Activation of beta-chemokines and CCR5 in persons infected with human immunodeficiency virus type 1 and tuberculosis

Tuberculosis (TB) in human immunodeficiency virus type 1 (HIV-1)-infected p ersons is associated with progression of HIV-1 disease. The expression of m acrophage inflammatory protein (MIP)-1 alpha and CCR5 was assessed in HIV-1 -infected patients with pulmonary TB (HIV-1/PTB) and without PTB (HIV-1/C), PTB patients not infected with HIV-1 (PTB), and control subjects. Mycobact erium tuberculosis (MTB)-induced MIP-1 production was lower in peripheral b lood mononuclear cells (PBMC) of HIV-1/PTB patients than in those of PTB pa tients (P < .05) and was lower in PBMC of HIV-1/C patients than in those of control subjects (P < .05). However, MIP-1 alpha production was higher in PBMC of HIV/PTB patients than in those of HIV-1/C patients (P < .01). The p attern of MTB-induced RANTES production was similar to that of MIP-1<alpha> . However, MTB induced greater expression of mRNA for CCR5 in PBMC of HIV-1 /PTB patients than in those of HIV-1/C patients (P < .04). Furthermore, the MTB-induced HIV p24 antigen level in PBMC of HIV-1/PTB patients with a CD4 cell count <500 cells/muL was higher (P < .05) than that in HIV-1/C patien ts. Thus, perturbations in chemokine pathways in HIV-1/PTB patients may acc elerate HIV-1 disease.