Autoimmune Disorders & COVID-19

Abstract

Coronavirus disease 2019 (COVID-19) can progress to severe pneumonia with respiratory failure and is aggravated by the deregulation of the immune system causing an excessive inflammation including the cytokine storm. Since 2019, several studies regarding the interplay between autoimmune diseases and COVID-19 infections is increasing all over the world. In addition, thanks to new scientific findings, we actually know better why certain conditions are considered a higher risk in both situations. There are instances when having an autoimmune disease increases susceptibility to COVID-19 complications, such as when autoantibodies capable of neutralizing type I IFN are present, and other situations in which having COVID-19 infection precedes the appearance of various autoimmune and autoinflammatory diseases, including multisystem inflammatory syndrome in children (MIS-C), Guillain-Barré syndrome, and Autoimmune haemolytic anaemia (AIHA), thus, adding to the growing mystery surrounding the SARS-CoV-2 virus and raising questions about the nature of its link with autoimmune and autoinflammatory sequelae. Herein, we discuss the role of host and virus genetics and some possible immunological mechanisms that might lead to the disease aggravation.

Comprehensive Investigations Relationship Between Viral Infections and Multiple Sclerosis Pathogenesis

“…SARS-CoV-2 is the seventh human coronavirus known as a positive sense non-segmented RNA virus [73][74][75]. Detecting coronaviruses in the CNS of patients with Alzheimer's disease (AD), Parkinson's disease (PD), and MS is prominent [14,[76][77][78]. A possible explanation is that infection occurs as spikes in viral glycoproteins bind to the angiotensin-converting enzyme 2 (ACE2) receptor, which is widespread in the brain [76,79].…”

“…In particular, some thoughts are required to examine the most recent data showing a lack of relationship with DMT exposure and a significant association between the Extended Disability Status Scale (EDSS) and the severity of COVID-19 and age [85]. The highest degree of heterogeneity in severe COVID-19 outcomes has been linked to EDSS, according to reports [14,76].…”

“…Both adaptive and innate immune responses are critical to preventing infection by the virus. Viral infections can be prevented by innate immunity with inhibition of natural killer (NK) cells and IFN-I as resistance is achieved within an adaptive immune response to immunity induced by T lymphocytes and antibodies, mainly CD8 + T-cells [14,87,88]. Therefore, the infection of COVID-19 triggering further amplification of immunity pathways in patients with pre-existing immunocompromised paths like MS can be speculated.…”

“…It has been observed in some of the MS plaques that the dystrophy of the oligodendrocyte cells and the precursors (without the mediation of IgG and complement) has happened, which causes a defect in the function of the blood-brain barrier (BBB) and the continuation of the disease [12]. Molecular mimicry: During this phenomenon, cross-reaction occurs, wherein myelin compounds are presented by class II major histocompatibility complex (MHC) on APCs to autoreactive CD4 + T-cell lymphocytes due to the similarity of myelin to some viral structures [12,14].…”

“…As a result, T and B lymphocytes became reactive [12]. Epitope expansion: damage to myelogenous cells causes myelin fragmentation in the inflammatory environment, which leads to additional epitopes with self-perpetuating destruction of myelin [12,14].…”