Neurotropism as a Mechanism of the Damaging Action of Coronavirus

Clinical evidence suggests that COVID-19 is accompanied by many symptoms of damage to the central and peripheral nervous system. This article outlines new aspects of pathogenesis that consider the principle of neurotropism as the leading cause of SARS-CoV-2 infection and central nervous system dysfunction. New data demonstrate additional mechanisms for coronavirus transfection. The description of some transmembrane proteins (neuropilin, etc.) serve as an additional argument for SARS-CoV-2 neurotropism, these molecules act as cofactors for virus transfection in the tissues of the lungs, brain, and other organs. The study of the damaging effect of SARS-CoV-2 at the level of an individual neuron is formulated as a task of neurotropism investigation. The use of the organoid methodology as a new approach in biomedical analysis for modeling the relationship between the host and the pathogen is described. Numerous data on the pathogenesis of COVID-19 indicate that astrocytes and microglia are targets of SARS-CoV-2. Neuroinflammation is considered as an inverse manifestation of neurotropism and a consequence of the neural and mental complications of pathogenesis.