How COVID-19 Triggers an Autoimmune Reaction

June 13, 2023

A paper published earlier this year clearly outlines how a Covid-19 infection may be triggering the development of autoimmune diseases through three different mechanisms, which may intersect at different points of the inflammatory process. 

The first mechanism involves SARS CoV-2 virus infecting cells by binding to the ACE2 receptors. These ACE2 receptors are part of the renin-angiotensin system which helps regulate blood pressure and normally plays an anti-inflammatory role; however, this function can be inhibited when the COVID-19 virus binds to the ACE2 receptors. This contributes to high levels of inflammation that are characteristic of the disease. There are more ACE2 receptors in some organs than in others, making certain organs more susceptible to SARS-CoV-2 infection. It is hypothesized that cases of Type 1 diabetes caused by a COVID-19 infection are due to this mechanism.

Molecular mimicry is also thought to play a significant role in the development of autoimmune diseases post-COVID-19-infection. SARS-CoV-2 spike proteins share a similar structure to many of our own proteins, so when the immune system creates antibodies that recognize the viral proteins, it can inadvertently create autoantibodies for proteins such as nuclear antigens, isolable nuclear antigen, thyroglobulin, as well as those of the mitochondria. This process of molecular mimicry is thought to be involved in the development of a number of autoimmune diseases post-infection. 

Another mechanism by which COVID-19 may trigger autoimmunity is the cytokine storm, a dangerous occurrence in which the immune system overreacts to the infection leading to high levels of inflammation. These high levels of inflammation may in turn lead to autoimmunity, though the precise route is not yet fully understood.

Researchers hypothesize that there are shared mechanisms between COVID-19 and various autoimmune diseases. Rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, Hashimoto’s thyroiditis, Graves disease, immune thrombocytopenia, autoimmune hemolytic anemia, antiphospholipid syndrome, Guillain-Barre syndrome, and Type 1 diabetes are all thought to share mechanisms with COVID-19, either through molecular mimicry, cytokine storm, or general inflammation.