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Title: Selected P. falciparum specific immune responses are maintained in AIDS adults in Burkina Faso.
Author: Migot F, Ouedraogo JB, Diallo J, Zampan H, Dubois B, Scott-Finnigan T, Sanou PT, Deloron P.
Journal: Parasite Immunol; 1996 Jul; 18(7):333-9. PubMed ID: 9229386.
Abstract:
In tropical areas where Plasmodium falciparum malaria is endemic, co-infection with HIV-1 does not lead to a worsening of malaria, raising questions about the immunological interactions between both infections. Alterations of immune response to malaria during HIV-1 infection was investigated in the town of Bobo Dioulasso, Burkina Faso. Sixty-six adults were enrolled, including 37 HIV-1 positive subjects with < 250 CD4+ cells/microliter and clinical AIDS, and 29 HIV-1, negative healthy subjects. In vitro lymphocyte proliferation and cytokine (IFN-gamma, IL-2 and IL-4) production were assessed in isolated mononuclear cells (PBMC) in presence of PHA, PPD or three malarial antigens: the baculovirus-expressed protein from P. falciparum Merozoite Surface Protein-I, a P. falciparum in vitro culture and a crude schizont extract. Compared with healthy subjects. AIDS patients presented with decreased levels of cell proliferation and of IFN-gamma and IL-2 production, in response to all antigens except the schizont extract. Similar levels of IL-4 production were obtained in both groups. Mitogenic stimulation of whole blood cultures was also performed, and revealed similar trends in cytokine production as in PBMC cultures. These results show that some components of the specific human immune responses to falciparum parasites may not be modified during AIDS, in spite of the strong cellular alterations induced by HIV, namely the decrease of the CD4+ lymphocyte subset. In tropical areas where Plasmodium falciparum malaria is endemic, concurrent HIV infection does not appear to increase malaria prevalence. To investigate the immunologic interactions between these two infections, 66 adults from Bobo Dioulasso, Burkina Faso, were enrolled in a study in May 1994. The group included 29 HIV-negative adults and 37 hospitalized HIV-positive adults with clinical AIDS and under 250 CD4+ cells per mcgl of blood. All subjects belonged to a population exposed to numerous falciparum malaria infections since birth and were thus presumed to have developed specific antimalarial protective immune mechanisms prior to HIV infection. AIDS patients had a reduced hemoglobin content and a lower number of CD3+ and CD4+ lymphocytes than healthy controls. All thick blood smears were negative for malaria parasites, but the mean level of antibodies to P. falciparum was lower and the total immunoglobulin G content of plasma was higher in AIDS patients than controls. In vitro lymphocyte proliferation and cytokine (IFN-psi, IL-2, and IL-4) production were assessed in isolated mononuclear cells (PBMC) in the presence of PHA, PPD, or 3 antimalarial agents: the baculovirus-expressed protein from P. falciparum Merozoite Surface Protein-1, a P. falciparum in vitro culture, and a crude schizont extract. AIDS patients presented with decreased levels of cell proliferation and of IFN-psi and IL-2 production compared to healthy controls in response to all antigens except the schizont extract. IL-4 production levels were similar in both groups. Mitogenic stimulation of whole blood cultures revealed similar trends in cytokine production as in PBMC cultures. These findings confirm that not all effector cells involved in the immune responses directed against malaria are affected by concurrent HIV infection and/or that important CD4+ independent mechanisms of protection against malaria are conserved. It has been proposed that HIV infection causes a selective depletion of T cell subsets that are not implicated in the antimalarial immune response.

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