About this Research Topic

Background

Coronaviruses represent a major group of viruses mostly affect human beings through zoonotic transmission. In the past twenty years, there have been already two instances of the emergence of a novel coronavirus, the severe acute respiratory syndrome (SARS) in 2003 and the Middle East respiratory syndrome coronavirus (MERS-CoV) in 2012. The third outbreak as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (COVID-19) was identified for the first time at Wuhan, China, in December 2019. In March 2020, the World Health Organization (WHO) declared the widespread of COVID-19 disease as a pandemic. As of January 1, 2022, a total of 350,292,163confirmed cases and 5,611,459casualities were reported to the WHO worldwide. In addition to acute respiratory symptoms, COVID-19 presents with manifestations that affect other body systems, including but not limited to neurological ones, resulting from either direct or indirect brain damage. The SARS-CoV-2 virus enters the central nervous system (CNS) via multiple routes: The first and significant entrance route of COVID-19 infection to CNS is through the olfactory bulb (retrograde neuronal pathway). The second routes in which the virus enters the CNS are through the hematogenous route, including infected leukocytes, endothelial cells of the BBB, epithelial cells of the blood-cerebrospinal fluid barrier, and viremia. in addition, angiotensin-converting enzyme 2 (ACE2) receptors in brain neurons are the third route to virus junction and entrance into CNS. This CNS entry subsequently activates microglial and inflammatory mediators, which in turn activate T-lymphocytes, plasma cells, monocytes, macrophages, and dendritic cells; afterward, these cells cause cytokine storm, lesions, and inflammation. As a consequence, immunopathological mechanisms such as autoimmunity, direct immune cytotoxicity, and indirect bystander damage are responsible for the neurological manifestations of COVID-19. It has also been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation. On the other hand, during the pandemic, the care of autoimmune patients has raised the question whether they are at higher risk of infection and/or worse outcome. Previous research showed that the use of corticosteroids in the treatment of autoimmune diseases is able to make diagnosis and treatment of COVID-19 more challenging by preventing the fever. Nonetheless, due to the common pathogenesis of COVID-19 and autoimmune diseases, the use of autoimmune drugs as a possible treatment option could help control the virus.

As such, in order to get a clear understanding of the relationship between the pandemic and autoimmunity, it is vital to investigate: 1- the possible effect the pandemic has had on patients with autoimmune diseases, and 2- whether or not COVID-19 infection could give rise to CNS autoimmunity.

We welcome submissions of Case reports/series, Original Research, Systematic Reviews and Meta-Analysis, and expect submissions relating to, but not limited to, the following topics:
•Epidemiological, clinical, and immunological aspects of the CNS autoimmune disorders during COVID-19
•COVID-19 induced CNS autoimmune disorders
•Neuroimmunological relations of the CNS autoimmune disorders with COVID-19
•COVID-19 Vaccination and CNS autoimmune disorders

Keywords: Central nervous system, Multiple sclerosis, Neuromyelitis optica, Encephalitis, COVID-19

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