Not a biologist, but reading the paper, the chain of reasoning appears to be summarized in this section:
> Taken together, the neuroinvasive propensity has been demonstrated as a common feature of CoVs. In light of the high similarity between SARS-CoV and SARS-CoV2, it is quite likely that SARS-CoV-2 also possesses a similar potential. Based on an epidemiological survey on COVID-19, the median time from the first symptom to dyspnea was 5.0 days, to hospital admission was 7.0 days, and to the intensive care was 8.0 days 15. Therefore, the latency period is enough for the virus to
enter and destroy the medullary neurons. As a matter of fact, it has been reported that some patients infected with SARS-CoV-2 did show neurologic signs such as headache (about 8%), nausea and vomiting (1%).
There's also this rather disquieting anecdote used as evidence of a link to the nervous system:
> According to the complaints of a survivor, the medical graduate student (24 years old) from Wuhan University, she
must stay awake and breathe consciously and actively during the intensive care. She said that if she fell asleep, she might die because she had lost her natural breath.
Supposing that this neurological link is real,
> the precaution with masks will absolutely be the most effective measure to protect against the possible entry of the virus into the CNS. It may also be expected that the symptoms of the patients infected via facal-oral [sic?] or conjunctival route will be lighter than those infected intranasally. The possible neuroinvasion of SARS-CoV-2 may also partially explain why some patients developed respiratory failure, while others not. It is very possible that most of the persons in Wuhan, who were the first exposed to this previously unknown virus, did not have any protective measure, so that the critical patients is much more in Wuhan than in other cities in China.
So let me ask a dumb question for someone with actual biomedical knowledge. Are they saying that infection of the CNS is somehow easier through the nose, in which case high-quality face masks actually do matter?
I'm also confused by this sentence in the introduction, which appears to contradict the hypothesis that the upper respiratory tract is a high-impact area?
> However, different from SARS-CoV, SARS-CoV-2-infected patients rarely showed prominent upper respiratory tract signs
and symptoms, indicating that the target cells of SARS-CoV-2 may be located in the lower airway.
I will note that, unlike some other papers on this topic, this one has been peer-reviewed in what seems to be a legitimate medical journal (Journal of Medical Virology), so there should be some genuine substance here.
1. I am not familiar with coronavirus biology, however, as to the general question about nasal -> brain routes if infection: yes this is a risk if the virus is able to infect the olfactory nerves and travel retrograde through the cribriform plate into the olfactory bulb. It is a little peculiar that it would lead to medullary viral replication, as the medulla is a few steps back and distal from the olfactory bulb. Other infectious agents can travel into the CNS via the cribriform plate, most terrifying is naegleria fowleri but other terrible fungal infections like mucor and rhizopus can do it as well. They don’t tend to grow in neurons but rather eat through the tissues.
2. Upper versus lower: when people have a URI the upper airways meaning the nasopharyngeal, oropharyngeal, and trachea are predominantly affected. The typical symptoms are runny nose, nasal congestion, sore throat. However, SARS/COVID tends to cause a lower respiratory syndrome affecting the small airways deep in the lungs, namely the alveoli and small bronchioles. It is entirely consistent to hypothesize that infection through the upper airway mucosa is “worse” but the target cells that primarily cause disease are in the lower airway.
> So let me ask a dumb question for someone with actual biomedical knowledge. Are they saying that infection of the CNS is somehow easier through the nose, in which case high-quality face masks actually do matter?
The olfactory receptors (nerves that smell) are among the most exposed nerves of the body, and IIRC they are single cells stretching from the mucus membrane in your nose all the way to the brain. And because smell is such an evolutionary ancient function, the relevant brain region is really close to the centre of the brain (and brainstem).
So it's really just two hops from the outside world to the command post of your autonomous nervous system (i. e. breathing)
> There's also this rather disquieting anecdote used as evidence of a link to the nervous system:
> According to the complaints of a survivor, the medical graduate student (24 years old) from Wuhan University, she must stay awake and breathe consciously and actively during the intensive care. She said that if she fell asleep, she might die because she had lost her natural breath.
Would that explain people collapsing suddenly on the streets as seen in Wuhan and Iran?
No, I think that'd be very unlikely because it'd be a late symptom after substantial damage has been done. Compared to the frequency of syncopal episodes I'd expect in people sick with any other cold or flu, I think it's overwhelmingly more likely to be from other causes.
And if it actually were causing neurological damage, I'd expect still more causes like seizures and the like.
> Taken together, the neuroinvasive propensity has been demonstrated as a common feature of CoVs. In light of the high similarity between SARS-CoV and SARS-CoV2, it is quite likely that SARS-CoV-2 also possesses a similar potential. Based on an epidemiological survey on COVID-19, the median time from the first symptom to dyspnea was 5.0 days, to hospital admission was 7.0 days, and to the intensive care was 8.0 days 15. Therefore, the latency period is enough for the virus to enter and destroy the medullary neurons. As a matter of fact, it has been reported that some patients infected with SARS-CoV-2 did show neurologic signs such as headache (about 8%), nausea and vomiting (1%).
There's also this rather disquieting anecdote used as evidence of a link to the nervous system:
> According to the complaints of a survivor, the medical graduate student (24 years old) from Wuhan University, she must stay awake and breathe consciously and actively during the intensive care. She said that if she fell asleep, she might die because she had lost her natural breath.
Supposing that this neurological link is real,
> the precaution with masks will absolutely be the most effective measure to protect against the possible entry of the virus into the CNS. It may also be expected that the symptoms of the patients infected via facal-oral [sic?] or conjunctival route will be lighter than those infected intranasally. The possible neuroinvasion of SARS-CoV-2 may also partially explain why some patients developed respiratory failure, while others not. It is very possible that most of the persons in Wuhan, who were the first exposed to this previously unknown virus, did not have any protective measure, so that the critical patients is much more in Wuhan than in other cities in China.
So let me ask a dumb question for someone with actual biomedical knowledge. Are they saying that infection of the CNS is somehow easier through the nose, in which case high-quality face masks actually do matter?
I'm also confused by this sentence in the introduction, which appears to contradict the hypothesis that the upper respiratory tract is a high-impact area?
> However, different from SARS-CoV, SARS-CoV-2-infected patients rarely showed prominent upper respiratory tract signs and symptoms, indicating that the target cells of SARS-CoV-2 may be located in the lower airway.
I will note that, unlike some other papers on this topic, this one has been peer-reviewed in what seems to be a legitimate medical journal (Journal of Medical Virology), so there should be some genuine substance here.