H. Mayanja-kizza et al., Activation of beta-chemokines and CCR5 in persons infected with human immunodeficiency virus type 1 and tuberculosis, J INFEC DIS, 183(12), 2001, pp. 1801-1804
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.