The coronavirus can distort the body’s defenses in a variety of ways – for example by deactivating the body’s early warning systems or by misfiring immune cells. However, a number of new studies suggest another insidious consequence: the infection can trigger the production of antibodies that mistakenly attack the patient’s own tissues instead of the virus.
The latest report, published online this week, suggests that so-called autoantibodies may persist months after the infection has cleared and can potentially cause irreparable damage. If other studies confirm the finding, it may explain some of the persistent symptoms in people who have recovered from Covid-19. The syndrome, sometimes called Long Covid, can include dementia, “brain fog” and joint pain.
Autoantibodies are nothing new to science: they are the misguided soldiers of the immune system associated with debilitating diseases like lupus and rheumatoid arthritis that arise when the body attacks its own tissues.
The latest study is small, with only nine patients, five of whom had autoantibodies for at least seven months. It has not yet been peer-reviewed for publication and the authors cautioned caution when interpreting the results.
“It’s a signal; It’s not final, ”said Dr. Nahid Bhadelia, Medical Director of the Department of Specific Pathogens at Boston Medical Center, who led the study. “We don’t know how widespread it is and whether or not it can be linked to Long Covid.”
The question of autoimmunity after coronavirus infection is urgent and important, added Dr. Bhadelia added. Every third Covid-19 survivor says they still have symptoms.
“This is a real phenomenon,” she said. “We’re seeing a second pandemic of people with persistent potential disabilities who may not be able to return to work, and it’s having a huge impact on health systems.”
A growing body of evidence suggests that autoimmunity contributes to the severity of Covid-19 in some people. A study published online in October found that among 52 patients with severe Covid-19, more than 70 percent had antibodies against their own DNA and against proteins that help blood clot.
In another study, also published online in October, the researchers discovered autoantibodies to carbohydrates that the body made in Covid-19 patients that could explain neurological symptoms. A November study in the journal Science Translational Medicine found that half of patients hospitalized for Covid-19 had at least temporary autoantibodies that cause blood clots and blockages in blood vessels.
The research that has been collected raises the worrying possibility that lingering autoantibodies can lead to autoimmune diseases in some people infected with the coronavirus.
“Once these autoantibodies are induced, there is no going back,” said Akiko Iwasaki, an immunologist at Yale University. “They will be an integral part of the person’s immune system.”
She added, “What does it do with the vaccine response? What does it do with newly acquired infections? These are all questions that need to be answered. “
The team of Dr. Iwasaki showed in December that critically ill patients had a dramatic increase in a variety of autoantibodies that target parts of the immune system, brain cells, connective tissue and clotting factors.
Jan. 28, 2021, 5:56 ET
“We are really seeing largely reactive autoantibody responses in these patients,” said Dr. Iwasaki. She suspected that autoimmunity might play a role, but “even I didn’t expect so much auto-reactivity to occur.”
Dr. Iwasaki and her colleagues collected blood from 172 patients with a range of symptoms, 22 infected health care workers and 30 uninfected health care workers.
Every fifth infected patient had autoantibodies against five proteins in their own body and up to 80 percent against at least one protein, the researchers found. Patients with severe Covid-19 had many more of these antibodies, which hampered their immune responses and made the disease worse. Of 15 patients who died during the study, 14 had autoantibodies against at least one component of the immune system.
The study convincingly shows that autoantibodies “change the course of the disease,” said Marion Pepper, an immunologist at the University of Washington in Seattle who was not involved in the research.
Autoimmunity after illness can not only be observed with the coronavirus. Other highly inflammatory infections, including malaria, leprosy, and respiratory viruses, are also known to trigger autoantibodies. But autoimmunity and Covid-19 could be a particularly dangerous mix, experts said.
An analysis of nearly 170,000 people with rare autoimmune rheumatic diseases such as lupus and scleroderma found that they are faced with an increased risk of death from Covid-19. A study of more than 130,000 people found that autoimmune diseases like type 1 diabetes, psoriasis, and rheumatoid arthritis increased the risk of respiratory complications and death from Covid-19.
Some of the antibodies appeared to be the result of congenital defects in the immune system. For example, a study in the journal Science in October found that around 10 percent of critically ill Covid-19 patients had autoantibodies that attack key components of the immune system that were supposed to kick in after exposure to the virus. Without this quick response, the body’s defense is hopelessly delayed and wages a losing battle against the replicating virus.
The mere presence of autoantibodies does not indicate harm, however. They’re in the general population and don’t always lead to disease, some experts noted.
“10 to 15 percent of the population have some level of auto-reactivity,” said Dr. Iñaki Sanz, an immunologist at Emory University. “The problem is, you need a lot of other events downstream of the autoantibodies to trigger disease.”
At least some patients clearly showed autoantibodies as a result of the disease, as the study by Dr. Iwasaki showed. Extreme inflammation caused by viral infections can cause cells to burst open, spit out their contents, and confuse the immune system’s ability to distinguish “self” from “other”.
However, autoantibodies induced in this way could weaken after a few months, said Dr. Shiv Pillai, immunologist at Harvard University: “The vast majority of Covid-19 patients probably develop autoantibodies in the acute phase and then decrease.”
“That being said – yes, it would be interesting if Covid could be explained by certain autoantibodies for a long time,” he added.
Several researchers, including Dr. Bhadelia and Dr. Iwasaki, follow patients over time to see how long autoantibodies have been around and whether they are causing permanent damage. Although scientists knew that acute infections could trigger their presence, the phenomenon has never been studied in such detail.
“That may be the only silver lining here,” said Dr. Pepper. “We are going to learn some basic principles about acute viral infections in people that have not been easy to study this way.”