Plasmodium infects red blood cells in the following manner : To begin, heparin activates the interaction and deforms the red blood cells slightly. The growth factor receptor (GFR) plays a role in the entry and replication of viruses. Numerous viruses attach to and enter human cells via GFR, including heparan sulfate proteoglycan (HSPG) . The second step is that the malaria parasite's actin-myosin causes the malaria proteins (EBA and PfRh) to bend red blood cells strongly. The malaria parasite protein then binds to the red blood cell receptor, forming a fusion pore. Along the pipeline, small molecules and invading components enter the red blood cell. The malaria protein is bound to the erythrocyte membrane skeletal protein (spectrum, actin, ankyrin, protein 4.1). The EBAs and Rhs are two major parasite protein families. Three EBAs are receptors for members of the glycophorin family . Complement receptor 1 (CD35, for example) has been identified as a PfRh4 receptor . Complement receptor type 1 (CR1, CD35) is a C1q receptor . PfRh5 is homologous to the antigen basigin of the Ok blood group (BSG, also known as CD147 , EMMPRIN, and M6) . The final step is the AMA1-RON2 interaction , which mediates tight junction formation and anchors for the internalization point. The motor, MTRAP (homolog of thrombin-sensitive protein), and other kinetic system proteins complete the process of plasmodium's rapid slide into red blood cells. If the COVID-19 virus also employs thrombin-sensitized protein-mediated entry into red blood cells, it may account for some of the systemic coagulation observed in severe patients.