Many unknown aspects and ambiguities regarding the immune response to SARS-CoV-2 still remain, a year and a half after the COVID-19 pandemic.
Some people have a severe or fatal reaction to the virus, while others have no or very mild symptoms. Some people recover quickly while others experience long-term complications called "long COVID", with symptoms that persist for a long time after recovery from the early stages of the disease.
Researchers are beginning to understand significantly how the human immune system contributes to the varied responses to COVID-19. Thus, it appears that the development of autoantibodies may be behind some of these complications. Autoantibodies are antibodies produced by the immune system that target - incorrectly - normal tissues in the body. Autoantibodies are found in a wide range of autoimmune diseases, such as systemic lupus erythematosus, vasculitis, rheumatoid arthritis and others. Of course, many people with low levels of autoantibodies in their blood do not have obvious symptoms or organ complications.
Professors of the Therapeutic Clinic of the Medical School of the National and Kapodistrian University of Athens, Efstathios Kastritis and Thanos Dimopoulos (Rector of EKPA) report that a recent study found that autoantibodies that existed before infection with SARS-CoV can be 2% or more of severe or fatal COVID-20 cases. The scientists wondered if infection with SARS-CoV-19 could also lead to the production of autoantibodies in people who did not have them before they became ill.
To address this question, the researchers tested a series of autoantibodies in blood samples from nearly 150 people treated with COVID-19 and 41 healthy volunteers. The results were published in the journal Nature Communications. The researchers found that about half of people treated for severe COVID-19 had at least one type of autoantibody in their bloodstream. In contrast, only 15% of healthy people had such antibodies.
About 50 of the people with COVID-19 received blood samples in more than one day, including the day they were first treated. The researchers found that about 20% of these patients did not have autoantibodies when they were first admitted to the hospital but developed them during their illness.
In some patients, autoantibody levels were very high, close to those seen in autoimmune diseases. Common targets of these misdirected antibodies included immune system proteins such as cytokines, which normally help coordinate the immune response.
The mechanisms behind the production of such autoantibodies are not yet clear. Extensive and long-term inflammation during severe COVID-19 can cause the immune system to produce antibodies against parts of the virus that it would not normally recognize. Some of these parts of the virus proteins can look a lot like human proteins and eventually cause the production of autoantibodies.
Excessive inflammation could also boost the production of autoantibodies that existed before but at very low levels. However, vaccination against COVID-19 is much less inflammatory than infection with the virus while exposing the immune system to fewer viral proteins (spike protein only) than infection with the virus itself, according to the EKPA Professors. In a separate study that looked at COVID vaccination, none of the healthy volunteers developed autoantibodies.
The team is also investigating whether autoantibodies produced during COVID-19 could lead to the development of autoimmune diseases later, after recovery from infection. More research is also needed to understand how autoantibodies contribute to COVID-19 symptoms.