BACKGROUND: Previously we demonstrated that monocyte phagolysosomal fusion is impaired in chronic HIV infection in adult patients. METHODS: We studied the phagolysosomal fusion of peripheral blood monocytes from 45 children vertically infected with HIV, 38 noninfected infants born to HIV-positive mothers and 14 children born to HIV-seronegative women, by a cytomorphologic method in which acridine orange is used as a fusion marker. RESULTS: The mean percentages of phagolysosomal fusion +/-SD were 42 +/- 16.1 for HIV-positive children, 55.3 +/- 15.5 for HIV-negative infants born to HIV-infected mothers and 58.2 +/- 12.7 for normal controls. Monocyte phagolysosomal fusion of HIV-infected children was significantly decreased in comparison to noninfected and normal infants (P < 0.001), while there was no difference between the two latter groups. Phagolysosomal fusion impairment in HIV-infected infants inversely correlated with age (r = -0.4527; P < 0.002) and directly correlated with CD4+ T cell counts (r = 0.393; P = 0.03). Moreover, phagolysosomal fusion strongly correlated with clinical manifestations; this function was significantly impaired in moderately and severely symptomatic HIV-infected children with respect to those who remained asymptomatic or mildly symptomatic (P < 0.05). CONCLUSIONS: Our results suggest that monocyte function in HIV-infected children progressively deteriorates, closely related to the severity of the clinical symptoms.
BACKGROUND: Previously we demonstrated that monocyte phagolysosomal fusion is impaired in chronic HIV infection in adult patients. METHODS: We studied the phagolysosomal fusion of peripheral blood monocytes from 45 children vertically infected with HIV, 38 noninfected infants born to HIV-positive mothers and 14 children born to HIV-seronegative women, by a cytomorphologic method in which acridine orange is used as a fusion marker. RESULTS: The mean percentages of phagolysosomal fusion +/-SD were 42 +/- 16.1 for HIV-positive children, 55.3 +/- 15.5 for HIV-negative infants born to HIV-infected mothers and 58.2 +/- 12.7 for normal controls. Monocyte phagolysosomal fusion of HIV-infectedchildren was significantly decreased in comparison to noninfected and normal infants (P < 0.001), while there was no difference between the two latter groups. Phagolysosomal fusion impairment in HIV-infectedinfants inversely correlated with age (r = -0.4527; P < 0.002) and directly correlated with CD4+ T cell counts (r = 0.393; P = 0.03). Moreover, phagolysosomal fusion strongly correlated with clinical manifestations; this function was significantly impaired in moderately and severely symptomatic HIV-infectedchildren with respect to those who remained asymptomatic or mildly symptomatic (P < 0.05). CONCLUSIONS: Our results suggest that monocyte function in HIV-infectedchildren progressively deteriorates, closely related to the severity of the clinical symptoms.