Study finds more than HALF of hospital patients with COVID-19 develop autoantibodies

About half of patients hospitalized with COVID-19 develop dangerous immune system proteins that attack the body’s own tissues, according to a new study.

Researchers at Stanford University studied blood samples from nearly 200 patients hospitalized with Covid in the early months of the pandemic and identified signals in the blood of these patients that were similar to those of patients with lupus and other autoimmune diseases.

Half of the patients developed so-called autoantibodies

About 20 percent of patients whose blood was drawn multiple times developed these “rogue antibodies” during their first week in the hospital, the researchers found.

“If you get sick enough from COVID-19 to end up in the hospital, you may not be out of the woods even after your recovery,” one of the study’s lead authors said.

Further study is needed to determine the links between these autoantibodies and severe symptoms of Covid, as well as potential links to long-term Covid.

From the start of the pandemic, doctors noticed that patients with severe cases of Covid share common symptoms with autoimmune diseases.

In autoimmune diseases, a person’s immune system mistakenly attacks other parts of the body instead of attacking a foreign virus or other type of invader.

These autoimmune diseases include lupus, celiac disease, and type 1 diabetes.

Autoimmune diseases often involve swelling, blood clots, fatigue, and fever – all symptoms doctors have seen in Covid patients.

Researchers have also suggested that an autoimmune reaction could be one of the driving forces behind a long Covid, in which patients suffer from symptoms much longer than a typical two-week infection period.

A new study – published Tuesday in Nature Communications – reveals how common autoimmune reactions can be in critically ill Covid patients.

The study was conducted by researchers at Stanford University, Philipps University in Marburg in Germany, and the University of Pennsylvania.

Researchers studied blood samples from patients hospitalized for Covid in March and April 2020.

This included 147 patients at Stanford-affiliated facilities and 48 patients at Kaiser Permanente, another California hospital system.

By studying these blood samples, the researchers looked for autoantibodies, which are types of proteins in the immune system that attack the body’s own tissues, often leading to autoimmune diseases.

Previous research has found autoantibodies in Covid patients and in children with multisystem inflammatory syndrome in children (MIS-C).

Stanford researchers looked for many different antibodies, including those associated with different autoimmune diseases like lupus and systemic sclerosis.

Overall, they found that more than half of Covid patients had at least one type of autoantibody in their blood, compared to less than 15% of healthy patients used as controls.

This autoimmune reaction can be caused by an intense and long-term Covid infection sending the immune system into “overdrive,” the researchers said in a press release.

For some patients, a coronavirus infection can trigger higher levels of natural immune system proteins that were present before the virus entered the body.

For others, the immune system may be triggered by coronavirus particles that look like human proteins.

“It is possible that during a poorly controlled SARS-CoV-2 infection – in which the virus persists too long while an intensifying immune response continues to break the virus particles into pieces – the system immune sees pieces of the virus that it has never seen before, ”explained Dr. PJ Utz, professor of immunology at Stanford and lead author of the study.

“If any of these viral pieces look too much like one of our own proteins, it could trigger the production of autoantibodies.”

About 60% of the patients had anti-cytokine antibodies, which attack proteins involved in cell signaling and are common in autoimmune diseases.

A quarter of the patients had antinuclear antibodies, another common autoantibody associated with these conditions.

And, in a specific blood test that looked for many different antibodies at once, 41 out of 51 (80%) patients tested positive for at least one autoantibody.

A small number of patients have tested positive for two or more autoantibodies, and some have even tested positive for these dangerous “rogue antibodies” early in their hospital stay.

“Within a week of registering at the hospital, about 20% of these patients had developed new antibodies against their own tissues that were not there on the day of their admission,” Utz said.

“In many cases, these autoantibody levels were similar to what you would see in a diagnosed autoimmune disease.”

These results may suggest that critically ill Covid patients could suffer from autoimmune-like illnesses after recovering from their initial infection.

Or, as Utz said, “If you get sick enough from COVID-19 to end up in the hospital, you may not be out of the woods even after your recovery.”

The results give Americans extra motivation to get vaccinated, Utz said, because the vaccination does not trigger the body’s autoimmune response the same way a Covid infection can.

“If you haven’t been vaccinated and you’re thinking, ‘Most people who get COVID get over it and are fine,’ remember you can’t know ahead of time when you will receive COVID-19, it will be a mild case, ‘Utz said.

“If you have a severe case, you could be setting yourself up for a life of trouble because the virus can trigger autoimmunity.”

Utz and his scientific colleagues plan to continue to study the links between autoimmunity and severe Covid disease, as well as the links between autoimmunity and long Covid.