Activation of β‐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 persons is associated with progression of HIV-1 disease. The expression of macrophage inflammatory protein (MIP)–1α 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. Mycobacterium tuberculosis (MTB)–induced MIP-1α production was lower in peripheral blood mononuclear cells (PBMC) of HIV-1/PTB patients than in those of PTB patients (P<.05) and was lower in PBMC of HIV-1/C patients than in those of control subjects (P<.005). However, MIP-1α production was higher in PBMC of HIV/PTB patients than in those of HIV-1/C patients (P<.01). The pattern of MTB-induced RANTES production was similar to that of MIP-1α. 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/μL was higher (P<.05) than that in HIV-1/C patients. Thus, perturbations in chemokine pathways in HIV-1/PTB patients may accelerate HIV-1 disease