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    CD4 + T-cell deficiency in HIV patients responding to antiretroviral therapy is associated with increased expression of interferon-stimulated genes in CD4 + T cells

    Access Status
    Open access via publisher
    Authors
    Fernandez, S.
    Tanaskovic, S.
    Helbig, K.
    Rajasuriar, R.
    Kramski, M.
    Murray, J.
    Beard, M.
    Purcell, D.
    Lewin, S.
    Price, Patricia
    French, M.
    Date
    2011
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Fernandez, S. and Tanaskovic, S. and Helbig, K. and Rajasuriar, R. and Kramski, M. and Murray, J. and Beard, M. et al. 2011. CD4 + T-cell deficiency in HIV patients responding to antiretroviral therapy is associated with increased expression of interferon-stimulated genes in CD4 + T cells. Journal of Infectious Diseases. 204 (12): pp. 1927-1935.
    Source Title
    Journal of Infectious Diseases
    DOI
    10.1093/infdis/jir659
    ISSN
    0022-1899
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/3445
    Collection
    • Curtin Research Publications
    Abstract

    Most patients with human immunodeficiency virus (HIV) who remain CD4 + T-cell deficient on antiretroviral therapy (ART) exhibit marked immune activation. As CD4 + T-cell activation may be mediated by microbial translocation or interferon-alpha (IFN-a), we examined these factors in HIV patients with good or poor CD4 + T-cell recovery on long-term ART. Messenger RNA levels for 3 interferon-stimulated genes were increased in CD4 + T cells of patients with poor CD4 + T-cell recovery, whereas levels in patients with good recovery did not differ from those in healthy controls. Poor CD4 + T-cell recovery was also associated with CD4 + T-cell expression of markers of activation, senescence, and apoptosis, and with increased serum levels of the lipopolysaccharide receptor and soluble CD14, but these were not significantly correlated with expression of the interferon-stimulated genes. Therefore, CD4 + T-cell recovery may be adversely affected by the effects of IFN-a, which may be amenable to therapeutic intervention. © 2011 The Author.

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