kadiot said:
It is likely that the virus is zoonotically transmitted from bats to humans. But since there are no bats sold in the Wuhan market, and that bats are not naturally found near the market, and that the lab is using live bats for research, which are the claims of the other study, it is possible that the real place of first infection are the labs, where the virus infected a lab worker, and not the market.
Are you claiming that the virus was transmitted directly from bats to humans? On what scientific basis do you make that claim?
Jarvis323 said:
I'm not a expert in the area, but one concern I have about the article is that they did not actually study the SARS-CoV-2 virus. Rather, they pseudotyped HIV (a virus known to infect T-cells) with the spike protein from SARS-CoV-2 virus. I don't have experience with these types of experiments, but is it possible that their findings are an artefact of using pseudotyped lentiviruses?
The authors do note that individuals infected with COVID-19 exhibit lymphocytopenia (low white blood cell counts), but
acute lymphocytopenia can be caused by other viral infections, such as influenza, hepatitis and even the
common cold (though some common colds are caused by other strains of coronavirus).
kyphysics said:
Here was one quote from the piece I didn't understand:
The gene behind the fusion function in Sars-CoV-2 was not found in other coronaviruses in human or animals.
But some deadly human viruses such as Aids and Ebola have similar sequences, prompting speculation that the novel Coronavirus might have been spreading quietly in human societies for a long time before causing this pandemic.
How are they extrapolating that this novel Coronavirus may have been spreading among humans "for a long time"?
I first read the paper published in
Molecular and Cellular Immunology being reported on by the SCMP article, then the SCMP article, and it's pretty clear that the person writing the SCMP article doesn't really understand the science. The explanations of the paper are mostly ok, especially when guided by quotes from the paper or the authors, but explanations of issues outside of the paper are confusing at best. I will note that the bolded statements do not appear in the published paper (indeed, the published scientific paper does not mention HIV, AIDS or ebola).
My guess about what the article is talking about is the presence of a
functional polybasic furin cleavage site in the spike protein of the virus. This site allows the protein to be cleaved in half by furin proteases found widely throughout the human body on the outside of cells (including the respiratory tract). Furin-mediated cleavage of the spike protein could facilitate entry of the virus into cells. See this paper from
Nature Medicine or this article from
the Atlantic for technical or simpler explanations of these features, respectively. Proteins from HIV and Ebola also contain furin cleavage sites as do many human proteins (the furin protease recognises a
fairly simple motif requiring the proximity of two arginine amino acids in an extracellular portion of the protein), so I don't think the presence of a furin cleavage site implies any relationship to these viruses. However, I don't know why the author of the SCMP piece claims this feature is unique: the MERS Coronavirus that infects humans as well as MERS-like coronaviruses found in bats
also contain these features.
The origin of the furin cleavage site in SARS-CoV-2 is unknown. Although we have found spike proteins from animal coronaviruses that closely resemble the SARS-CoV-2 spike protein, these lack the furin cleavage site. These findings offer two possible explanations (discussed further in the
Nature Medicine article): 1) evolution of the site in an animal host (because we have very few Coronavirus sequences from animals, we could very likely have missed the "missing link" between animal coronaviruses and the current SARS-CoV-2 virus behind the COVID-19 outbreak) or 2) evolution of the site in humans (which would suggest that the virus may have been transmitting in humans long before the current outbreak). While possibility #2 is unlikely (genetic studies of the virus suggest a relatively recent origin ~late Nov 2019 to early Dec 2019), it can't completely be ruled out yet. Potentially, studies of banked samples from the Wuhan region (especially those looking for antibodies against SARS-CoV-2 in blood samples pre-dating the outbreak) could help resolve this question.