Particles were detected only in the brain, but not in the lung, indicating that infection in the CNS was more important for the high mortality observed in infected mice 11 . Among the brain regions involved, the brainstem is heavily infected by SARS-CoV 30, 35 or MERS-CoV 11.
The exact route by which SARS-CoV or MERS-CoV enters the CNS has not yet been reported. However, the hematogenous or lymphatic route seems impossible, especially in the early stage of infection, because almost no virus particles have been detected in it.
Non-neuronal cells in the infected areas of the brain 32-34. On the other hand, it is increasing
Evidence suggests that CoVs may first invade peripheral nerve terminals and gain access to the CNS through a synapse-connected pathway 9-10, 19, 36. Transsynaptic transmission is well documented for other coronaviruses, such as HEV67 9-10, 18-19 and avian bronchitis virus 36-37.
HEV 67N is the first coronavirus to attack the pig brain, and shares
> 91% homology with HCoV-OC43 38-39. HEV first oronasally infects the nasal mucosa, tonsils, lungs and small intestine in lactating Granger animals, and then is delivered retrograde through the peripheral nerves to the medullary neurons responsible for the function of the gastrointestinal tract, resulting in the so-called vomiting disease 18 – 19 . HEV67N transport between neurons has been shown by our previous ultrastructural studies to use a clathrin-coating-mediated endo-/exocytotic pathway.
10.
Similarly, transsynaptic transmission has been reported for avian bronchitis virus 36-37. Intrauterine inoculation has been reported in mice with avian influenza virus, which causes neuroinfection in addition to bronchitis or pneumonia 36. Of interest, viral antigens have been detected in the brainstem, where infected areas include the nucleus of the solitary tract and the nucleus accumbens. The nucleus of the solitary tract receives sensory information from mechano- and chemoreceptors in the lung and airways 40 – 42 , while extrinsic fibers from the nucleus accumbens and the nucleus of the solitary tract provide muscle, glands, and smooth blood vessels of the airways. . Such neural and neural connections suggest that the death of infected animals or patients may be due to dysfunction of the cardiorespiratory center in the brainstem.
11, 30, 36.
Taken together, neural propensity has been shown to be a common feature of CoVs. Given the high similarity between SARS-CoV and SARS-CoV2, it is quite possible that SARS-CoV-2 has a similar potential. According to an epidemiological study on COVID-19, the average time from the first symptoms to dyspnea was 5.5 days, hospitalization was 7.0 days, and for intensive care was 8.0 days 15. Therefore, the latency period is sufficient for the virus
Enter and destroy medullary neurons. In fact, some patients infected with SARS-CoV-2 have been reported to show neurological symptoms such as headache (about 8%), nausea and vomiting (1%).
Potential neurological consequences of SARS-CoV-2
As an emerging virus, no effective treatment has been developed for the disease caused by SARS-CoV-2. Therefore, awareness of possible entry
SARS-CoV-2 entry into the CNS will be important for prevention and treatment.
If neurotransmission of SARS-CoV-2 plays a role in the development of respiratory failure in patients with COVID-19, precaution with masks would be the most effective measure to protect against potential entry of the virus into the CNS. It can also be expected that the symptoms of patients who are infected through the face-mouth route or conjunctiva will be lighter than those who are infected inside the body. Possible neurotransmission of SARS-CoV-2 may also partially explain why some patients developed respiratory failure, while others did not. It is very possible that most of the people in Wuhan, who were first exposed to this previously unknown virus, did not have any protective measures, so that the critically ill patients in Wuhan are much more than in other Chinese cities.
This post is written by Farshadboy000