tetano
Editor, Senior Moderator
Eur J Immunol
. 2023 Sep 21;e2250230.
doi: 10.1002/eji.202250230. Online ahead of print. Nervous system-related tropism of SARS-CoV-2 and autoimmunity in COVID-19 infection
Robert Weissert[SUP] 1 [/SUP]
Affiliations
The 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 central nervous system-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 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. Better understanding of nervous-system-related immunity in COVID-19 might support 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 for the nervous system resulting into various disease conditions. Prevention of SARS-CoV-2 infection by means of vaccination is currently the best strategy for prevention of subsequent tissue damage involving the nervous system. This article is protected by copyright. All rights reserved.
Keywords: COVID-19; SARS-CoV-2; lymphocyte; nervous system; post-COVID.
. 2023 Sep 21;e2250230.
doi: 10.1002/eji.202250230. Online ahead of print. Nervous system-related tropism of SARS-CoV-2 and autoimmunity in COVID-19 infection
Robert Weissert[SUP] 1 [/SUP]
Affiliations
- PMID: 37733584
- DOI: 10.1002/eji.202250230
The 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 central nervous system-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 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. Better understanding of nervous-system-related immunity in COVID-19 might support 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 for the nervous system resulting into various disease conditions. Prevention of SARS-CoV-2 infection by means of vaccination is currently the best strategy for prevention of subsequent tissue damage involving the nervous system. This article is protected by copyright. All rights reserved.
Keywords: COVID-19; SARS-CoV-2; lymphocyte; nervous system; post-COVID.