Scientists figure out mechanism of brain damage by COVID-19

Scientists in the UK and Switzerland have found out how the coronavirus affects the human brain.

The infection does not cause neuronal death, but provokes inflammatory reactions that can explain neurological symptoms, a study published in the bioRxiv preprint repository noted.

The scientists studied the spread and effect of the COVID-19 in the central nervous system (CNS) of K18-hACE2 transgenic mice that expressed the human ACE2 enzyme, a protein that allows coronavirus to enter the cell. One group of rodents was infected with low doses of coronavirus, and another was first infected with the influenza A virus, and then 3 days later with the coronavirus. The third group of animals was used for control. Mice were euthanized 3-7 days after the dose of SARS-CoV-2.

Scientists found that the COVID-19 entered the central nervous system and spread through neurons on the seventh day of infection. First, it affected the olfactory bulb and then penetrated the lower regions of the brain and spinal cord. The virus did not cause nerve cell death, axonal damage or demyelination, but there was an increased activity of the immune cells of the nervous system - macrophages and T cells, which caused moderate inflammation. All this was accompanied by the death of microglial and endothelial cells during apoptosis.

Microgliosis and apoptosis of immune cells indicate that it is microglial cells that may play an important role in the mechanism of development of neurological disorders during prolonged COVID-19.

Scientists have long found that the SARS-CoV-2 coronavirus affects not only the respiratory system but also affects the brain, causing neurological symptoms such as loss of smell and taste, headache, fatigue or more serious complications, such as cerebrovascular disease.