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.

恶性疟原虫（pf）疟疾是威胁人类红细胞（RBC）的生命之一，它会破坏相应的双层膜的拓扑结构，并在井中导致其各自的剪切模量增加10倍。感染进展的显着环，滋养体和裂殖体阶段。表征pf -iRBC膜的整体剪切刚度的先前努力包括体外拉伸试验和少量模拟，这些模拟能够部分描述膜的弹性，同时假设剪切模量均匀。尽管这些结果为pf的轴向变形提供了很好的见解-iRBCs，计算出的横向直径与实验值未显示出相似的一致性。本工作的目的是建立一个计算模型，该模型可以模拟健康和感染的RBC的拉伸测试，以更好地了解疾病进展的机理及其对RBC膜弹性特性的影响。为此，开发了一种新的修补技术，以模拟通过将细胞膜分解为被感染的成对斑块和准斑块而引起的感染进展。-正常的膜片段。使用非线性超弹性Skalak本构模型对不可压缩膜进行建模，该模型通过在3-D ABAQUS / Explicit有限元模型框架内的VUMAT子例程实现。在高级Schizont阶段中，假定具有类似剪切模量的类球形几何体，而在其他两个阶段中，分别采用直径为2.4和4 µm且具有自适应剪切模量的较大圆形补丁来复制较硬的一对-补丁。Skalak模型表明，Schizont细胞的整体剪切模量增加了8倍，与已发表的实验结果更好地吻合。有趣的是，对于所有其他中间感染阶段，总剪切模量随感染面积百分比呈线性增加，准正常的膜片段。