Research is still preliminary – but already provides several new lines of evidence to support a largely unprovable theory.
According to the paper, which was led by Yale immunologist Akiko Iwasaki, the virus is able to replicate inside the brain, and its presence stares near oxygenated brain cells, although the spread of this is not yet clear.
S. Andrew Josephson, chairman of the Department of Neurology at the University of California, San Francisco, praised the techniques used in the study and said “understanding whether the brain’s direct viral involvement is exceptionally important.”
But he also said that he would be vigilant until the paper was peer reviewed.
It would not be completely shocking if SARS-CoV-2 is capable of destroying the blood-brain-barrier, a structure that encircles the brain’s blood vessels and tries to block foreign substances.
For example, the zika virus also does this – causing considerable damage to the brain of the fetus.
But doctors have so far believed that the neurological effect seen in about half of all patients may be the result of an abnormal immune response known as a cytokine storm that causes brain inflammation – rather than To attack the virus directly.
Iwasaki and colleagues decided the question in three ways: by infecting mice, infecting the lab-brain mini-brain known as the brain organ, and examining the brain tissue of COVID-19 patients who died. Were.
In the organoids of the brain, the team found that the SARS-CoV-2 virus is capable of infecting neurons and then hijacking the neuron cell’s machinery to make copies of itself.
The infected cells, in turn, promoted the death of surrounding cells by inhibiting oxygen supply.
A main argument against the theory of direct brain invasion was that the brain lacks high levels of a protein called ACE2, which depends on the coronovirus, and is found abundantly in other organs such as the lungs.
But the team found that organoids had sufficient ACE2 to facilitate the entry of the virus, and proteins were also present in the brain tissue of deceased patients.
He demonstrated a spinal tap to a hospitalized Kovid-19 patient suffering from delirium and found that the person had neutralized antibodies against the virus in his spinal fluid – further evidence in favor of his theory .
The team then looked at two groups of mice – one set that had been genetically altered, so it had ACE2 receptors only in his lungs, and another only in his brain.
Those infected with their lungs showed few signs of lung injury, while those infected in the brain rapidly lost weight and died early, indicating a potentially increased malignancy when the virus entered this organ. Does.
Finally, they examined the brains of three patients who had died of severe Kovid-19 related complications, all to varying degrees of evidence for the virus.
Intuitively, infected areas did not show signs of infiltration by immune cells, such as T-cells, which visit the site of other viruses, such as zika or herpes, to kill infected cells.
This may indicate that the overloaded immune response known as cytokine storm that is responsible for the damage observed in the lungs of Kovid-19 patients is probably not the main cause of neurological symptoms.
It is envisaged that the nose can provide a pathway to the brain, but the authors wrote the need to validate it through more study.
He said that more corpses would be needed to know how the brain could become infected.
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