Effects of malaria infection in human immunodeficiency virus type 1-infected Ugandan children.

BACKGROUND: Malaria causes severe morbidity and mortality in many areas of Africa where HIV-1 infection is also prevalent. Immunosuppression is associated with both diseases but most reports do not find significant interactions between them. METHODS: A collaborative study of HIV-1 infection in Ugandan women and their infants was established between the Ministry of Health, Makerere University, Kampala, and Case Western Reserve University in 1988. Four hundred fifty-eight infants, including 77 HIV-1-infected, 232 seroreverter and 125 control children born to HIV-1-negative mothers and 24 of indeterminate status were followed closely from birth for 4 years. Data on these infants were reviewed with respect to episodes of general illness and infections, suspected and confirmed episodes of malaria, onset and frequency of malaria, use of chloroquine and occurrence of selected illnesses after episodes of febrile illnesses. Thick and thin blood smears for malaria were obtained from children with fever. RESULTS: There was no association between occurrence of febrile illnesses and childrens' HIV-1 category. The relative rates of occurrence were 1.0 (95% confidence interval (CI), 0.8 to 1.2) and 1.1 (95% CI 0.9 to 1.4) for the HIV seroreverter and control children compared with the HIV-infected children. Although there was no association (P = 0.83) between HIV-1 status and a smear being taken during a febrile episode, there was an increase in smears positive for malaria parasitemia among seroreverter (risk ratio, 1.5; 95% CI 1.1 to 1.9) and control infants (risk ratio, 1.6; 95% CI 1.2 to 2.2) compared with HIV-1-infected infants. The level of parasitemia was similar in each group. A greater proportion of malaria episodes among the HIV-infected group than among the control groups resulted in hospitalizations (P = 0.001) and blood transfusions (P = 0.02). There was a positive association between time to clinical AIDS and absence of malaria (adjusted for follow-up age) in infected children (P = 0.02). Use of chloroquine was similarly high in each HIV-1 category (80%). CONCLUSIONS: In this group of HIV-infected children there was no significant increase in malarial episodes as compared with their HIV-negative controls. The results suggest a possibility that malaria may offer some protection against HIV-1 progression or that chloroquine used to treat malaria may have a direct effect against the HIV-1 virus.

PIP: A prospective study of 458 infants from Kampala, Uganda, who were followed from birth to 48 months of age, documented a reduced risk of malaria in children infected with HIV-1. Included in the analysis were 77 HIV-infected children, 232 seroreverters, 125 HIV-negative children born to uninfected mothers, and 24 children of indeterminate HIV status. Thick and thin blood smears for malaria were obtained from children with fever. 51% of all children had at least 1 positive malaria smear during the study period, for a total of 653 documented malaria episodes. HIV-infected children had 3.5 episodes of malaria per 100 child months of observation compared with 5.0 episodes among seroreverters and 5.5 episodes among seronegative children. The relative rates of occurrence of malaria were 1.0 (95% confidence interval [CI], 0.8-1.2) in seroreverters and 1.1 (95% CI, 0.9-1.4) There was an increase in smears positive for malaria parasitemia among seroreverters (risk ratio, 1.5; 95% CI, 1.1-1.9) and HIV-negative controls (risk ratio, 1.6; 95% CI, 1.2-2.2) compared with HIV-infected children. Parasitemia levels during episodes of malaria were not significantly different between groups. Although the HIV-infected children had fewer episodes of malaria, they had a greater percentage of severe malaria episodes than controls and more frequent hospitalizations and blood transfusions per acute malarial episode. Within the HIV-positive group, mortality and progression to AIDS were delayed (although not significantly) among children who had malaria compared with those without malaria. It is possible that HIV-1 suppresses Plasmodium infection by creating a milieu that is suboptimal for parasite growth.

Growth failure as a prognostic indicator of mortality in pediatric HIV infection.

OBJECTIVE: To study the effect of perinatally acquired human immunodeficiency virus (HIV) on somatic growth and examine the relationship of nutritional status to mortality in HIV-infected infants. METHOD: Pregnant women attending the antenatal clinic at Mulago hospital in Kampala, Uganda, were enrolled. All live-born babies born to HIV-1 seropositive (HIV+) women, and to every fourth age-matched HIV-1 seronegative (HIV-) woman, were followed for 25 months. RESULTS: The mean weight-for-age and length-for-age curves of HIV+ children were significantly lower than those of HIV- controls and seroeverters. Forty-five (54%) of the 84 HIV+ infants died before their second birthday, as compared with a 1.6% and 5.6% mortality in HIV- and seroeverters. HIV+ infants with an average weight-for-age Z-score below -1.5 in the first year of life have a nearly fivefold risk of dying before 25 months of age compared with noninfected controls. CONCLUSION: Perinatally acquired HIV infection is associated with early and progressive growth failure. The severity of growth failure is associated with an increased risk of mortality. The effect of early, aggressive nutritional intervention in delaying HIV progression and mortality should be evaluated by controlled intervention studies.