Part of anti-covid therapy based on a theoretical model describing mechanics of contact interaction between coronavirus and cell membrane

Abstract

This article proposes a theoretical model of mechanical feedback in pattern formation on deforming a membrane when coronavirus enters a cell. Coronavirus stiff and flexible spike proteins attach to ACE2 receptors on the cell membrane of the target cell. TMPRSS2 triggers the fusion of the viral and cell membranes with the formation of a fusion pore leading to opening of a capsid surrounded by the coronavirus envelope and viral RNA release into the cell. Based on mechanical feedback analysis of contact interaction and elastic shell theory, a critical value of cell radius, at which a fusion pore is formed and membrane damage occurs locally, is determined. The results revealed that the smaller the cell size, the less likely that the cell will be damaged mechanically when exposed to the virus. One of the ways to reduce the cell size is to decrease intracellular fluid volume through the use of medicines - diuretics. The critical value of cell radius is inversely proportional to the value of binding energy at the time of attachment of the coronavirus to the cell membrane. Further research is required to improve our knowledge of the dependency of binding energy on the shape and sizes of spikelike bumps for various types of coronavirus strains. It may be predicted that when a new coronavirus strain will emerge, it may produce lower binding energy to cell surface and the severity of the disease may decrease. It is necessary to verify the conclusions of the theoretical study by experimental methods.