Johns Hopkins University, School of Hygiene and Public Health, Johns Hopkins University, School of Medicine, Division of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Makerere Medical School, Baltimore, Maryland, Uganda
We conducted a cross-sectional study to determine the serological response to malaria in an HIV-1 infected population and in a control population in a region of high malaria transmission. The study group consisted of 66 hospitalized patients with clinical acquired immunodeficiency syndrome (AIDS) and 70 trauma patients without clinical AIDS (controls). Mean optical densities of antibody produced against RESA-4, RESA-8, RESA-11, (PNAN)5 and (NAAG)5 synthetic peptides of Plasmodium falciparum were compared between HIV-1 seropositive and HIV-1 seronegative patients using non-parametric statistics. HIV-1 seropositive patients with clinical AIDS had significantly less antibody to the synthetic P. falciparum ring stage peptide, RESA-8 (P = 0.001), than a comparable group of seronegative patients. Antibody levels were also low for the other ring stage peptides, RESA-4 (P = 0.024) and RESA-11 (P = 0.024). Although not statistically significant, antibody levels among the HIV-1 seropositive trauma patients were higher than among the HIV-1 seronegative trauma patients. During HIV-1 infection, a polyclonal B cell activation may occur as noted in the HIV-1 seropositive trauma patients, but with increased immunosuppression in advanced clinical AIDS, B cell stimulation appears to be diminished. This results in decreased production of malaria antibody.