COVID-19 Outbreak (Update: More than 2.9M cases and 132,313 deaths in US) (37 Viewers)

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Why would we be required to act on incomplete -- or even bad -- information?
What action was it asking to take? I must have missed that part.

Just sharing what that research is showing what we've been discussing all along. That if it's able to spread through the Phillipines and a cruise ship then it's likely not impacted by temps as much as the POTUS may be implying.
 
Well, I think it's pretty obvious how easy this thing spreads.
I don't think this is obvious, actually. I had been likening it's spread to that of most varieties of common-cold viruses (some, but not all, of which are coronaviruses). However, I will do some research to see if I have overlooked some information.
 
What action was it asking to take? I must have missed that part.

Just sharing what that research is showing what we've been discussing all along. That if it's able to spread through the Phillipines and a cruise ship then it's likely not impacted by temps as much as the POTUS may be implying.
I got "taking action" from your phrase "what they have to go on". Who's "they"? What does "have to go on" mean in this context if not making decisions, taking action, etc.?

I am not trying to be curt here -- I'm just trying to get away from fuzzy, indeterminate, and undefined thinking about this outbreak and the information it's been spawning. I guess when things are unknown and out of our control ... we fill in the knowledge gaps out own way and from out own biases. That's natural and I can't hold it against anyone.
 
The "it lasts nine days on surfaces!" study (which didn't even study COVID-19, but no one ever mentions that) did seem to demonstrate that various other coronaviruses do deactivate a lot faster on warm surfaces (room temperature and up) than on cool or cold ones. To be fair ... that study, too, is still a pre-print.

I posted that study earlier on this thread. I was quite clear that it was not 2019-nCoV (name at the time) - but based on another coronavirus.

But you make a good point. There is a way to talk about these things without drawing conclusions. I think I said "there is evidence that coronaviruses may be able to survive on surfaces up to nine days." That is an entirely reasonable way to characterize that study as it may relate to the Wuhan coronavirus. It doesn't mean the study is conclusive. It doesn't mean Wuhan will show the same characteristics, it is just part of the body of information that may be relevant - in the wide scope.

I guess it's just human nature to want to speak in conclusions and definitives - even when the reality doesn't support it. And it isn't just the alarmists doing it, there are cynics doing the same thing.
 
I posted that study earlier on this thread. I was quite clear that it was not 2019-nCoV (name at the time) - but based on another coronavirus.

But you make a good point. There is a way to talk about these things without drawing conclusions. I think I said "there is evidence that coronaviruses may be able to survive on surfaces up to nine days." That is an entirely reasonable way to characterize that study as it may relate to the Wuhan coronavirus. It doesn't mean the study is conclusive. It doesn't mean Wuhan will show the same characteristics, it is just part of the body of information that may be relevant - in the wide scope.
This is fair. Accordingly, I have changed that post to read " ... which didn't even study COVID-19, but that's rarely mentioned".

I'm sure we have all seen this particular nugget of info get bowdlerised in the wild, haven't we?
 
This is fair. Accordingly, I have changed that post to read " ... which didn't even study COVID-19, but that's rarely mentioned".

I'm sure we have all seen this particular nugget of info get bowdlerised in the wild, haven't we?

For sure, I didn't mean to suggest that you were wrong that people were treating it as a verified trait of the virus.
 

This situation really doesn’t surprise me. With the very small places people live in generally, the difference in sanitation standards, and such makes transmission very easy. Also, while being asymptomatic, was there sneezing? A runny nose? We’re they sharing food? There are a lot of ways in that situation things can spread way easier than in a more open environment. I would think it falls under a possible but not probable.
 
The Proximal Origin of SARS-CoV-2

NOTE: link might be broken for some users. Here is the text of the link, may need to paste it into address bar (NOTE 2: Never mind, the article just got embedded):


Pre-print (not yet peer-reviewed) addressing the "virus is man-made" theories. Unfortunately, much of the content is technical and not written for the layman. Skip down to the "Theories of SARS-CoV-2 origins" section about halfway down:

It is improbable that SARS-CoV-2 emerged through laboratory manipulation of an existing SARS-related coronavirus. As noted above, the RBD of SARS-CoV-2 is optimized for human ACE2 receptor binding with an efficient binding solution different to that which would have been predicted. Further, if genetic manipulation had been performed, one would expect that one of the several reverse genetic systems available for betacoronaviruses would have been used. However, this is not the case as the genetic data shows that SARS-CoV-2 is not derived from any previously used virus backbone.

This peer-reviewed paper (Nov 9, 2015) was cited after the words "previously used virus backbone". Of interest therein, the abstract which I have spoiler-boxed for length:

The emergence of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome (MERS)-CoV underscores the threat of cross-species transmission events leading to outbreaks in humans. Here we examine the disease potential of a SARS-like virus, SHC014-CoV, which is currently circulating in Chinese horseshoe bat populations. Using the SARS-CoV reverse genetics system, we generated and characterized a chimeric virus expressing the spike of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone. The results indicate that group 2b viruses encoding the SHC014 spike in a wild-type backbone can efficiently use multiple orthologs of the SARS receptor human angiotensin converting enzyme II (ACE2), replicate efficiently in primary human airway cells and achieve in vitro titers equivalent to epidemic strains of SARS-CoV. Additionally, in vivo experiments demonstrate replication of the chimeric virus in mouse lung with notable pathogenesis. Evaluation of available SARS-based immune-therapeutic and prophylactic modalities revealed poor efficacy; both monoclonal antibody and vaccine approaches failed to neutralize and protect from infection with CoVs using the novel spike protein. On the basis of these findings, we synthetically re-derived an infectious full-length SHC014 recombinant virus and demonstrate robust viral replication both in vitro and in vivo. Our work suggests a potential risk of SARS-CoV re-emergence from viruses currently circulating in bat populations.
 
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New cases in Japan popping up in various prefectures and cities. If this arc continues, other nations are going to have to start implementing containment measures for Japan as well.
 
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