For example, evidence from animal studies supports the idea that antibodies targeting the SARS-CoV-2 spike protein, the same protein used by many vaccines to trigger a protective immune response, could cause collateral damage, he notes.
Harald Prüss, neurologist at the German Center for Neurodegenerative Diseases (DZNE) and the Charité University Hospital in Berlin.
In 2020, while researching antibody therapies for COVID-19, he and his colleagues found that of the 18 antibodies identified with potent effects against SARS-CoV-2, four also targeted healthy tissue in mice, a sign that they could trigger problems. autoimmune.”We shouldn’t be against adverse events.”William Murphy, University of California, Davis
The first clinical data point in a similar direction. In the past year, research groups have found unusually high levels of autoantibodies, which can attack the cells and tissues of the body, in people after a SARS-CoV-2 infection.
In Nature in May 2021, immunologists Aaron Ring and Akiko Iwasaki of Yale School of Medicine and their colleagues reported finding autoantibodies in acute COVID-19 patients that affect the immune system and the brain; now they are studying how long the autoantibodies persist and whether they can damage tissues.
This month, Cedars-Sinai Medical Center
cardiologist Susan Cheng and protein chemist Justyna Fert-Bober wrote in the Journal of Translational Medicine that autoantibodies could last up to 6 months after infection, although the researchers did not. persistence of autoantibodies correlated with ongoing symptoms.
Partly to figure out whether these autoantibodies harm people, DZNE is checking the cerebrospinal fluid of Long Covid patients for antibodies that react to mouse brain tissue – if they react, they could attack human neural tissues as well.
In a paper that Prüss and his colleagues are about to present, they describe the discovery of autoantibodies that attack mouse neurons and other brain cells in at least a third of those patients.
A group from Northwestern
University, meanwhile, reported in an August 2021 preprint that in people with neurological complications after COVID-19, a subset of T cells are persistently activated as would happen with a SARS-CoV infection. 2 ongoing, suggesting some sort of aberrant immune response or persistent virus.
Researchers are looking into another possible culprit of Long Covid: tiny blood clots. In an acute SARS-CoV-2 infection, small clots can form that can damage the cells that line the blood vessels.
Resia Pretorius, a physiologist at Stellenbosch University in South Africa, and her colleagues published preliminary evidence in cardiovascular diabetes in August that microscopic clots can persist after an infection has resolved. They could interfere with oxygen delivery, which could explain some symptoms of Long Covid such as brain fog. Pretorius is now collaborating with colleagues to develop diagnostics for this microcoagulation and study ways to treat it in Long Covid.