More than a year after a bout with COVID-19, Rebekah Hogan still suffers from severe brain fog, pain and fatigue that leave her unable to do her nursing job or handle household activities.
Long COVID has her questioning her worth as a wife and mother.
“Is this permanent? Is this the new norm?’’ said the 41-year-old Latham, New York, woman, whose three children and husband also have signs of the condition. “I want my life back.’’
More than a third of COVID-19 survivors by some estimates will develop such lingering problems. Now, with omicron sweeping across the globe, scientists are racing to pinpoint the cause of the bedeviling condition and find treatments before a potential explosion in long COVID cases.
Could it be an autoimmune disorder? That could help explain why long COVID-19 disproportionately affects women, who are more likely than men to develop autoimmune diseases. Could microclots be the cause of symptoms ranging from memory lapses to discolored toes? That could make sense, since abnormal blood clotting can occur in COVID-19.
As these theories and others are tested, there is fresh evidence that vaccination may reduce the chances of developing long COVID.
It’s too soon to know whether people infected with the highly contagious omicron variant will develop the mysterious constellation of symptoms, usually diagnosed many weeks after the initial illness. But some experts think a wave of long COVID is likely and say doctors need to be prepared for it.
With $1 billion from Congress, the National Institutes of Health is funding a vast array of research on the condition. And clinics devoted to studying and treating it are popping up around the world, affiliated with places such as Stanford University in California and University College London.
Why does it happen?
Momentum is building around a few key theories.
One is that the infection or remnants of the virus persist past the initial illness, triggering inflammation that leads to long COVID.
Another is that latent viruses in the body, such as the Epstein-Barr virus that causes mononucleosis, are reactivated. A recent study in the journal Cell pointed to Epstein-Barr in the blood as one of four possible risk factors, which also include pre-existing Type 2 diabetes and the levels of coronavirus RNA and certain antibodies in the blood. Those findings must be confirmed with more research.
A third theory is that autoimmune responses develop after acute COVID-19.
In a normal immune response, viral infections activate antibodies that fight invading virus proteins. But sometimes in the aftermath, antibodies remain revved up and mistakenly attack normal cells. That phenomenon is thought to play a role in autoimmune diseases such as lupus and multiple sclerosis.
Justyna Fert-Bober and Dr. Susan Cheng were among researchers at Cedars-Sinai Medical Center in Los Angeles who found that some people who have had COVID-19, including cases without symptoms, have a variety of these elevated “autoantibodies" up to six months after recovering. Some are the same ones found in people with autoimmune diseases.
Another possibility is that tiny clots play a role in long COVID. Many COVID-19 patients develop elevated levels of inflammatory molecules that promote abnormal clotting. That can lead to blood clots throughout the body that can cause strokes, heart attacks and dangerous blockages in the legs and arms.
In her lab at Stellenbosch University in South Africa, scientist Resia Pretorius has found microclots in blood samples from patients with COVID-19 and in those who later developed long COVID. She also found elevated levels of proteins in blood plasma that prevented the normal breakdown of these clots.
She believes that these clotting abnormalities persist in many patients after an initial coronavirus infection and that they reduce oxygen distribution to cells and tissue throughout the body, leading to most if not all symptoms that have been linked to long COVID.