Presuming that we were able to find a person who was never exposed to any of the human seasonal coronaviruses (part of the viruses that cause the common cold), would the virus be just as deadly for that person as the SARS-CoV-2 currently circulating around the world? Or is SARS-CoV-2 uniquely dangerous?

  • 4
    +1 because I suggested this question. The minor quibble I can make right now is that it's a bit misleading to say "human coronavirus", as there were at least 4 (not counting SARS and MERS); see the figure in my answer to a q on Skeptics: skeptics.stackexchange.com/a/46088/29579 Also that question is not quite the same as this one, as the claim there was more silly, namely that even with the exposure we have to the [alpha]coronavirus "geckos" as I dubbed them (229E, NL63, OC43, HKU1), they were just as deadly as SARS-CoV-2. Your question is a bit less obvious how to answer. Apr 2, 2020 at 5:28
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    I like this article, which suggests that the answer is mostly yes (to the title question), unlike @GrahamChiu's answer below, but it's mostly speculative, and I think GrahamChiu's reasoning also makes sense theinsight.org/p/novelty-means-severity-the-key-to
    – That Guy
    Feb 2, 2022 at 22:41

2 Answers 2


The seasonal coronaviruses attach exclusively to cells with a ciliated epithelium.

Coronaviruses invade the respiratory tract via the nose. After an incubation period of about 3 days, they cause the symptoms of a common cold, including nasal obstruction, sneezing, runny nose, and occasionally cough (Figs. 60-1 and 60-2). The disease resolves in a few days, during which virus is shed in nasal secretions. There is some evidence that the respiratory coronaviruses can cause disease of the lower airways but it is unlikely that this is due to direct invasion. Other manifestations of disease such as multiple sclerosis have been attributed to these viruses but the evidence is not clear-cut.

Studies in both organ cultures and human volunteers show that coronaviruses are extremely fastidious and grow only in differentiated respiratory epithelial cells. Infected cells become vacuolated, show damaged cilia, and may form syncytia. Cell damage triggers the production of inflammatory mediators, which increase nasal secretion and cause local inflammation and swelling. These responses in turn stimulate sneezing, obstruct the airway, and raise the temperature of the mucosa.

So, the mechanism of infection is such that they only attack the upper airways.

The SARS-CoV-2 is totally different. It attaches to the ACE2 surface receptor which is found deep in alveolar pneumocytes. Their damage causes loss of surfactant in the alveoli, the collapse of these air cells that perform oxygen exchange and subsequently ARDS.

So, seasonal coronaviruses give you a runny nose but don't kill. SARS-CoV-2 collapses the air sacs that allow oxygenation to occur.


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    "Coronaviruses invade the respiratory tract via the nose" and not the mouth too ? Apr 3, 2020 at 19:30
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    The mouth doesn't have a ciliated epithelium. Apr 3, 2020 at 21:38
  • And the eyes? I’ve heard the virus can enter thorough the eyes. Apr 11, 2020 at 11:39
  • @Albrecht Hügli: “[T]ransmission from droplet spread may occur when viral particles in tears are drained through the nasolacrimal duct into the respiratory tract,” per cebm.net/wp-content/uploads/2020/03/Spreading-SARS.pdf
    – goodside
    Apr 11, 2020 at 15:01

I should add here that there has been a case of ARDS reported for the alphacoronavirus 229E (i.e. a "common cold" coronavirus) in 2018. But ARDS occurrences are of course, much less common in these "common colds" than in Covid-19 infections. The case report for 229E discusses the few other such occurrences:

HCoV-229E has been associated with bronchitis, acute exacerbations of COPD, and pneumonia in infants, children, and elderly persons with underlying illnesses [11–13]. Life-threatening infections have only been described in immunocompromised patients [7, 8], but the correlation of HCoV-229E with LRTI in healthy adult individuals is uncertain [9]. An adult patient with pneumonia tested positive for HCoV-229E has been described in a study conducted in rural Thailand, but it is not made clear if other comorbidities were present [14]. Nine Italian patients hospitalized with LRTI have also been tested positive for HCoV-229E; however, their age is not specified [15]. Αlthough numerous studies have tentatively linked 229E infections to severe respiratory tract illness over many years, no study controlling for age and underlying illness has demonstrated an epidemiologic association between infection with HcoV-229E in healthy adults and any illness other than the common cold. Furthermore, no case of HCoV-229E-associated ARDS has been reported in immunocompetent adults. Only a few cases of pulmonary infection and ARDS have been described in a 76-year-old woman infected with the closely related alpha coronavirus HCoV-NL63 [16] and in a 39-year-old woman with poorly controlled DM and infected with the beta coronavirus HCoV-OC43.

For severely immunocompromised patients however, there have been cases of 229E infection, triggering pneumonia e.g. as reported in (the papers referenced from the prviousone):

But this is like a handful of cases in toto (for 229E).

The ARDS case cited/mentioned in that (first) paper for NL63 was reported in 2016. This was also diagnosed by BAL + electron microscopy. This latter paper also suggests that in immunocompromised patients NL63 may be a bit more problematic (than 229E):

In 2010, a case of fatal HCoV-NL63 pulmonary infection during the late-engraftment phase was reported (6). An Australian study reported that 2% of patients presenting to the hospital because of respiratory symptoms tested positive for HCoV-NL63, and 81% of these patients were diagnosed with lower respiratory tract disease; all of them required admission to the hospital, 56% had an abnormal chest xray, and one immunocompromised patient died, yet none of these patients had ARDS (7).

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