Cerebral malaria pathogenesis: revisiting parasite and host contributions.
Cerebral malaria is one of a number of clinical syndromes associated with infection by human malaria parasites of the genus Plasmodium. The etiology of cerebral malaria derives from sequestration of parasitized red cells in brain microvasculature and is thought to be enhanced by the proinflammatory status of the host and virulence characteristics of the infecting parasite variant. In this article we examine the range of factors thought to influence the development of Plasmodium falciparum cerebral malaria in humans and review the evidence to support their role.
Vascular Immunology Unit, Department of Pathology, Sydney Medical School, The University of Sydney, Camperdown NSW 2042, Australia. ggrau@med.usyd.edu.au
Georges Emile Raymond
GE
Grau
Alister Gordon
AG
Craig
D000818:Animals; D001921:Brain / Q000276:immunology / Q000469:parasitology / Q000473:pathology; D002448:Cell Adhesion; D003072:Cognition Disorders / Q000276:immunology / Q000469:parasitology / Q000473:pathology; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism / Q000469:parasitology; D004912:Erythrocytes / Q000276:immunology / Q000469:parasitology*; D006790:Host-Parasite Interactions; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000469:parasitology; D016779:Malaria, Cerebral / Q000276:immunology / Q000469:parasitology* / Q000473:pathology*; D016778:Malaria, Falciparum / Q000276:immunology / Q000469:parasitology / Q000473:pathology; D010963:Plasmodium falciparum / Q000276:immunology / Q000378:metabolism / Q000472:pathogenicity*; D015800:Protozoan Proteins / Q000378:metabolism; D015398:Signal Transduction; D037521:Virulence Factors / Q000378:metabolism
D015800:Protozoan Proteins; D037521:Virulence Factors; C085731:erythrocyte membrane protein 1, Plasmodium falciparum