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The headaches, confusion and delirium experienced by some Patients with Covid-19 may be the result of direct invasion of 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.
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According to the paper, 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.
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 will remain cautious until the document is 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 attempts to block foreign substances.
Zika virus, for example, also does: it damages the brains of fetuses.
But doctors until now believed that the neurological effects noticed in about one part of all patients could be the result of an immune reaction known as cytokine typhoon that causes inflammation in the brain, rather than direct invasion of the virus.
Prevalence unknown
Iwasaki and his colleagues manipulated the factor in three ways: infecting mini lab brains called brain organoids, infecting mice, and examining the brain factor of deceased Covid-19 patients.
In the organoids of the brain, the team discovered that the SARS-CoV-2 virus infects neurons and then hijacks the neural cell machinery to make copies of itself.
Inflamed cells promote the death of surrounding cells by disrupting their oxygen supply.
One of the main arguments against the theory of direct invasion of the brain is that the brain lacks the maximum levels of a protein called ACE2 on which the coronavirus blocks and that 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 proteins were provided in the brain tissue of patients who died.
They also performed a lumbar puncture on a patient hospitalized by 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 tested two teams of mice, one that had been genetically modified to have ACE2 receptors in their lungs and the other in their brains.
Other infected people in their lungs showed symptoms of lung damage, while those inflamed in the brain temporarily lost weight and died temporarily, indicating a potentially higher fatality when the virus enters the organ.
Finally, they tested the brains of 3 patients who died of severe Covid-19 headaches, locating the virus in all of them to varying degrees.
Interestingly, the inflamed regions showed no symptoms of infiltration of immune cells, such as T lymphocytes, which rush to attack other viruses such as Zika or herpes to kill the inflamed cells.
This may also simply recommend that the overloaded immune reaction known as the cytokine storm, which is guilty of much of the damage observed in the lungs of Covid-19 patients, may not be the main 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 should be validated by an additional study.
They added that additional autopsies will be needed to determine the prevalence of brain infection.
Agence France-Presse