Abstract
We investigate numerically the microscale blood flow in which red blood cells (RBCs) are partially infected by Plasmodium falciparum, the malaria parasite. The infected RBCs are modeled as more rigid cells with less deformability than healthy ones. Our study illustrates that, in a 10 μm microvessel in low-hematocrit conditions (18% and 27%), the Plasmodium falciparum-infected red blood cells (Pf-IRBCs) and healthy ones first form a train of cells. Because of the slow moving of the Pf-IRBCs, the local hematocrit (H(ct)) near the Pf-IRBCs is then increased, to approximately 40% or even higher values. This increase of the local hematocrit is temporary and is kept for a longer length of time because of the long RBC train formed in 27%-H(ct) condition. Similar hematocrit elevation at the downstream region with 45%-H(ct) in the same 10 μm microvessel is also observed with the cells randomly located. In 20 μm microvessels with 45%-H(ct), the Pf-IRBCs slow down the velocity of the healthy red blood cells (HRBCs) around them and then locally elevate the volume fraction and result in the accumulation of the RBCs at the center of the vessels, thus leaving a thicker cell free layer (CFL) near the vessel wall than normal. Variation of wall shear stress (WSS) is caused by the fluctuation of local H(ct) and the distance between the wall and the RBCs. Moreover, in high-hematocrit condition (45%), malaria-infected cells have a tendency to migrate to the edge of the aggregates which is due to the uninterrupted hydrodynamic interaction between the HRBCs and Pf-IRBC. Our results suggest that the existence of Pf-IRBCs is a nonnegligible factor for the fluctuation of hematocrit and WSS and also contributes to the increase of CFL of pathological blood flow in microvessels. The numerical approach presented has the potential to be utilized to RBC disorders and other hematologic diseases.