As the COVID pandemic progresses and the number of survivors increases, they have been found to have antibodies that attack the body instead of the virus.
The immune system is in jeopardy, as more Covid-19 survivors have worrying signs of autoimmune problems leading to potentially debilitating diseases like lupus and rheumatoid arthritis.
At some point, the body’s defense system in these patients changed to attack itself, rather than the virus. Patients are producing molecules called “autoantibodies” that target the genetic material of human cells, rather than the virus.
This wrong immune response can exacerbate severe Covid-19. It can also explain why so-called “long-haul carriers” have persistent problems months after their initial illness has resolved and the virus has cleared from their bodies.
The findings have important implications for treatment: Using existing tests that can detect autoantibodies, doctors could identify patients who might benefit from the treatments used for lupus and rheumatoid arthritis. There is no cure for these diseases, but some treatments decrease the frequency and severity of flare-ups.
“You may be able to hit the appropriate patients harder with some of these more aggressive drugs and expect better results,” said Matthew Woodruff, an immunologist at Emory University in Atlanta and lead author on the paper.
"En los primeros días de la pandemia, muchos inmunólogos, incluyéndome a mí, asumimos que los pacientes que producían grandes cantidades de anticuerpos al inicio de la infección no tendrían la enfermedad. Nos equivocamos" Matthew Woodruff , Universidad de Emory
— Miguel Angel Grullon C. (@miguel78910) October 10, 2020
The results were reported Friday on the MedRxiv prepress server and have yet to be published in a scientific journal. But other experts said the researchers who conducted the study are known for their careful and meticulous work, and that the findings are not unexpected because other viral diseases also trigger autoantibodies.
“I’m not surprised, but it’s interesting to see what is really happening,” said Akiko Iwasaki, an immunologist at Yale University. “It is possible that even moderate to mild disease can induce this type of antibody response.”
For months it has been clear that the coronavirus can cause the immune system to go haywire in some people, ultimately causing more damage to the body than the virus itself. (Dexamethasone, the steroid that Donald Trump took after his Covid diagnosis, has been shown to be effective in some people with severe Covid in controlling this over-exuberant immune response.)
Viral infections cause the death of infected human cells. Sometimes cells die silently, but sometimes, and especially in the midst of a severe infection, they can explode and spread throughout the gut. When that happens, the DNA, normally cloistered in bundles coiled within the nucleus, is scattered and suddenly seen.
In the typical response to a virus, cells known as immune B cells produce antibodies that recognize and bind to viral RNA fragments of the virus.
But in conditions like lupus, some B cells never learn to do this and instead produce autoantibodies that stick to the DNA debris of dead human cells, mistaking themselves for intruders.
Something similar may be happening in Covid-19 patients, the research suggests. “Every time that combination of inflammation and cell death occurs, there is the potential for autoimmune diseases and autoantibodies to arise, more importantly,” said Marion Pepper, an immunologist at the University of Washington in Seattle.