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.