Journal Article

Oxidant Stress Is Increased during Treatment of Human Immunodeficiency Virus Infection

Todd Hulgan, Jason Morrow, Richard T. D'Aquila, Stephen Raffanti, Michael Morgan, Peter Rebeiro and David W. Haas

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 37, issue 12, pages 1711-1717
Published in print December 2003 | ISSN: 1058-4838
Published online December 2003 | e-ISSN: 1537-6591 | DOI: http://dx.doi.org/10.1086/379776
Oxidant Stress Is Increased during Treatment of Human Immunodeficiency Virus Infection

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Some diseases and environmental exposures, including those that are risk factors for atherosclerosis, are associated with increased oxidant stress. The objective of this cross-sectional, observational study was to determine whether oxidant stress is increased during human immunodeficiency virus type 1 (HIV-1) infection or its therapy. To quantify oxidant stress, plasma F2 isoprostane (F2-IsoP) concentrations were determined by gas chromatography/mass spectroscopy. A total of 120 subjects were enrolled during routine primary care visits. The median CD4+ T cell count was 341 cells/mm3, the median HIV-1 RNA level was 3.4 log10 copies/mL, and 74% of patients were receiving antiretroviral therapy. Plasma F2-IsoP concentrations were 12–149 pg/mL (median, 31 pg/mL). In univariate analysis, higher F2-IsoP concentrations were associated with lower log10 plasma HIV-1 RNA levels (P = .009) and with efavirenz use (P = .02). Both factors remained associated with plasma F2-IsoP concentrations in multivariate analysis. Oxidant stress associated with therapeutic control of viral replication may have important implications for long-term complications of antiretroviral therapy.

Journal Article.  3330 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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