LOS ANGELES - A year into the ongoing coronavirus pandemic, medical experts continue to be baffled by the residual effects of the virus found in COVID-19 patients. Among extraordinary impacts of the novel coronavirus are reports of the immune system turning on itself.
An international team of researchers found that in some people with severe COVID-19, the body — specifically the immune system — goes rogue and attacks one of its own key defenses instead of fighting the coronavirus. Most of the subjects with the immune response aberrations were men, helping to explain why the virus may be hitting men harder than women.
The international study, published in October in the medical journal "Science," uncovered two reasons why the immune system may become scrambled. In blood from nearly 1,000 severe COVID-19 patients, researchers found 1 in 10 had what are called auto-antibodies — antibodies that mistakenly attack needed virus fighters.
The findings are especially surprising, since autoimmune disorders tend to be more common in women — but 95% of the affected COVID-19 patients who were studied were men. The researchers didn’t find the damaging molecules in patients with mild or asymptomatic COVID-19.
In another group of 660 severely ill patients, the same international team found 3.5% had gene mutations that didn’t produce Type I interferons.
Usually, when a virus invades a cell, proteins called Type I interferons spring into action, defending the cell by interfering with viral growth. But new research shows those crucial molecules were essentially absent in a subset of people with severe COVID-19.
A separate National Institutes of Health study published in January studying antiviral antibody responses in 147 hospitalized COVID-19 patients found auto-antibodies in approximately 50% of the patients.
Inflammation — which is the body’s response to fighting harmful and unwanted infections, injuries or toxins — has been known to be over-triggered by COVID-19.
Another study published on June 25, 2020 in the journal "Cell Reports Medicine" found that while COVID-19 is commonly known as a respiratory illness, the disease has also been known to instigate inflammatory responses in the body which can negatively affect the function of one’s heart and brain.
According to the study, researchers observed SARS-CoV-2 infecting human heart cells that were grown from stem cells in a lab. Within 72 hours of infection, the virus managed to spread and replicate, killing the heart cells.
There are two main arms of the immune system. Innate immunity is the body’s first line of defense. As soon as the body detects a foreign intruder, key molecules, such as interferons and inflammation-causing cytokines, launch a wide-ranging attack.
Innate immune cells also alert the slower-acting "adaptive" arm of the immune system, the germ-specific sharpshooters, to gear up. B cells start producing virus-fighting antibodies, the proteins getting so much attention in the vaccine hunt.
In another NIH study published in December, researchers uncovered blood vessel damage and inflammation in the brains of 19 deceased COVID-19 patients.
"We found that the brains of patients who contract infection from SARS-CoV-2 may be susceptible to microvascular blood vessel damage. Our results suggest that this may be caused by the body’s inflammatory response to the virus" said Dr. Avindra Nath, clinical director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS).
Nath, the senior author of the study added that while COVID-19 is most commonly known to be a respiratory illness, he hopes this study will help the medical community recognize the scope of complications that can arise out of contracting the deadly coronavirus.
"We were completely surprised. Originally, we expected to see damage that is caused by a lack of oxygen. Instead, we saw multifocal areas of damage that is usually associated with strokes and neuroinflammatory diseases," said Nath.
Researchers were expecting to find damage caused by a lack of oxygen since COVID-19 attacks the lungs preventing oxygen from getting to other organs that desperately need it to function properly.
"So far, our results suggest that the damage we saw may not have been not caused by the SARS-CoV-2 virus directly infecting the brain," said Dr. Nath. "In the future, we plan to study how COVID-19 harms the brain’s blood vessels and whether that produces some of the short- and long-term symptoms we see in patients."
The Associated Press contributed to this story.