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Herbert Samuel Kiyingi, Thomas Gordon Egwang, Maria Nannyonga. Prolonged elevation of viral loads in HIV-1-infected children in a region of intense malaria transmission in Northern Uganda: a prospective cohort study. The Pan African Medical Journal. 2010;7:11 Key words: HIV infection, Plasmodium falciparum, Malaria, children living with AIDS, viral loads Permanent link: http://www.panafrican-med-journal.com/content/article/7/11/full Received: 08/10/2010 - Accepted: 26/10/2010 - Published: 09/11/2010 © Herbert Samuel Kiyingi et al. The Pan African Medical Journal - ISSN 1937-8688. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
Prolonged elevation of viral loads in HIV-1-infected children in a region of intense malaria transmission in Northern Uganda: a prospective cohort study
Herbert Samuel Kiyingi1,2, Thomas Gordon Egwang1,&, Maria Nannyonga1
1Homecare Department, St. Raphael of St. Francis Nsambya Hospital/Elizabeth Glaser Pediatric AIDS Foundation Collaboration, 2Centers for Disease Control and Prevention, Uganda
&Corresponding author
Thomas Gordon Egwang, Med-biotech laboratories, Muyenga Tank Hill By-pass, Lugwana Close, Plot 3438, P.O. Box 9364, Kampala Tel.+256-312-266-153, Uganda
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/µl) 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/µl), 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.
