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Research Article Free access | 10.1172/JCI119608

Do beta-chemokines have clinical relevance in HIV infection?

C E Mackewicz, E Barker, G Greco, G Reyes-Teran, and J A Levy

Department of Medicine and Cancer Research Institute, University of California, School of Medicine, San Francisco, California 94143-1270, USA.

Find articles by Mackewicz, C. in: JCI | PubMed | Google Scholar

Department of Medicine and Cancer Research Institute, University of California, School of Medicine, San Francisco, California 94143-1270, USA.

Find articles by Barker, E. in: JCI | PubMed | Google Scholar

Department of Medicine and Cancer Research Institute, University of California, School of Medicine, San Francisco, California 94143-1270, USA.

Find articles by Greco, G. in: JCI | PubMed | Google Scholar

Department of Medicine and Cancer Research Institute, University of California, School of Medicine, San Francisco, California 94143-1270, USA.

Find articles by Reyes-Teran, G. in: JCI | PubMed | Google Scholar

Department of Medicine and Cancer Research Institute, University of California, School of Medicine, San Francisco, California 94143-1270, USA.

Find articles by Levy, J. in: JCI | PubMed | Google Scholar

Published August 15, 1997 - More info

Published in Volume 100, Issue 4 on August 15, 1997
J Clin Invest. 1997;100(4):921–930. https://doi.org/10.1172/JCI119608.
© 1997 The American Society for Clinical Investigation
Published August 15, 1997 - Version history
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Abstract

The role of beta-chemokines in HIV infection was evaluated. The kinetics of regulated upon activation of normal T cell expressed and secreted, macrophage inflammatory protein-1alpha, and macrophage inflammatory protein 1beta production by stimulated T lymphocytes did not differ substantially between HIV-infected (asymptomatic and with AIDS) and uninfected subjects. Maximal production of these beta-chemokines by activated peripheral blood cells was higher in the infected individuals than in uninfected individuals, but no significant difference was observed between healthy infected subjects and AIDS patients. Evaluation of the effect of HIV replication on beta-chemokine production indicated that acute infection of CD4+ T cells with non-syncytia-inducing (NSI) viruses generally increased beta-chemokine production two to eightfold, whereas with SI strains, it led to decreased production. The sensitivity of an individual's virus to beta-chemokine-mediated inhibition correlated with the NSI virus phenotype and a healthy clinical state. 50% of the AIDS patients, however, had NSI viruses that were sensitive to beta-chemokines. Finally, anti-beta-chemokine-neutralizing antibodies caused a more rapid release of HIV by CD4+ T cells naturally infected by NSI, but not SI, viruses indicating that endogenously produced chemokines can affect HIV production in culture. These findings suggest that beta-chemokines may affect HIV replication when an NSI virus is involved, but provide little evidence that they substantially influence HIV infection and pathogenesis.

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