A large international study has shown that after some people are infected with SARS-CoV-2, antibodies against our own immune defense elements are a key driver of serious illness and death. These rogue antibodies, called autoantibodies, are also present in a small group of healthy, uninfected individuals – their prevalence increases with age, which may help explain why the elderly suffer from severe COVID- 19 has a higher risk.
Research results were published on August 19 Scientific Immunology, To provide strong evidence to support the observations made by the same research team last October. Led by Jean-Laurent Casanova, an immunologist at Rockefeller University in New York City, researchers found that approximately 10% of severely ill patients with COVID-19 have autoantibodies that can attack and block Type 1 interferon, a protein molecule in the blood that plays a key role in fighting viral infections.
“Last year’s preliminary report may be one of the most important papers in the pandemic,” said Aaron Ring, an immunologist at Yale University School of Medicine in New Haven, Connecticut, who was not involved in the work. “What they are doing in this new study is really digging deeper into the ubiquity of these antibodies in the general population-it turns out they are very common.”
The international research team focuses on detecting autoantibodies that can neutralize lower and more physiologically relevant concentrations of interferon. They studied 3,595 COVID-19 critically ill patients from 38 countries/regions, which means that these people are sick enough to be admitted to the intensive care unit. Overall, 13.6% of these patients have autoantibodies, ranging from 9.6% under 40 to 21% over 80. Autoantibodies are also present in 18% of people who die of the disease.
Casanova and his colleagues suspect that these cunning antibodies are the key cause of COVID-19, not the consequences. There are signs that this may be the case-the team had previously found that about 4 of the 1,000 healthy people who collected samples before the pandemic had autoantibodies. The team also found that individuals with genetic mutations that disrupt the activity of type 1 interferon are at higher risk of life-threatening diseases.
To further investigate this connection, researchers looked for autoantibodies in large blood samples collected from nearly 35,000 healthy people before the pandemic. They found that 0.18% of people aged 18 to 69 have autoantibodies against type 1 interferon, and this proportion increases with age: about 1.1% of people aged 70 to 79 have autoantibodies. More than 3.4% of people have autoantibodies. 80 years old.
Casanova said that with age, the “prevalence rate will increase substantially.” “This largely explains the high risk of severe COVID in the elderly.” He added that these findings have clear clinical significance, and suggested that hospitals should check patients for the presence of these autoantibodies, as well as block type 1 interventions. Interferon-related mutations. This can identify people who are more likely to be seriously ill due to COVID-19 and help doctors adjust their treatment plans appropriately.
Ring stated that the sample of more than 30,000 people is “too big to ignore.” “This just shows that this is something we need to consider.” He added that researchers should now consider whether autoantibodies play a role in driving other infectious diseases. Ring’s team has found evidence of autoantibodies against various immune system components in COVID-19 patients, and he and his colleagues are now investigating further. “I suspect we are just beginning to touch the fur,” Ring said.
This article is reproduced with authorization and is First published August 31, 2021.