Detection of EBV RNA (EBER-1 and EBER-2) in malaria lymph nodes by in situ hybridization.

Acute Plasmodium falciparum malaria in African children allows expansion of latent Epstein-Barr virus infection, leading to colonization of lymph nodes by virus-infected lymphoblasts in 60% of cases as demonstrated by in situ hybridization for the detection of EBER-1 and EBER-2 RNA. This probably arises against a background of malaria-induced immunosuppression to EBV and concurrent lymphoid activation. The relevance of the results to the pathogenesis of African endemic Burkitt's lymphoma is discussed.

Erythrocytes carrying mutations in spectrin and protein 4.1 show differing sensitivities to invasion by Plasmodium falciparum.

The role of the erythrocyte skeleton in the invasion process of Plasmodium falciparum was evaluated using genetically variant erythrocytes containing well-defined molecular defects in alpha spectrin (alpha Sp) or protein 4.1 from eight unrelated families. Invasion into red cells from subjects of three black families with hereditary pyropoikilocytosis (HPP) due to inheritance of alpha I/74 mutant spectrin was significantly reduced in cells both from the patients and from the relatives of these who carried asymptomatic hereditary elliptocytosis (HE).

Malaria antigens stimulate neopterin secretion by PBMC and U937 cells.

Lysates of Plasmodium falciparum parasitized human erythrocytes stimulate U937 cells to secrete neopterin during a 48 hr co-culture period. Neopterin secretion by U937 cells was enhanced by the addition of human interferon gamma (IFN-gamma). Several P.

High levels of anti-phospholipid antibodies in uncomplicated and severe Plasmodium falciparum and in P. vivax malaria.

The majority (75%) of adult patients with uncomplicated Plasmodium falciparum and P. vivax malaria are positive for anti-phospholipid antibodies (aPLA) as demonstrated by ELISA using a panel of anionic and cationic phospholipids. The highest IgG and IgM binding was to the anionic phospholipids, phosphatidylserine (PS), phosphatidic acid (PA) and cardiolipin (CL), but excluding phosphatidylinositol (PI) to which only low antibody levels were found.

Elevated plasma levels of P-selectin (GMP-140/CD62P) in patients with Plasmodium falciparum malaria.

The plasma concentration of soluble P-selectin (GMP-140/CD62P/PADGEM), a selectin produced by activated platelets and endothelial cells, was quantitated in a group of adults and East African negro children presenting with either non-severe or severe (cerebral) malaria caused by Plasmodium falciparum. Sixty percent of adults with non-severe malaria had immunoreactive levels of P-selectin above 200 ng/ml (the maximum recorded for any normal healthy adult in the assay) and 86% of all African children with malaria had concentrations above normal irrespective of their clinical categorization, and most exceeded the maximum limits of the assay (> 640 ng/ml). There was no correlation between P-selectin levels and parasitemia.

Cytokine-induced inhibition of Plasmodium falciparum erythrocytic growth in vitro.

The addition of recombinant cytokines to Plasmodium falciparum in vitro cultures retarded the growth of the parasite with the effect of recombinant IL-2 (rIL-2) > interferon-gamma (IFN-gamma) > tumour necrosis factor-beta (TNF-beta). The process was concentration dependent, being greatest at 30,000 U/ml and required a 72-h period of continuous exposure for maximum effect. Growth inhibition, as determined morphologically and radiometrically, was a consequence of defective schizont maturation rather than inhibition of merozoite invasion.

Cytotoxicity of human natural killer (NK) cell subsets for Plasmodium falciparum erythrocytic schizonts: stimulation by cytokines and inhibition by neomycin.

Quantification of human peripheral blood NK subsets has been made in a group of Kenyan adults and children with acute P. falciparum malaria. Results were compared with data obtained from three age- and sex-matched control cohorts: parasitaemic but asymptomatic children; aparasitaemic children and adults; and adult Caucasians with no previous history of malaria.

In vitro analysis of Epstein-Barr virus: host balance in patients with acute Plasmodium falciparum malaria. I. Defective T-cell control.

Peripheral blood lymphocytes from healthy, Epstein-Barr virus (EB-virus)-seropositive donors and from patients with acute Plasmodium falciparum malaria were tested for their cytotoxicity towards autologous EB-virus-infected B-cells using an in vitro regression assay. Of the 18 cultures from control donors, 88.8% showed the normal pattern of regression.

Abnormal features of peripheral blood films from Gambian children with malaria.

A series of peripheral blood films taken from Gambian children with either acute or low-grade Plasmodium falciparum infections were examined for abnormal features of the red and white cells. Hypochromia and polychromasia with cytoplasmic stippling were predominant features in both groups. Lymphocytosis, granulocytosis and plasmacytosis were common white cell abnormalities.

Stimulation of autoantibody production in normal blood lymphocytes by malaria culture supernatants.

Supernatants from Plasmodium falciparum cultures containing soluble parasite material were mitogenic for normal human peripheral blood mononuclear cells (MNC) in vitro. This was evidenced by blast transformation and significant incorporation of 3H-thymidine and confirms earlier reports of the mitogenic potential of malaria parasites. Lymphocyte activation by these malaria derived products was polyclonal as demonstrated by increased secretion of IgA, IgG and IgM by the stimulated cells.

Plasmodium falciparum products enhance human lymphocyte transformation by Epstein-Barr virus.

Supernatants obtained from the in vitro culture of Plasmodium falciparum infected erythrocytes induced prolonged lymphocyte survival in culture for more than 8 weeks in six cultures and permanent cell lines were established in four of these. The cells in the latter showed lymphoblastoid features similar to those seen in parallel cultures to which transforming Epstein-Barr (EB) virus instead of P. falciparum derived substances had been added.

Merozoites of P. falciparum require glycophorin for invasion into red cells.

The importance of the red cell membrane sialoglycoproteins in the invasion of P. falciparum merozoites has been assessed. Human erythrocytes deficient in glycophorin A (En(a-)cells) or B (S-s-U-, S-s-U+ cells) showed significant resistance to invasion.

Erythrocyte sialoglycoproteins and Plasmodium falciparum invasion.

Human erythrocytes with a deficiency in glycophorin A (En(a-) cells) and glycophorin B (S-s-U- and S-s-U+ cells) show significant resistance in vitro to invasion by Plasmodium falciparum merozoites. Treatment of normal erythrocytes with trypsin and chymotrypsin also reduced invasion. Trypsinization of S-s- and En(a-) red cells, a process which removes the T1 peptide of glycophorins A and C, produced cells almost refractory to invasion.