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Washington – The headaches, confusion and delirium that some COVID-19 patients experience are possibly the result of the direct invasion of the coronavirus into the brain, according to a study published Wednesday.
The studies are still initial, but they provide several new resources of evidence of what was largely unproven in the past.
According to the document, led by Yale immunologist Akiko Iwasaki, the virus is able to replicate internally in the brain and its presence deprives nearby brain cells of oxygen, the prevalence of this is not yet clear.
S. Andrew Josephson, director of the Department of Neurology at the University of California, San Francisco, praised the techniques used in the study and said that “understanding whether there is or is direct viral involvement of the brain is incredibly important. “
But he added that he would remain cautious until the document was peer-reviewed.
It would not be absolutely surprising if SARS-CoV-2 crossed the blood brain barrier, a design that surrounds the blood vessels of the brain and tries to block foreign substances.
Zika virus, for example, also does, causing brain damage to fetuses.
But doctors have believed in the past that the neurological effects observed in about one part of all patients may be the result of an immune reaction known as cytokine typhoon that causes inflammation of the brain, rather than direct invasion of the virus.
Iwasaki and his colleagues to deal with the factor in three ways: infecting mini lab brains known as brain organoids, infecting mice and examining the brain factor of deceased COVID-19 patients.
In brain organoids, the team discovered that the SARS-CoV-2 virus is able to infect neurons and then divert machinery from neural cells to copies.
Inflamed cells promote the death of surrounding cells by quelling their oxygen supply.
One of the main arguments that opposes the theory of direct brain invasion is that the brain lacks the maximum levels of a protein called ACE2 in which the coronavirus is blocked and that it is discovered in abundance in other organs such as the lungs. .
But the team found that organoids had enough ACE2 to facilitate access to the virus and that proteins were provided in the brain tissue of deceased patients.
They also performed a lumbar puncture on a patient hospitalized with COVID-19 who suffered from delirium and discovered that the individual had neutralizing antibodies opposed to the virus in his cerebrospinal fluid, additional evidence in favor of his theory.
The team then observed two teams of mice: one that had been genetically modified to have ACE2 receptors in his lungs and the other in his brain.
Other people infected in his lungs showed symptoms of lung damage, while inflammations in the brain temporarily lost weight and died temporarily, indicating potentially greater lethality when the virus enters the organ.
Finally, they tested the brains of 3 patients who died of severe COVID-19-like headaches, locating the virus to varying degrees.
Surprisingly, inflamed regions have shown no symptoms of infiltration through immune cells, such as T cells, that rush to attack other viruses such as Zika or herpes to kill inflamed cells.
This recommends that the overloaded immune reaction known as cytokine storm, which is guilty of much of the damage observed in the lungs of COVID-19 patients, may not be the leading cause of neurological symptoms.
The hypothesis was raised that the nose could simply provide the trace to the brain, but the authors wrote that this needed to be validated through other studies.
They added that additional autopsies would be needed to determine the prevalence of brain infection.
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