Ectopic Expression of Genes in Affects Cytoadhesion via Increased Expression of Specific Genes.

-infected erythrocytes (IEs) adhere to endothelial cell receptors (ECRs) of blood vessels mainly via EMP1 proteins to escape elimination via the spleen. Evidence suggests that -infected reticulocytes (IRs) also bind to ECRs, presumably enabled by VIR proteins, as shown by inhibition experiments and studies with transgenic expressing genes. To test this hypothesis, our study investigated the involvement of VIR proteins in cytoadhesion using gene-expressing transfectants. Those VIR proteins with a putative transmembrane domain were present in Maurer's clefts, and some were also present in the erythrocyte membrane. The VIR protein without a transmembrane domain (PVX_050690) was not exported. Five of the transgenic cell lines, including the one expressing PVX_050690, showed binding to CD36. We observed highly increased expression of specific genes encoding EMP1s in all CD36-binding transfectants. These results suggest that ectopic expression regulates expression through a yet unknown mechanism. In conclusion, the observed cytoadhesion of expressing genes depended on EMP1s, making this experimental unsuitable for characterizing VIR proteins.