Influence of active tuberculosis on chemokine and chemokine receptor expression in HIV-infected persons.

Hanna, L.E.; Bose, J.C.; Nayak, K.; Subramanyam, S.; Swaminathan, S.

Aids Research and Human Retroviruses; 2005; 21; 997–1002.

Abstract: Tuberculosis (TB) is the major opportunistic infection of HIV-1-infected patients in developing countries. Concurrent infection with TB results in immune cells having enhanced susceptibility to HIV-1 infection, which facilitates entry and replication of the virus. Cumulative data from earlier studies indicate that TB provides a milieu of continuous cellular activation and irregularities in cytokine and chemokine circuits that favor viral replication and disease progression. To better understand the interaction of the host with HIV-1 during active tuberculosis, we investigated in vivo expression of the HIV-1 coreceptors, CCR5 and CXCR4, and circulating levels of the inhibitory b -chemokines, macrophage inflammatory protein-1- a (MIP-1 a ), macrophage inflammatory protein-1- b (MIP-1 b ), and regulated upon activation T cell expressed and secreted (RANTES), in HIV-positive individuals with and without active pulmonary tuberculosis. We found a significant decrease from normal in the fraction of CD4 + T cells expressing CCR5 and CXCR4 in individuals infected with HIV. However, CCR5 and CXCR4 expression did not differ significantly between HIV patients with and without tuberculosis. Higher amounts of MIP-1 a , MIP-1 b , and RANTES were detected in plasma of HIV-1-positive individuals, particularly those with dual infection, although the increase was not found to be statistically significant.

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