THE NEW CORONAVIRUS SARS-COV-2 WAS ORIGINALLY THOUGHT TO BE A RESPIRATORY VIRUS, BUT AS THE NUMBER OF CASES INCREASES GLOBALLY, IT WAS RECOGNIZED THAT THE VIRUS NOT ONLY CAUSES RESPIRATORY SYMPTOMS, BUT ALSO SPREADS TO MULTIPLE OTHER ORGAN SYSTEMS, WITH THE NERVOUS SYSTEM BEARING THE BRUNT.
A study of hospitalized patients in the UNITED Kingdom found that during the acute infection of the new crown, the most common neurological symptoms of patients include: loss of smell, stroke, delirium, brain inflammation, brain lesions, etc.
Not only that, but in the months after an acute infection, loss of taste and smell, inattention, headaches, sensory disturbances, sleep disturbances, depression and even mental illness may also persist as sequelae of COVID-19 in some patients in the recovery phase, even in young mild patients.
However, we have not yet understood the mechanism of the new crown virus damage to the brain, and the current mainstream view is that the new crown virus may affect the function of the nervous system through immune activation, nerve inflammation and cerebrovascular damage.
The autopsy results of the new crown pneumonia patients showed that there was obvious inflammation in the brains of these deceased patients with the activation and infiltration of immune cells.
Compared with influenza, the risk of stroke in patients with acute COVID-19 infection has increased significantly, and even after adjusting for stroke risk factors, this correlation persists, and an increase in intra-organ thrombosis and infarction similar to that of stroke patients has been found in patients with COVID-19.
A recent research team from Tulane University in the United States used a non-human primate model infected with the new crown virus to reproduce the autopsy results of human cases, showing in detail how the new crown virus affects the nervous system. Even more surprising is that infected monkeys, who have no obvious respiratory symptoms, have brain damage changes in their brains. The study was published in Nature Communications on April 1, 2022.
Eight adult monkeys, including four rhesus macaques (RM) and four African green monkeys (AGMs), were enrolled in the experimental group of eight adult monkeys who were infected with the original strain of the new coronavirus (2019-nCoV strain) by multi-channel mucosal inoculation or aerosol atomization.
In addition, 2 adult rhesus monkeys and 2 African green monkeys were inoculated with virus-free medium through multi-channel mucosa as a control group.
Within a week, the monkeys in the experimental group were successfully infected with the new crown virus, except for the early death of AGM1 and AGM2, the other monkeys survived to the end of the experiment.
AGM1 fell into a coma on the 8th day after infection, responded only mildly to stimuli, developed dyspnea, hypothermia, and hypoxemia, and was euthanized after anesthesia. AGM2 also showed a similar manifestation on the 22nd day after infection, also with euthanasia.
After the end of the experiment, the monkey specimens of the experimental group and the control group were collected and compared, and the results showed that compared with the experimental group infected with the new coronavirus and the control group, there was a significant inflammatory response in the brain of the monkeys in the experimental group and the activation of a wide range of microglia and astrocytes.
After infection, the brain neurons of the monkeys in the experimental group underwent different degrees of nuclear lysis, and neuronal apoptosis, especially in the cerebellum and brain stem positions.
Not only that, the monkeys in the experimental group also had a larger number of micro-bleeding points in the brain, accompanied by the formation of micro-thrombosis, especially in the brain of the earliest death of AGM1, a large number of bleeding points were found, which is likely to be one of the reasons for its rapid death.
Cerebrovascular damage will cause local brain tissue blood supply, oxygen supply is insufficient, during the infection, the blood sample saturation of the monkeys in the experimental group fluctuates between 89% and 99%, most of the time it is less than 95%, although it does not reach the warning value, but it also means the presence of mild hypoxemia, corresponding to the concentration of carbon dioxide in the blood of the monkeys in the experimental group exceeds the normal physiological range.
The brain is a very metabolic organ, it is highly dependent on the ATP energy supply produced by aerobic glycolysis, long-term or intermittent decrease in blood oxygen saturation will cause brain hypoxia, energy metabolism disorders, affect nerve cell activity, and eventually lead to nerve cell death, brain damage occurs.
The evidence of cerebral hypoxia after infection with COVID-19 is that compared with the control group, the expression of the hypoxia inducing factor HIF-1a in multiple brain regions of the experimental group increased significantly, and the brain cells Purkinye neurons and their surrounding cells, which are very sensitive to hypoxia conditions, degenerated and went to apoptosis.
Finally, the researchers tried to look for traces of the new crown virus in the brains of infected monkeys, and similar to the results of human autopsies, they could only find a few new coronaviruses in the blood vessels, suggesting that the brain tissue lesions of the monkeys in the experimental group were unlikely to be caused by the direct invasion of the new crown virus into the brain.
Based on the above findings, researchers believe that cerebral hypoxia plays an important role in the process of covid-19 infection to the appearance of neurological symptoms, which may be caused by systemic hypoxemia plus cerebrovascular damage, which can be very mild, but as long as it takes a long time, it will cause nerve cell damage and death.
More importantly, cerebral hypoxia does not only occur in severe cases of dyspnea, but also in those infected people with inconspicuous respiratory symptoms, indicating that cerebral hypoxia is likely to be a common feature after the new crown infection.
As with all ages, with or without complications, infected people with post-infection severity are likely to develop COVID-19 neurological symptoms.
"Because infected people did not develop significant respiratory symptoms, no one expected that these infected people might have potential brain damage," researcher Tracy Fischer said.
She hopes that this study and more future studies of the new crown virus and brain will point the way to treating and improving the neurological symptoms of acute and long-term new crown.
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