMC) isolated from HIV-infected subjects, compared to HIV-seronegative (HIV−) subjects, and were not correlated with plasma levels of HIV-RNA, cytokines, or activation markers. These results are consistent with the hypothesis that a self-reinforcing mechanism exists between TNF-α production and generalized immune activation on one hand with HIV replication on the other.
ISSN:0090-1229
1090-2341
DOI:10.1006/clin.1997.4364