Type I interferons (IFN-I) are antiviral proteins produced by every cell in the body in response to virus entry. IFN-I cause infected cells to produce proteins that attack the virus and inhibit its replication. Type I interferons attract immune cells to the infection site and warn healthy neighboring cells to prepare their defenses.

Scientists have studied how the body’s production of type I interferons affects the course of COVID-19. One study found that in 3.5% of patients with severe COVID-19, the body’s production and use of type I interferon is impaired due to congenital genetic abnormalities. These gene mutations are at the root of life-threatening flu and other viral diseases. Therefore, it is essential to develop treatment methods aimed at enhancing the response to type I interferon.

Another study found that 10% of patients with severe COVID-19 have an autoimmune disease in which the body produces antibodies against type I interferon. These antibodies attack the interferon produced by the body, making the cells unable to resist the virus’s invasion. However, patients with mild and asymptomatic SARS-CoV-2 infection did not have such antibodies.

Even though women suffer from autoimmune diseases more often than men, 94% of patients with anti-interferon antibodies are men. The reason is that women have two X chromosomes that contain a gene that regulates immune activity. Therefore, men have a higher risk of severe COVID-19.

However, antibodies that attack their interferon are also found in women. Among the seriously ill patients with coronavirus was a patient with a rare disease in which one of the X-chromosomes is inactive. This patient also had antibodies against IFN-I.

The presence of antibodies against interferon shows why the risk of developing severe COVID-19 in the elderly is high. Half of the severely ill patients with anti-IFN-I antibodies were over 65 years of age.

Some scientists hypothesize that antibodies attacking interferon are not the cause of severe coronavirus, but its consequence. However, this hypothesis is opposed because, in some patients, such antibodies were detected even before infection with SARS-CoV-2.

Numerous clinical trials have confirmed the effectiveness of interferon as a cure for SARS-CoV-2. But synthetic interferons will not help patients who have mutations that interfere with interferon function and who have antibodies that attack interferon.

Even though the early treatment of IFN-α is unlikely to benefit this group of patients, therapy with injectable or sprayed IFN-β may have positive effects, because in patients with type I interferon antibodies, antibodies against IFN-β are rare.

One of the methods of treatment for coronavirus infection is the introduction of plasma from recovered patients. The plasma of recovered patients contains a large number of antibodies to the SARS-CoV-2 virus. But if there are also antibodies against interferon in the plasma, such treatment will harm the patient because it will disable the patient’s antiviral interferon.

Scientists have confirmed this fact. A plasma of recovered patients with type I anti-interferon antibodies neutralized the ability of IFN-α2 to block infection of SARS-CoV-2 cells, which was not observed with a plasma of recovered patients without anti-interferon antibodies. These data confirm that the blood of recovered patients contains a sufficiently large amount of anti-interferon antibodies to neutralize type I interferons in a sick patient and block their antiviral activity. Therefore, it is vital to test plasma donors for the presence of antibodies that attack interferon.

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