Proteins left behind by COVID-19 long after initial infection can cause cortisol levels in the brain to plummet, inflame the nervous system and prime its immune cells to hyper-react when another stressor arises, according to new animal research by University of Colorado Boulder scientists. The study, in the journal , sheds new light on what might underlie the neurological symptoms of long COVID, an intractable syndrome which impacts as many as 35% of those infected with the virus. The findings come as COVID makes a striking summer comeback, with cases and numerous high-profile athletes at the Paris Olympics testing positive.
"Our study suggests that low cortisol could be playing a key role in driving many of these physiological changes that people are experiencing with long COVID," said lead author Matthew Frank, Ph.D., a senior research associate with the Department of Psychology and Neuroscience at CU Boulder.
Previous research has shown that SARS-CoV-2 antigens, immune-stimulating proteins shed by the virus that causes COVID-19, linger in the blood stream of long COVID patients as much as a year after infection. They've also been detected in the brains of COVID patients who have died. To explore just how such antigens impact the brain and , the research team injected an antigen called S1 (a subunit of the "spike" protein) into the spinal fluid of rats and compared them to a .
After 7 days, in rats exposed to S1, levels of the cortisol-like hormone corticosterone plummeted .