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, published in the journal Brain Behavior and Immunity , sheds new light on what might underly 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 rising in 84 countries 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." Matthew Frank, PhD, lead author, 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 nervous system, 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 control group. After 7 days, in rat.