Headaches, confusion and delusions experienced by some COVID-19 patients could be the result of a direct invasion of the brain by the Coronavirus, according to a study published this past week. Although the research is still preliminary, it provides new evidence to support what was until now just an unproven theory.
According to the study, led by Akiko Iwasaki, an immunologist at Yale University, the virus can duplicate itself within the brain and its presence deprives nearby brain cells of oxygen. How often this situation occurs is not yet clear.
Andrew Josephson, head of the department of neurology at the University of California, San Francisco, praised the techniques used in the study, stressing that “understanding whether or not there is direct viral involvement in the brain is extremely important.” However, he added that he would be cautious until the investigation was the subject of a peer review.
Not a surprise
It wouldn’t be entirely surprising if SARS-CoV-2 were able to penetrate the blood-brain barrier, a structure that surrounds blood vessels in the brain and tries to block foreign substances.
But doctors until now believed that the neurological consequences seen in about half of hospitalized patients with COVID-19 could be the result of an abnormal immune response, “the cytokine storm,” that caused brain swelling rather than a invasion of the brain by the virus.
Various methods
Professor Iwasaki and colleagues decided to tackle the problem in three ways: infecting lab-created mini-brains (so-called brain organoids), infecting mice, and examining the brains of patients who died from COVID-19.
In brain organoids, the team discovered that the virus could infect neurons and then “hack” the machinery of the neuronal cell to duplicate itself. The infected cells caused the death of the surrounding cells by depriving them of oxygen.
One of the main arguments against the theory of direct brain invasion was that the brain does not have high levels of a protein called ACE2, to which the Coronavirus attaches itself and which is found in abundance in other organs such as the lungs.
But the team found that the organoids had enough ACE2 to facilitate entry of the virus and that the proteins were also present in the brains of deceased patients. The researchers also looked at two groups of mice: one that had been genetically modified to have ACE2 receptors only in the lungs, and the other, only in the brain.
Mice infected in the lungs had lesions in these organs; animals infected in the brain lost weight and died rapidly, a potential sign of increased lethality when the virus enters the brain. The brains of three patients who died from serious Coronavirus-related complications also showed traces of the virus, to varying degrees.
