Mechanics of deformation of malaria-infected red blood cells

Citation:
Eraky, M. T., A. I. Abd El-Rahman, M. H. Shazly, and M. M. Abdelrahman, "Mechanics of deformation of malaria-infected red blood cells", Mechanics Research Communications, vol. 113, pp. 103666, 2021.

Abstract:

Plasmodium Falciparum (pf) Malaria is one of the life-threatening infections for human red blood cells (RBCs), which deteriorates the topology of the corresponding bi-layer membranes and causes a 10-fold increase in their respective shear modulus during the well-distinguished Ring, Trophozoite and Schizont stages of infection progression. Previous efforts to characterize the bulk shear stiffness of pf-iRBC membranes include both in-vitro stretching tests and few simulations that enabled partial description of the membrane elasticity while assuming a uniform shear modulus. Although these results provided good insights into the axial-deformation of pf-iRBCs, the computed transverse diameter did not show similar agreement with the experimental values. The aim of the present work is to build a computational model that simulates the stretching tests of healthy and infected RBCs to better understand the mechanics of disease progression and its influence on the elastic properties of RBC membranes. For this purpose, a new patching technique is developed to mimic the infection progression through the decomposition of the cell membrane into infected pair patches and quasi-normal membrane segments. The incompressible membranes are modeled using the non-linear hyper-elastic Skalak constitutive model implemented through a VUMAT subroutine within the framework of a 3-D ABAQUS/Explicit finite-element model. In the advanced Schizont stage, a spheroidal-like geometry with uniform shear modulus is assumed, whereas in the other two stages, sizable circular patches of 2.4 and 4 µm in diameters, respectively, with adaptive shear moduli are implemented to replicate the stiffer pair-patches. The Skalak model indicates an 8-fold increase in the bulk shear modulus of the Schizont-cell beside showing better agreement with the published experimental results. Interestingly, for all other intermediate stages of infection, the bulk shear modulus is found to increase linearly with the percent area-infection, whereas nearly-constant shear modulus in the range of 14 µm is obtained for the quasi-normal membrane segments.

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