Background: Raised HIV viral load in blood has been associated with accelerated disease progression and increased transmission of infection. To assess the effect of Plasmodium falciparum malaria on concentrations of HIV in blood, we did a prospective cohort study in Malawi.
Methods: We recruited 367 HIV-1-infected adults. Among 334 people aparasitaemic at baseline, 148 had at least one malaria episode during follow-up and received antimalarial treatment. Of these, 77 had HIV-1-RNA measurements at baseline, during malaria, and post-malaria. We used linear regression with generalised estimating equations to assess effect of four definitions of malaria (any parasitaemia, parasite density > or =2000/microL, febrile parasitaemia, and febrile parasitaemia with parasite density > or =2000/microl) on changes in log HIV-1 RNA, overall and by baseline CD4 count.
Findings: With malaria defined as any parasitaemia, HIV-1-RNA concentration almost doubled between baseline (median 96215 copies per mL) and malaria (168901 copies per mL), a 0.25 (95% CI 0.11-0.39) log increase in mean RNA concentration. HIV-1-RNA concentration fell to median 82058 copies per mL by about 8-9 weeks post-malaria. Increases in HIV-1-RNA were greatest for people with fever, parasite density 2000/microL or greater, and CD4 count more than 300 cells per muL, in whom concentrations rose from median 38483 copies per mL at baseline to 196098 copies per mL during malaria, a mean log increase of 0.82 (95% CI 0.55-1.10, p<0.0001), and fell to median 75331 copies per mL post-malaria. People who remained aparasitaemic showed no changes in HIV-1-RNA concentration.
Interpretation: HIV-infected individuals with malaria have a significantly increased viral load, which might enhance HIV transmission and accelerate disease progression.