COVID-19 disease and autoimmune disorders: A mutual pathway

Abstract

Coronavirus disease 2019 (COVID-19) is a real challenge for humanity with high morbidity and mortality. Despite being primarily a respiratory illness, COVID-19 can affect nearly every human body tissue, causing many diseases. After viral infection, the immune system can recognize the viral antigens presented by the immune cells. This immune response is usually controlled and terminated once the infection is aborted. Nevertheless, in some patients, the immune reaction becomes out of control with the development of autoimmune diseases. Several human tissue antigens showed a strong response with antibodies directed against many severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) proteins, such as SARS-CoV-2 S, N, and autoimmune target proteins. The immunogenic effects of SARS-CoV-2 are due to the sizeable viral RNA molecules with interrupted transcription increasing the pool of epitopes with increased chances of molecular mimicry and interaction with the host immune system, the overlap between some viral and human peptides, the viral induced-tissue damage, and the robust and complex binding between sACE-2 and SARS-CoV-2 S protein. Consequently, COVID-19 and its vaccine may trigger the development of many autoimmune diseases in a predisposed patient. This review discusses the mutual relation between COVID-19 and autoimmune diseases, their interactive effects on each other, the role of the COVID-19 vaccine in triggering autoimmune diseases, the factors affecting the severity of COVID-19 in patients suffering from autoimmune diseases, and the different ways to minimize the risk of COVID-19 in patients with autoimmune diseases.

Autoimmune Diseases Affecting Hemostasis: A Narrative Review

“…In summary, both COVID-19 and vaccination against COVID-19 may trigger similar pathways to development or exacerbation of autoimmune diseases [ 111 ], and both may be associated with development of various autoimmune events [ 112 , 113 ] in addition to those we have described here.…”

Long-Term Effects of SARS-CoV-2 in the Brain: Clinical Consequences and Molecular Mechanisms

“…It is also shown that SARS-CoV-2 infections can result in autoimmune disorders [29,34,35]. Viral infections may trigger an autoimmune disease, especially in COVID-19 patients who are already at risk of developing autoimmune conditions [34].…”

“…Autoimmune manifestations of SARS-CoV-2 have been reported and can contribute to the neurological symptoms associated with this virus. Al-Beltagi and collaborators [35] suggested that one potential mechanism for the development of autoimmune diseases could be the binding of the SARS-CoV-2 spike protein to the ACE2 receptor. This may cause long-term disabilities for a group of vulnerable patients reacting to the viral infection with a sustained inflammatory reaction.…”

COVID-19 and antiphospholipid antibodies

“…The S1 subunit allows the virus to attach to the host cell receptor while S2 mediates fusion of the viral capsid with the host cell membrane [ 31 ]. In molecular mimicry, the S1 and S2 glycoprotein subunits of the SARS-CoV-2 viral S protein form a phospholipid-like epitope that induces formation of aPL, which can trigger an autoimmune response if the antigenic determinants are similar to host human tissue [ 69 ]. The neoepitope model postulates that oxidative stress in COVID-19 causes a change in confirmation of β2GPI, a plasma protein involved in hemostasis and immunity, creating a neoepitope for the generation of aβ2GPI [ 70 ].…”