Objective:To find out host gene expression profiles after malarial infection.Methods:Further time-course microarray analysis of peripheral blood mononuclear cells focusing on malaria pathogenesis was performed.Results:Up-rcgulation of coagulation-related genes,heal shock proteins,glycolytic enzymes,glucose transporters,and vacuolar H~+-ATPascs was found in acute febrile malaria.In early malaria,prior to detectable parasitemia,CD36 and ICAM1 were up-regulated.During acute malaria,there is correlation between IL-1β and heal shock proteins.CD163,a hemoglobin scavenger receptor,was up-regulated in acute malaria to potentially facilitate free hemoglobin up-takc by leukocytes.In acute malaria,high MafB gene expression was negatively correlated with hemoglobin and platelet counts.Consistent with hemoglobin down-regulation,peripheral red blood cell counts tended to increase during acute malaria.Up-regulations of red blood cell and leucocyte binding mediators like CD36.ICAM1,thrombospondin and thrombomodulin may contribute to the pathogenesis of cerebral malaria.Similarly,up-regulation of correlated glycolytic enzymes,glucose transporter and H~+-ATPases may contribute to the hypoglycemia and metabolic acidosis frequently observed in serious malaria patients.Overall gender effects on gene expression profiles between male and female were not apparent,except for some hemoglobins were significantly downregulated in male versus female,which suggesting males are prone to malaria-related anemia.Conclusions:Leucocyte gene expression profiles can explain the pathogenesis of malarial complication such as fever,metabolic acidosis,hypoglycemia,anemia,and coagulopathy. Objective: To find out host gene expression profiles after malarial infection. Methods: Further time-course microarray analysis of peripheral blood mononuclear cells focusing on malaria pathogenesis was done. Results: Up-rcgulation of coagulation-related genes, heal shock proteins, glycolytic enzymes , glucose transporters, and vacuolar H ~ + -ATPascs was found in acute febrile malaria. In early malaria, prior to detectable parasitemia, CD36 and ICAM1 were up-regulated. With acute malaria, there is a correlation between IL-1β and heal shock proteins .CD163, a hemoglobin scavenger receptor, was up-regulated in acute malaria to potentially facilitate free hemoglobin up-takc by leukocytes. In acute malaria, high MafB gene expression was negatively correlated with hemoglobin and platelet counts. Consistent with hemoglobin down-regulation, peripheral red blood cell counts tended to increase during acute malaria. Up-regulations of red blood cell and leucocyte binding mediators like CD36. ICAM1, thrombospondin and Thrombomodulin may contribute to the pathogenesis of cerebral malaria. Similar, up-regulation of correlated glycolytic enzymes, glucose transporter and H ~ + -ATPases may contribute to the hypoglycemia and metabolic acidosis frequently observed in serious malaria patients. Overall Gender Effects on gene expression profiles between male and female were not apparent, except for some hemoglobins were significantly downregulated in male versus female, which suggests males are prone to malaria-related anemia. Conclusions: Leucocyte gene expression profiles can explain the pathogenesis of malarial complication such as fever, metabolic acidosis , hypoglycemia, anemia, and coagulopathy.