Antioxidant defenses influence HIV-1 replication and associated cytopathic effects

Paul A. Sandstrom, Judith Murray, Thomas M. Folks, Alan M. Diamond

    Research output: Contribution to journalArticlepeer-review

    52 Scopus citations


    HIV-infected cells often exhibit reduced levels of antioxidant enzymes and thiols. To investigate the role of cellular antioxidant defenses in the progression of an acutely spreading HIV-1 infection, human Sup-T1 T cells were engineered to overexpress the selenium-dependent glutathione peroxidase, GSHPx-1. This enzyme represents a major cellular defense mechanism against toxicity associated with reactive oxygen species (ROS). T cells engineered to produce elevated GSHPx-1 activity displayed accelerated viral replication and associated cytopathic effects compared to control cells. Conversely, the inhibition of the synthesis of glutathione with buthione sulfoximine (BSO) resulted in the attenuation of viral replication in Sup-T1 cells. Similarly, exposure of human peripheral blood lymphocytes (PBLs) to low, nontoxic levels of BSO resulted in an approximately 80% decline in HIV-1 replication as indicated by Western blot analysis of viral proteins.

    Original languageEnglish (US)
    Pages (from-to)1485-1491
    Number of pages7
    JournalFree Radical Biology and Medicine
    Issue number9
    StatePublished - Jun 1998


    • BSO
    • Free radical
    • Glutathione
    • Glutathione peroxidase
    • HIV-1
    • Selenium

    ASJC Scopus subject areas

    • Biochemistry
    • Physiology (medical)


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