Cell mechanics and signalisation: SARS-CoV-2 hijacks membrane liquid crystals and cytoskeletal fractal topology

Abstract

We highlight changes to cell signaling under virus invasion (with the example of SARS-CoV-2 ), involving disturbance of membranes, (plasma, mitochondrial, endothelial-alveolar) and of nanodomains, modulated by the cytoskeleton. Virus alters the mechanical properties of the membranes, impairing mesophase structures mediated by the fractal architecture initiated by actomyosin. It changes the topology of the membrane and its lipid composition distribution. Mechanotransduction, self-organization and topology far from equilibrium are omnipresent. We propose that the actomyosin contractility generates the cytoskeleton's fractal organization. We focus on three membranar processus: -The transition from lamellar configuration in cell and viral membranes to a bi-continuous organization in the presence of ethanolamine; (The energy for this transition is provided by change of the folding of the viral fusion protein from metastable to stable state).-The action of mitochondrial antiviral signaling protein on the external mitochondrial envelope in contact with mitochondrial-associated membranes, modified by viral endoribonuclease, distorting innate immune response.-The increased permeability of the epithelial-alveolar-pulmonary barrier involves the cytoskeleton membranes. The pulmonary surfactant, is also perturbed in its liquid crystal state. Viral subversion disorganizes membrane structure and functions and thus the metabolism of the cell. We advocate systematic multidisciplinary exploration of membrane mesophases and their links with fractal dynamics, to enable novel therapies for SARS-CoV-2 infection.