Infection of asexual stage of the malaria parasite Plasmodium falciparum induce morphologic, functional and antigenic changes in their host erythrocyte membranes. The consequence of these changes is that infected erythrocyte develop the ability to sequester by binding to capyllary endothelial cells, venula and to uninfected erythrocyte is termed rosette formation. Recently, rosette formation be interesting phenomenon because it was presumed imprtant to phatogenesis of severe malaria such as cerebral malaria through sequesteration of parasite in microvasculature. Rossete formation is a binding mechanism between Plasmodium falciparum infected erythrocyte to the normal ones, which involve the role of parasite protein ligands such as PfEMP1 expressed on infected eythrocyte as surface antigen through DBL1-alfa domain that bind to CR-1 receptor and/or A-antigen on the uninfected erythrocyte as target cell. Taking into accounts that all strains of P. falciparum parasite could cause rosette formation, therefore information of rosette formation still needed such as site of sequesteration, identity receptors, haemodinamic enviroment of microvascular and domain mapping on rosette formation to elucidate the role of rosette formation in phatogenesis of severe malaria.
|Makara Journal of Health Research
|Published - Jun 2001