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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. This Article Full Text (PDF) All Versions of this Article: 2004-11-4272v1 105/12/4730    most recent e-Letter: Submit a Response Alert me when this article is cited Alert me when e-Letters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Aukrust, P. Articles by Bjoras, M. Search for Related Content PubMed PubMed Citation Articles by Aukrust, P. Articles by Bjoras, M. Social Bookmarking                         What's this?  Previous Article  |  Next Article  Submitted November 8, 2004 Accepted February 4, 2005 Impaired base excision repair and accumulation of oxidative base lesions in CD4+ T cells of HIV-infected patients Pal Aukrust, Luisa Luna, Thor Ueland, Rune F Johansen, Fredrik Muller, Stig S Froland, Erling C Seeberg, and Magnar Bjoras* Section of Clinical Immunology and Infectious Diseases, University of Oslo, The National Hospital, Oslo, Norway Research Institute for Internal Medicine, University of Oslo, The National Hospital, Oslo, Norway Section of Endocrinology, Medical Department, University of Oslo, The National Hospital, Oslo, Norway Department of Molecular Biology, Institute of Medical Microbiology, University of Oslo, The National Hospital, Oslo, Norway; Centre for Molecular Biology and Neuroscience, University of Oslo, The National Hospital, Oslo, Norway * Corresponding author; email: magnar.bjoras{at}medisin.uio.no. Several studies have reported enhanced oxidative stress in HIV infection. An important pathophysiological 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 8-oxoguanine (8-oxoG) levels, as a marker of oxidative DNA damage, and DNA glycosylase activities in CD4+ and CD8+ T cells from HIV-infected patients and controls. These results showed that HIV-infected patients, particularly those with advanced disease, were characterized by increased accumulation of 8oxoG in CD4+ T cells accompanied by a marked decline in DNA glycosylase activity for 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 accompanied by normalization of 8-oxoG levels. This imbalance between accumulation of oxidative DNA damage and the capacity to repair such lesions in CD4+ T cells may represent a previous unrecognized mechanism involved in the numerical and functional impairment of CD4+ T cells in HIV infection. CiteULike    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

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