According to a new study, the immune system could be at the origin of the persistent symptoms of Covid long.
New information has just been discovered about the virus of the Covid-19more specifically the Covid long. Indeed, a new study published in the journal Brain has just revealed that the immune response to SARS-CoV-2 would cause damage to the brain, potentially being responsible for the symptoms of long Covid.
In detail, the researchers explain: “The mechanisms by which SARS-CoV-2 leads to acute and long-term neurological manifestations remain unclear. We wanted to characterize neuropathological changes in patients with the disease and determine the underlying pathophysiological mechanisms.”
The immune system in question of the symptoms of Covid long
To reach this conclusion, the study examined the brains of nine adults aged 24 to 73, who died during the first wave of the Covid-19 epidemic. We also learn that these patients died shortly after being infected. To carry out their work, the researchers explain that they carried out “a descriptive analysis of the pathological changes and quantitative analyzes of the infiltrates (a pathological infiltration of a tissue by cells) and vascular changes”.
A severe impact on the brain
The results thus revealed the presence of no trace of the Covid-19 virus in the brains of the patients. However, the antibodies produced by the body in response to SARS-CoV-2 infection came damage blood vessels in the brain, causing inflammation. The researchers thus suggest that the immune response could possibly be the cause of the symptoms of long Covid, such as taste and smell disorders, sleep disorders, pain or even intense fatigue.
The researchers then compared the brains of the nine dead people to those of ten people in a control group in order to analyze the immune response and neuronal inflammation. They find that “the most likely initiating event that leads to vascular leakage, platelet aggregation, neuroinflammation and neuronal damage” is the ability of antibodies to mistakenly destroy endothelial cells, making up the blood-brain barrier.