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 Blood, 15 June 2005, Vol. 105, No. 12, pp. 4730-4735.
Prepublished online as a Blood First Edition Paper on February 10, 2005; DOI 10.1182/blood-2004-11-4272.

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IMMUNOBIOLOGY

Impaired base excision repair and accumulation of oxidative base lesions in CD4+ T cells of HIV-infected patients

Pål Aukrust, Luisa Luna, Thor Ueland, Rune F. Johansen, Fredrik Müller, Stig S. Frøland, Erling C. Seeberg, and Magnar Bjørås

From the Section of Clinical Immunology and Infectious Diseases, the Research Institute for Internal Medicine, the Section of Endocrinology, Medical Department, the Department of Molecular Biology, Institute of Medical Microbiology, and the Centre for Molecular Biology and Neuroscience, University of Oslo, The National Hospital, Oslo, Norway.

Several studies have reported enhanced oxidative stress in patients with HIV infection. An important pathophysiologic consequence of increased oxidative stress is endogenous DNA damage, and the base excision repair pathway is the most important mechanism to withstand such deleterious effects. To investigate the role of base excision repair in HIV infection, we examined 7,8-dihydro-8-oxoguanine (8-oxoG) levels as a marker of oxidative DNA damage and DNA glycosylase activities in CD4+ and CD8+ T cells of HIV-infected patients and controls. These results showed that the HIV-infected patients, particularly those with advanced disease, had increased levels of 8-oxoG in CD4+ T cells and marked declines in DNA glycosylase activity for the repair of oxidative base lesions in these cells. In contrast, CD8+ T cells from HIV-infected patients, with 8-oxoG levels similar to those in healthy controls, showed enhanced capacity to repair oxidative DNA damage. Finally, highly active antiretroviral therapy induced increased glycosylase activity in CD4+ T cells and normalized 8-oxoG levels. This imbalance between the accumulation of oxidative DNA damage and the capacity to repair such lesions in CD4+ T cells may represent a previously unrecognized mechanism involved in the numerical and functional impairment of CD4+ T cells in patients with HIV infection. (Blood. 2005; 105:4730-4735)


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