Objective: To investigate the effect of placental Plasmodium falciparum malaria infection on peripheral and/or placental HIV-1 viral load.
Design: A cross-sectional study of HIV-infected pregnant women, with and without placental malaria, delivering at Queen Elizabeth Central Hospital in Malawi.
Methods: Peripheral blood samples were collected from consenting women and tested for HIV. HIV-infected women received nevirapine at the onset of labor. At delivery, placental blood and tissue specimens were collected. HIV-1 RNA concentrations were measured in peripheral and placental plasma samples, and malaria infection was determined by placental histopathology.
Results: Of the 480 HIV-infected women enrolled, 304 had placental histopathology performed, of whom 74 (24.3%) had placental malaria. Compared with women without placental malaria, those with placental malaria had a 2.5-fold higher geometric mean peripheral HIV-1 RNA concentration (62 359 versus 24 814 copies/ml; P = 0.0007) and a 2.4-fold higher geometric mean placental HIV-1 RNA concentration (11 733 versus 4919 copies/ml; P = 0.008). In multivariate analyses, after adjusting for CD4 cell count and other covariates, placental malaria was associated with a 1.7-fold increase in geometric mean peripheral HIV-1 RNA concentration (47 747 versus 27 317 copies/ml; P = 0.02) and a 2.0-fold increase in geometric mean placental HIV-1 RNA concentration (9670 versus 4874 copies/ml; P = 0.03).
Conclusion: Placental malaria infection is associated with an increase in peripheral and placental HIV-1 viral load, which might increase the risk of mother-to-child transmission of HIV.
From the aDepartment of Community Health, the bDepartment of Obstetrics and Gynecology and the cMalawi-Liverpool-Wellcome Trust Clinical Research Programme, College of Medicine, Blantyre, Malawi, the dDepartment of Epidemiology and the eDepartment of Anthropology University of Michigan, Ann Arbor, Michigan, USA, the fDepartment of Medicine, University of Melbourne, Parkville, Australia, and the gDepartments of Epidemiology and Microbiology, University of North Carolina, Chapel Hill, North Carolina, USA.
Correspondence to: Dr. S. R. Meshnick, University of North Carolina School of Public Health, Department of Epidemiology, CB 7435, Chapel Hill, North Carolina 27599, USA.
Received: 17 June 2003; revised: 4 December 2003; accepted: 28 January 2004.