The main cause of severe cases of COVID-19 is autoaggressive antibodies or autoantibodies: it is because of them that the functioning of the immune system is disrupted. Scientists from Yale University found this out, and the results of their research were published in the journal Nature.
The study authors used a high-throughput autoantibody detection method called REAP (Rapid Extracellular Antigen Profling). It is aimed at identifying, through sequencing (decoding of the amino acid sequence), antibodies that target the exoproteome – a collection of extracellular and secreted proteins.
Scientists analyzed blood samples from 194 medical workers and patients infected with the SARS-CoV-2 coronavirus for the presence of autoantibodies against 2,770 exoproteome proteins. As it turned out, patients with COVID-19 showed a sharp increase in autoantibody reactivity compared to uninfected people.
Most commonly, autoantibodies have been targeted against immunomodulatory proteins, including cytokines, chemokines, the complement system, and cell surface receptors. All this leads to the fact that the immune system ceases to effectively cope with the coronavirus, which in turn leads to complications.
Experiments on transgenic mice with the human ACE2 protein (which serves as a gateway for the virus to infect cells) showed that animals with autoantibodies were more likely to die when infected with SARS-CoV-2.
These autoantibodies remain in the human body after recovery, which explains the long-term postcoid syndrome. Interestingly, even mild infections can trigger the production of autoantibodies, which can lead to long-term health problems.
