An international study involving several teams of researchers confirmed the ability of SARS-Cov-2 to infect neurons and identified several consequences, including damage from oxygen deprivation.
A growing body of scientific evidence suggests that the SARS-Cov-2 virus is not without consequences for our brains. For example, in addition to the significant respiratory damage that SARS-Cov-2 infection can cause, neurological symptoms have been reported very quickly in patients, ranging from headaches to loss of smell to loss of consciousness and stroke. A recent study by researchers at the National Institutes of Health suggests the possibility of blood vessel damage and inflammation after examining samples of brain tissue from patients who died shortly after contracting the disease.
But although traces of the virus’ RNA were found in the brains of patients who died of Covid-19, and viral proteins were found in some cells of their olfactory bulbs, the virus’s ability to infect brain cells and the potential consequences had not been demonstrated until then. To address this challenge, a team of Yale University and researchers from several French organizations, including INSERM and the Pitié-Salpêtrière AP-HP hospital, used three different approaches to study infection in the brain: 3D brain cell cultures, a mouse model of SARS-Cov-2 infection, and brain tissue from deceased Covid-19 patients.
Which “pathway” leads to the neurons?
The 3D brain cell culture results showed the ability of SARS-Cov-2 to enter neurons and use their components to proliferate. This leads to metabolic changes in the infected cells without destroying them. In addition, cells adjacent to infected neurons are deprived of oxygen and eventually die. In the brains of patients who died from Covid-19, the virus was found in cortical neurons, along with pathological damage associated with infection, such as ischemic stroke, death of brain tissue due to insufficient blood and oxygen supply to the brain.
But how the virus gets into neurons is another matter. The researchers explain, “Previous data have shown that in the rest of the body, the virus uses the ACE 2 protein, which is present on the surface of cells. This is particularly prominent in the lungs, which explains why the coronavirus attacks this particular organ. However, this pathway had not yet been detected in neurons. “Using a mouse model of SARS-Cov-2 which also has an ACE 2 receptor, the researchers were able to confirm the importance of this pathway in infecting brain cells.
When neurological symptoms persist
Finally, the analysis also revealed that the infected brain regions in the mice studied showed significant remodeling of the cerebral vascular network. Therefore, the researchers believe that there may be a link between the penetration of the virus into neurons observed in brain cell cultures and brain tissue postmortem and the hypoxia and ischemic strokes observed in the patients’ brains. “These results confirm the brain tropism of SARS-Cov-2 and its ability to infect neurons. The neurological symptoms observed in Covid-19 could be a consequence of this direct involvement of the central nervous system,” they concluded.
However, studies are still needed to identify the pathway the virus uses to enter the brain and to confirm the link between the cellular changes observed in neurons and the reported neurological symptoms. Last December, an AP-HP study on the exact nature of “long COVID” symptoms identified 50 different manifestations of the disease based on responses from 600 people who described their symptoms in detail. Those of a neurological nature were found to be the most numerous, with headaches, brain fog, dizziness, memory problems, and always a loss of smell and/or taste.