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Prolonged elevation of viral loads in HIV-1-infected children in a region of intense malaria transmission in Northern Uganda: A prospective cohort study
Abstract
Introduction: Malaria and HIV-1 infection cause significant morbidity and mortality in children in sub-Saharan Africa. Recurrent malaria infection increases HIV-1 viral load in adults and increases the rate of progression of HIV-1 infection to AIDS. The effect of malaria on viral loads in children
living with AIDS (CLWA) is not clearly known.
Methods: One hundred thirty five afebrile HIV-1 positive children having negative blood slides for malaria were recruited at Apac Hospital and followed up for one year. They were monitored for development of Plasmodium falciparum malaria,
which was treated with chloroquine (CQ) + sulfadoxine-pyrimethamine (SP) and the children followed up for 28 days. HIV-1 viral loads were measured over three time-points: at enrolment (no malaria), during an episode of malaria, and at a visit about 8 weeks (range 6-19 weeks) after the malaria visit when the child had neither parasites nor any intervening malaria episodes (post-malaria). Primary analyses were restricted to
children who on follow up had HIV-1 viral loads measured at the three relevant time-points.
Results: Malaria increased HIV-1 viral load significantly in CLWA. Low parasitemia (200-4000/Cl) transiently increased viral load by 0.42 log (95% CI 0.29-0.78, p = 0.0002), higher than that
reported in adults. These patients’ viral loads returned to levels similar to those at baseline after treatment. In 13 patients with high parasitemia (>4000/Cl), the mean increase in viral load was 0.53 log (95% CI 0.14 to 0.51), p<0.0001, remaining significantly higher than at baseline after treatment i.e. mean difference (signed-rank test) in viral load “before” and “after” malaria was significant. Conclusion: Plasmodium falciparum
malaria is associated with increasing HIV-1 viral loads in children, with some viral loads remaining significantly elevated several weeks after antimalarial treatment. Prolonged post-treatment elevation has important implications for the clinical course in pre-ART HIV-1 positive children and
the potential for transmission in sexually active adults.
living with AIDS (CLWA) is not clearly known.
Methods: One hundred thirty five afebrile HIV-1 positive children having negative blood slides for malaria were recruited at Apac Hospital and followed up for one year. They were monitored for development of Plasmodium falciparum malaria,
which was treated with chloroquine (CQ) + sulfadoxine-pyrimethamine (SP) and the children followed up for 28 days. HIV-1 viral loads were measured over three time-points: at enrolment (no malaria), during an episode of malaria, and at a visit about 8 weeks (range 6-19 weeks) after the malaria visit when the child had neither parasites nor any intervening malaria episodes (post-malaria). Primary analyses were restricted to
children who on follow up had HIV-1 viral loads measured at the three relevant time-points.
Results: Malaria increased HIV-1 viral load significantly in CLWA. Low parasitemia (200-4000/Cl) transiently increased viral load by 0.42 log (95% CI 0.29-0.78, p = 0.0002), higher than that
reported in adults. These patients’ viral loads returned to levels similar to those at baseline after treatment. In 13 patients with high parasitemia (>4000/Cl), the mean increase in viral load was 0.53 log (95% CI 0.14 to 0.51), p<0.0001, remaining significantly higher than at baseline after treatment i.e. mean difference (signed-rank test) in viral load “before” and “after” malaria was significant. Conclusion: Plasmodium falciparum
malaria is associated with increasing HIV-1 viral loads in children, with some viral loads remaining significantly elevated several weeks after antimalarial treatment. Prolonged post-treatment elevation has important implications for the clinical course in pre-ART HIV-1 positive children and
the potential for transmission in sexually active adults.
