Is the Coronavirus Primarily a Human Virus?

In summary, the article discusses how the coronavirus is unique in terms of its genome and how it is optimized for binding to the human receptor ACE2. It also mentions that the spike protein has a functional polybasic (furin) cleavage site at the S1-S2 boundary, which is predicted to result in the acquisition of three O-linked glycans.
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Phil Core
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I keep wondering why we do not know more about the virus? How hard is it to expose some mice to Coronavirus and see what happens? Then I considered that perhaps the virus is primarily a human virus and does not effect other life forms like lab mice. There have been cases with dogs and the origin is suppose to be bats (this info - how it effects bats is nonexistence).

So if the virus primarily effects humans, what is it about the virus's structure that makes this the case.

If I had to speculate I would venture that the transcribed DNA is well suited to human ribosomal structure. This seems odd to me.
 
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Phil Core said:
I keep wondering why we do not know more about the virus? How hard is it to expose some mice to Coronavirus and see what happens? Then I considered that perhaps the virus is primarily a human virus and does not effect other life forms like lab mice. There have been cases with dogs and the origin is suppose to be bats (this info - how it effects bats is nonexistence).

So if the virus primarily effects humans, what is it about the virus's structure that makes this the case.

If I had to speculate I would venture that the transcribed DNA is well suited to human ribosomal structure. This seems odd to me.
Some evidence of other mammals.
https://www.nature.com/articles/d41586-020-00984-8
 
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Interesting article.

Found this especially interesting - "The authors of the latest preprint also found that ferrets are highly susceptible to infection with the COVID-19 coronavirus, which they suggest makes the animals a suitable model for testing potential vaccines and drugs. Ferrets are already used as models in influenza studies, and several labs have started COVID-19 research on them. "

What is it about ferrets? Seems like we would have some good data on this by now.

I am still at a loss as to why we do not know more about the virus. It is only 32,000 nucleotides long.

I don't have the links but if memory serves, a large portion of this is devote to housekeeping tasks and frame alignment.

I have lost the reference but a group in China made mention of a section of the virus on the end of the chain that made it unique.

We do know that there is something about this virus that makes it very infectious. Part of the article mentioned that this unique chain was associcated with the production of a protein that made it easier for the virus to transgress the boundary of a health cell - the Crowns.

Hard to understand how a protein or two could make this big a change.

Facts about Coronvirus

1. Highly contagious to mainly humans - I find this to be very suspect
2. Seems to be restricted to a relatively small subset of Life - This only seems to reinforce (1.)
 
  • #4
Found this interesting

quoted by Ygg 3/17/2020

Our comparison of alpha- and betacoronaviruses identifies two notable genomic features of SARS-CoV-2: (i) on the basis of structural studies7,8,9 and biochemical experiments1,9,10, SARS-CoV-2 appears to be optimized for binding to the human receptor ACE2; and (ii) the spike protein of SARS-CoV-2 has a functional polybasic (furin) cleavage site at the S1–S2 boundary through the insertion of 12 nucleotides8, which additionally led to the predicted acquisition of three O-linked glycans around the site.

How do you get something that is optimized for binding to the human receptor ACE2, when the virus is thought to have originated in bats.

Also amazing that the insertion of just 12 nucleotides could make such a big difference.
 
  • #5
Actually the Coronaviruses are quite a large family of pathogens that infect a wide range of different species, like most pathogenic viruses they tend to infect only one or a few different animal species and are even selective in the types of cell they infect. Its really not surprising that we haven't come across this one before, our knowledge of viruses is really confined to the ones that are of significance to us, which is only a tiny fraction really.
While most tend to be species specific its not unusual for them to jump species and cause sporadic outbreaks, this is most likely if the target species is exposed to a very high viral load and has impaired immune functioning. When a virus infects a new host it is exposed to selective pressures that try to optimise it to its new host, in fact the ability to be transmitted between the new species is a very significant problem requiring very specific mutations to occur. Its this problem that effectively prevented MERS and SARS, the other two coronaviruses known to have jumped species becoming a major problem.
Its worth considering that one of the suggested binding sites, the ACE2 receptor, is common across a wide range of animal species and there may be other binding sites involved. It does seem that there may have been some adaptation in the virus soon after it was observed in humans, its suggested that there are two subspecies, the first appears to have caused a more sever illness but was less infectious, the more common subspecies causing a less sever infection but being more infectious. These changes are in fact consistent with natural selection facilitating the virus in increasing its fitness.
I've seen people describing the emergence of a new disease pandemic as a hundred year event, they are really not that unusual, just unusual in our lifetime. However the early warning systems were really focussed on identifying a new pandemic influenza, which has always been considered to be the greatest threat
 
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Phil Core said:
If I had to speculate I would venture that the transcribed DNA is well suited to human ribosomal structure.

Phil Core said:
Found this interesting

quoted by Ygg 3/17/2020

Our comparison of alpha- and betacoronaviruses identifies two notable genomic features of SARS-CoV-2: (i) on the basis of structural studies7,8,9 and biochemical experiments1,9,10, SARS-CoV-2 appears to be optimized for binding to the human receptor ACE2; and (ii) the spike protein of SARS-CoV-2 has a functional polybasic (furin) cleavage site at the S1–S2 boundary through the insertion of 12 nucleotides8, which additionally led to the predicted acquisition of three O-linked glycans around the site.

How do you get something that is optimized for binding to the human receptor ACE2, when the virus is thought to have originated in bats.

Also amazing that the insertion of just 12 nucleotides could make such a big difference.

As you seem to have figured out, a major determinant of the species specificity of a virus is how well the virus can attach to the cells of a particular species and enter those cells. (There are other factors that could be involved as well, such as how well the virus is able to evade some of the innate immune defenses of a particular species, but most of the time, the virus-receptor interactions determine a lot about the species and tissue specificity of a virus). It is unlikely that the ribosome would contribute to specificity; you can stick genes from bacteria into humans and get human ribosomes to translate those genes into proteins just fine.

While most of the SARS-CoV-2 virus resembles related coronaviruses in bats, the spike protein (the main protein on the outside of the virus that interacts with the cellular ACE2 receptor) is quite different from the spike protein in bat coronaviruses. Rather the spike protein resembles the spike protein found in pangolin coronaviruses (e.g. see https://www.nature.com/articles/s41586-020-2169-0). It is possible that the ACE2 protein from pangolins could more closely resemble the ACE2 protein from humans, which could account for why SARS-CoV-2 is more efficient at human-to-human transmission than other bat coronaviruses.

Indeed, for all of the coronaviruses that we've seen emerge as human pathogens in recent years (SARS, MERS and COVID-19), an intermediary species has been thought to be involved in all three (civet cats for SARS, camels for MERS and pangolins for COVID-19). It is thought that propagating these viruses in intermediate hosts that are more similar to humans than bats could allow the viruses to evolve into forms that are more capable of spreading through human populations. The aformentioned mutation to create the furin cleavage site may be the "lucky" mutation that has made COVID-19 much harder to contain than SARS or MERS.
 
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I read that great apes are at risk. Just saw it as a headline so don't know if that's an assumption based on known similarities between them/us or if it's based on empirical evidence.
 
  • #8
Ygggdrasil said:
As you seem to have figured out, a major determinant of the species specificity of a virus is how well the virus can attach to the cells of a particular species and enter those cells. (There are other factors that could be involved as well, such as how well the virus is able to evade some of the innate immune defenses of a particular species, but most of the time, the virus-receptor interactions determine a lot about the species and tissue specificity of a virus). It is unlikely that the ribosome would contribute to specificity; you can stick genes from bacteria into humans and get human ribosomes to translate those genes into proteins just fine.

While most of the SARS-CoV-2 virus resembles related coronaviruses in bats, the spike protein (the main protein on the outside of the virus that interacts with the cellular ACE2 receptor) is quite different from the spike protein in bat coronaviruses. Rather the spike protein resembles the spike protein found in pangolin coronaviruses (e.g. see https://www.nature.com/articles/s41586-020-2169-0). It is possible that the ACE2 protein from pangolins could more closely resemble the ACE2 protein from humans, which could account for why SARS-CoV-2 is more efficient at human-to-human transmission than other bat coronaviruses.

Indeed, for all of the coronaviruses that we've seen emerge as human pathogens in recent years (SARS, MERS and COVID-19), an intermediary species has been thought to be involved in all three (civet cats for SARS, camels for MERS and pangolins for COVID-19). It is thought that propagating these viruses in intermediate hosts that are more similar to humans than bats could allow the viruses to evolve into forms that are more capable of spreading through human populations. The aformentioned mutation to create the furin cleavage site may be the "lucky" mutation that has made COVID-19 much harder to contain than SARS or MERS.

I was wrong about the structure of the human ribosome being a factor. That was just me using the little I know.

I read the link you provided about the pangolin. (Did not know what a pangolin was and had to look it up.) Seemed rather incredulous that a virus would go from bat to anteater to human. All of the comments associated with the article pan it as bad science.
What was very interesting is what was found in the comments.

1st note
"more similar to humans than bats" According to first note the virus is less similar in the anteater than the bat?

2nd note
"Why do you keep pushing this idea that the virus had to jump from an intermediate when we have peer reviewed research & government research into gain of function using the Coronavirus? The Chinese literally built a lab around this research.
'U.S. Government Gain-of-Function Deliberative Process and Research Funding Pause on Selected Gain-of-Function Research Involving Influenza, MERS, and SARS Viruses'
This seems like a whole lot of revisionist history when people published this as an issue in 2007.
Your disclaimer should literally say that you cannot disprove it."

FYI - Gain of function research given green light again in US in 2018.Not a big fan of "lucky" mutation. Is this the mutation you are talking about - "the spike protein of SARS-CoV-2 has a functional polybasic (furin) cleavage site at the S1–S2 boundary through the insertion of 12 nucleotides"?
Relative to the positioning of the RNA chain where is this chain located?

There are 2 parts here

1. Emergence of the basic virus - spike virus - where did it come from?
a. What type of virus do you have is you take the 12 nucleotides out?
2. Divergence of less contagious more sever to more contagious less sever. Difference in nucleotides? Are the nucleotides both in the same position as the spike protein mentioned above.
a. Can both forms of the virus inhabit the same host?

Heard that the Coronavirus was not prone to mutate due to some proof reading protein??
 
  • #9
Phil Core said:
I read the link you provided about the pangolin. (Did not know what a pangolin was and had to look it up.) Seemed rather incredulous that a virus would go from bat to anteater to human. All of the comments associated with the article pan it as bad science.

The paper was published in a peer-reviewed journal, so it had to be reviewed and approved by experts. Comments from random people on the internet (especially some that seem to advocate disproven conspiracy theories). This is also not the only study that has come to this conclusion; various independent research teams have come to similar conclusions about the origin of the virus:

Isolation and Characterization of 2019-nCoV-like Coronavirus from Malayan Pangolins
https://www.biorxiv.org/content/10.1101/2020.02.17.951335v1

Evidence of recombination in coronaviruses implicating pangolin origins of nCoV-2019
https://www.biorxiv.org/content/10.1101/2020.02.07.939207v1

Now, it's important to be specific about what these studies show. These studies note a genetic similarity between the spike protein from SARS-CoV-2 and the spike protein found in coronaviruses from pangolins. This points to the involvement of pangolins in the evolutionary origin of the virus, but it does not say that the virus passed directly from pangolins to humans. That questions still remains unknown, and although we know some pieces of the story (e.g. that the virus likely originated from the recombination of bat and pangolin coronaviruses) many pieces remain unknown. For a good popular press discussion see: https://www.theguardian.com/world/2...-it-really-bats-pangolins-wuhan-animal-market

1st note
"more similar to humans than bats" According to first note the virus is less similar in the anteater than the bat?
Most of the SARS-CoV-2 RNA resembles a bat Coronavirus except for the spike protein, which more closely resembles the pangolin spike protein. This indicates that the virus resulted from the recombination of bat and pangolin coronaviruses (recombination of viruses is common in nature; for example, new influenza strains are constantly evolving by swapping and recombining their hemaglutinin [H] and neuramididase [N] genes to create varieties, e.g. H1N1, H3N2, etc). When, where and in what species the recombination occurred is not known.

2nd note
"Why do you keep pushing this idea that the virus had to jump from an intermediate when we have peer reviewed research & government research into gain of function using the Coronavirus? The Chinese literally built a lab around this research.
'U.S. Government Gain-of-Function Deliberative Process and Research Funding Pause on Selected Gain-of-Function Research Involving Influenza, MERS, and SARS Viruses'
This seems like a whole lot of revisionist history when people published this as an issue in 2007.
Your disclaimer should literally say that you cannot disprove it."

FYI - Gain of function research given green light again in US in 2018.

The conspiracy theory that the SARS-CoV-2 was bioengineered has been disproven by a number of genetic studies, including the one you cited from my post earlier. See:
https://directorsblog.nih.gov/2020/03/26/genomic-research-points-to-natural-origin-of-covid-19/
https://www.nature.com/articles/s41591-020-0820-9

Not a big fan of "lucky" mutation. Is this the mutation you are talking about - "the spike protein of SARS-CoV-2 has a functional polybasic (furin) cleavage site at the S1–S2 boundary through the insertion of 12 nucleotides"?
Relative to the positioning of the RNA chain where is this chain located?

Here's a figure from the Nature Medicine paper cited above showing the relative positioning of the furin cleavage site relative to the spike protein and the RNA genome: https://www.nature.com/articles/s41591-020-0820-9/figures/1

There are 2 parts here
1. Emergence of the basic virus - spike virus - where did it come from?
a. What type of virus do you have is you take the 12 nucleotides out?

1. The majority of SARS-CoV-2 is likely derived from a bat coronavirus. The spike protein is likely derived from a pangolin coronavirus. How these two coronaviruses got together to recombine is currently not known, and the path of that recombined Coronavirus to humans is also not known.

a. It is not known how or when the furin cleavage site evolved. It is not found in known pangolin coronaviruses, which could mean a number of possibilities, including 1) it is present in some unknown pangolin Coronavirus (since I'm sure there are many viruses out there that we have not identified yet) and that was the origin or 2) it evolved sometime after the bat and pangolin coronaviruses recombined. Because recent papers have suggested that the virus can exist in a number of other species, including many in close contact with humans (https://science.sciencemag.org/content/early/2020/04/07/science.abb7015), it is possible that species other than pangolins and bats were invovled in the chain of transmission to humans.

2. Divergence of less contagious more sever to more contagious less sever. Difference in nucleotides? Are the nucleotides both in the same position as the spike protein mentioned above.
a. Can both forms of the virus inhabit the same host?

The paper making the claim about two different strains of the virus has been criticized by other researchers in the field:
An analysis of genetic data from the ongoing COVID-19 outbreak was recently published in the journal National Science Review by Tang et al. (2020) 84. Two of the key claims made by this paper appear to have been reached by misunderstanding and over-interpretation of the SARS-CoV-2 data, with an additional analysis suffering from methodological limitations. [...] Given these flaws, we believe that Tang et al. should retract their paper, as the claims made in it are clearly unfounded and risk spreading dangerous misinformation at a crucial time in the outbreak.
http://virological.org/t/response-to-on-the-origin-and-continuing-evolution-of-sars-cov-2/418

According to the Tang paper, the two strains they identify are primarily differentiated by two mutations, one in the orf1ab gene and the other in the ORF8 gene. Neither of these genes are expressed on the surface of the virion, so the mutations will not affect immunity to the virus, and I would expect immunity to one "strain" to confer immunity to the other "strain." The spike protein is the main protein on the surface of the virus, so scientists should monitor mutations in the spike protein to find potential mutations that could affect immunity against the virus.

Heard that the Coronavirus was not prone to mutate due to some proof reading protein??

Yes, that is correct. See: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3127101/

For an explanation of how the proofreading process could work, see: https://www.physicsforums.com/threa...different-from-the-others.985500/post-6315740
 
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Related to Is the Coronavirus Primarily a Human Virus?

1. Is the coronavirus primarily a human virus?

Yes, the coronavirus is primarily a human virus. It is a zoonotic virus, meaning it originated in animals and then spread to humans. However, it is now primarily transmitted between humans through respiratory droplets.

2. What animals can get the coronavirus?

The coronavirus is believed to have originated in bats, but it can also infect other animals such as pangolins, cats, and dogs. However, it is important to note that the virus primarily spreads among humans and there is no evidence that pets can transmit the virus to humans.

3. Can the coronavirus mutate and become more dangerous?

Yes, viruses are constantly mutating and changing. However, most mutations are insignificant and do not affect the virus's ability to cause illness. Scientists are closely monitoring the coronavirus for any significant mutations that could make it more dangerous.

4. How long does the coronavirus survive on surfaces?

The coronavirus can survive on surfaces for varying lengths of time, depending on the type of surface and environmental conditions. Studies have shown that it can survive on plastic and stainless steel for up to 72 hours, on cardboard for up to 24 hours, and on copper for up to 4 hours. However, the risk of transmission from surfaces is low compared to person-to-person contact.

5. Can people get reinfected with the coronavirus?

There have been a few reported cases of people getting reinfected with the coronavirus. However, it is not yet clear if this is due to a new strain of the virus or if the individual's immune system did not produce enough antibodies to protect them from reinfection. More research is needed to fully understand reinfection with the coronavirus.

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