A recent study, published in the journal Science Immunology, provides robust evidence that these rogue antibodies targeted against elements of our own immune defences may cause severe disease and death in some patients following COVID-19 infection.
These rogue antibodies, known as autoantibodies, are also present in a tiny percentage of healthy, uninfected people — and their incidence increases with age, which may help to explain why elderly people are more likely to develop severe COVID-19.
The study, led by immunologist Jean-Laurent Casanova from the Rockefeller University in New York City, revealed that around 10 percent of people with severe COVID-19 infection had autoantibodies that strike and block type 1 interferons, protein molecules in the blood that have a critical role in fighting off viral infections.
The research team concentrated on identifying autoantibodies capable of neutralizing lower, more physiologically appropriate interferon concentrations. They looked at 3,595 patients from 38 countries who had serious COVID-19, which meant they were sick enough to be hospitalized to an intensive-care unit.
Autoantibodies were found in 13.6 percent of these individuals, ranging from 9.6 percent of those under the age of 40 to 21 percent of those over the age of 80. Autoantibodies were also found in 18 percent of those who died from the condition.
The study authors hypothesised that these cunning antibodies were the source, rather than the result, of severe COVID-19. There were clues that this might be the case – the researchers previously discovered that autoantibodies were present in approximately 4 out of 1,000 healthy patients whose samples were gathered prior to the pandemic. Individuals with genetic abnormalities that alter the function of type 1 interferons are also at a higher risk of life-threatening sickness, according to the researchers.
To investigate this link further, the researchers looked for autoantibodies in a large collection of blood samples collected from nearly 35,000 healthy adults prior to the pandemic. They discovered that 0.18 percent of persons aged 18 to 69 had autoantibodies to type 1 interferon, and that this proportion doubled with age: autoantibodies were present in approximately 1.1 percent of those aged 70 to 79, and 3.4 percent of those over the age of 80.
“There is a massive increase in prevalence” with age, said the study author.
“This largely explains the high risk of severe COVID in people in the elderly population.”
According to the study authors, these findings have significant clinical consequences, and that hospitals should screen patients for these autoantibodies, as well as mutations linked to type 1 interferon blocking. This could help doctors identify those who are more prone to become critically ill from COVID-19, allowing them to modify their treatment accordingly.
A sample of more than 30,000 people is “too big to ignore”, according to the authors.
“It just shows that this is something that we need to think about.”
They recommend that experts should now consider whether autoantibodies play a part in driving other infectious diseases.
The team has already found evidence of autoantibodies against various immune-system components in people with COVID-19, and they are now investigating further.
The findings of the study were published in Science Immunology.
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