BACKGROUND: To avoid spleen-dependent killing mechanisms parasite-infected 
erythrocytes (IE) of Plasmodium falciparum malaria patients have the capacity to 
bind to endothelial receptors. This binding also known as sequestration, is 
mediated by parasite proteins, which are targeted to the erythrocyte surface. 
Candidate proteins are those encoded by P. falciparum multicopy gene families, 
such as var, rif, stevor or PfMC-2TM. However, a direct in vivo proof of IE 
sequestration and expression of multicopy gene families is still lacking. Here, 
we report on the analysis of IE from a black African immigrant, who received the 
diagnosis of a malignant lymphoproliferative disorder and subsequently underwent 
splenectomy. Three weeks after surgery, the patient experienced clinical 
falciparum malaria with high parasitemia and circulating developmental parasite 
stages usually sequestered to the vascular endothelium such as late 
trophozoites, schizonts or immature gametocytes.
METHODOLOGY/PRINCIPAL FINDINGS: Initially, when isolated from the patient, the 
infected erythrocytes were incapable to bind to various endothelial receptors in 
vitro. Moreover, the parasites failed to express the multicopy gene families 
var, A-type rif and stevor but expression of B-type rif and PfMC-2TM genes were 
detected. In the course of in vitro cultivation, the parasites started to 
express all investigated multicopy gene families and concomitantly developed the 
ability to adhere to endothelial receptors such as CD36 and ICAM-1, 
respectively.
CONCLUSION/SIGNIFICANCE: This case strongly supports the hypothesis that 
parasite surface proteins such as PfEMP1, A-type RIFIN or STEVOR are involved in 
interactions of infected erythrocytes with endothelial receptors mediating 
sequestration of mature asexual and immature sexual stages of P. falciparum. In 
contrast, multicopy gene families coding for B-type RIFIN and PfMC-2TM proteins 
may not be involved in sequestration, as these genes were transcribed in 
infected but not sequestered erythrocytes.