Nervous system‐related tropism of SARS‐CoV‐2 and autoimmunity in COVID‐19 infection

Abstract

AbstractThe effects of SARS‐CoV‐2 in COVID‐19 on the nervous system are incompletely understood. SARS‐CoV‐2 can infect endothelial cells, neurons, astrocytes, and oligodendrocytes with consequences for the host. There are indications that infection of these CNS‐resident cells may result in long‐term effects, including emergence of neurodegenerative diseases. Indirect effects of infection with SARS‐CoV‐2 relate to the induction of autoimmune disease involving molecular mimicry or/and bystander activation of T‐ and B cells and emergence of autoantibodies against various self‐antigens. Data obtained in preclinical models of coronavirus‐induced disease gives important clues for the understanding of nervous system‐related assault of SARS‐CoV‐2. The pathophysiology of long‐COVID syndrome and post‐COVID syndrome in which autoimmunity and immune dysregulation might be the driving forces are still incompletely understood. A better understanding of nervous‐system‐related immunity in COVID‐19 might support the development of therapeutic approaches. In this review, the current understanding of SARS‐CoV‐2 tropism for the nervous system, the associated immune responses, and diseases are summarized. The data indicates that there is viral tropism of SARS‐CoV‐2 in the nervous system resulting in various disease conditions. Prevention of SARS‐CoV‐2 infection by means of vaccination is currently the best strategy for the prevention of subsequent tissue damage involving the nervous system.