A new study is shedding more light on what could be causing severe COVID-19 infection in SARS-CoV-2 patients.
Stanford researchers revealed this week their interesting discovery upon examining a number of hospitalized COVID-19 patients. In a press release published on Stanford Medicine’s website Tuesday, the team indicated that they found self-attacking antibodies in 1 in 5 patients.
The Breakthrough Study
For the study, senior author PJ Utz, M.D. and his team examined blood samples taken from 147 patients at three university-affiliated hospitals between March and April 2020. They also used samples from 48 patients at healthcare company Kaiser Permanente in California. For the controls, they used samples drawn from the same people prior to the pandemic.
Utz, who is a professor of immunology and rheumatology at Stanford Medicine, and his team determined and measured the levels of antibodies targeting SARS-CoV-2, antibodies directed against cytokines and autoantibodies in the samples, and they reported their findings in their study, which was was published in the peer-reviewed journal Nature Communications.
“Within a week after checking in at the hospital, about 20% of these patients had developed new antibodies to their own tissues that weren’t there the day they were admitted. In many cases, these autoantibody levels were similar to what you’d see in a diagnosed autoimmune disease,” Utz said in the press release.
The Alarming Discovery
The autoantibodies the researchers found targeted the patients’ own tissues or other substances secreted in the blood by their immune cells. This is an alarming discovery since autoantibodies are considered early harbingers of full-blown autoimmune disease — a condition wherein the body’s natural defenses are unable to differentiate normal from foreign cells, causing the body to attack normal cells.
Utz shared their theories on what could have led to the rise in autoantibodies in the patients. One theory is that their immune systems might have experienced an inflammatory shock during the COVID-19 infection, causing a spike in previously undetected and possibly harmless levels of autoantibodies present in some of the patients prior to their SARS-CoV-2 infection.
Another theory is that the noticeable spikes in autoantibodies could have resulted from the exposure of their bodies to viral materials that look similar to their own natural proteins. Utz said their immune systems might have seen bits and pieces of the virus that “closely resemble one of [their] own proteins,” and this triggered autoantibody production.
According to Utz, their study’s finding bolsters the argument for COVID-19 vaccination amid the global health crisis. Since the vaccines contain only a single protein or the genetic instructions for producing SARS-CoV-2’s spike protein, the probability of autoantibody production during a coronavirus infection is significantly diminished.
“Patients who, in response to vaccination, quickly mount appropriate antibody responses to the viral spike protein should be less likely to develop autoantibodies,” Utz explained.
Meanwhile, a similar study published early this year suggested that the self-attacking antibodies could be driving the worst cases of SARS-CoV-2 infection. The team behind the study found evidence that some patients had developed autoantibodies against their blood vessels, heart and brain, but they were unable to establish causal link between the autoantibodies and the COVID-19 symptoms affecting the aforesaid organs.