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13 minutes ago, WizeGuy said:

Pretty crazy to think that Oxford's vaccine may have 2 billion produced by Sept. Does this mean there may be some optimism surrounding the vaccine? 

That's my logic around it but I'm an optimist for the most part. Why use that many resources for something you're not feeling, at the very least, "good" about? I'm not an expert in vaccine production, believe it or not, but I'm sure it's not cheap

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41 minutes ago, JTagg7754 said:

That's my logic around it but I'm an optimist for the most part. Why use that many resources for something you're not feeling, at the very least, "good" about? I'm not an expert in vaccine production, believe it or not, but I'm sure it's not cheap

The only thing I will say about this is that AZ is a wildly successful pharmaceutical company with very deep pockets. That goes both ways, they have shown they know what they are doing but they are also willing to throw some money around. Basically they have all the infrastructure in place around the world to produce the vaccine, they would just halt current production of some of their current drug staples. It wouldn't end up costing AZ as much as other companies would have to spend(on equipment,validation, infrastructure, FDA GMP commercial viability, etc) to be able to produce the vaccine at that rate.   

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2 hours ago, seriously27 said:

The only thing I will say about this is that AZ is a wildly successful pharmaceutical company with very deep pockets. That goes both ways, they have shown they know what they are doing but they are also willing to throw some money around. Basically they have all the infrastructure in place around the world to produce the vaccine, they would just halt current production of some of their current drug staples. It wouldn't end up costing AZ as much as other companies would have to spend(on equipment,validation, infrastructure, FDA GMP commercial viability, etc) to be able to produce the vaccine at that rate.   

Well they just received more funding also:

https://www.reuters.com/article/us-health-coronavirus-astrazeneca-idUSKBN23G0ZG?taid=5edfd4060d010d000127de20&utm_campaign=trueAnthem:+Trending+Content&utm_medium=trueAnthem&utm_source=twitter

Looks like people are going all in on this one. Luckily there's still quite a few others in current trials so I'm sure we have a winner, it's just now isolating and championing it as well as others that may prove positive as well.

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4 hours ago, WizeGuy said:

Pretty crazy to think that Oxford's vaccine may have 2 billion produced by Sept. Does this mean there may be some optimism surrounding the vaccine? 

100%.

4 hours ago, bucsfan333 said:

 

For the love of god guys this isn't that hard.

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Good News Guy is back to break you from your typical doomer and gloomer!!..... At least potential good news....

Is the virus weakening like it's like brother did many years ago?? It's possible. Also possible it's just a weaker variant that exists. This mutation could potentially lower virulence.

https://www.biorxiv.org/content/10.1101/2020.06.08.140152v1

"#Abstract
The iconic 'red crown' of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is made of its spike (S) glycoprotein. The S protein is the Trojan horse of coronaviruses, mediating their entry into the host cells. While SARS-CoV-2 was becoming a global threat, scientists have been accumulating data on the virus at an impressive pace, both in terms of genomic sequences and of three-dimensional structures. On April 21st, the GISAID resource had collected 10,823 SARS-CoV-2 genomic sequences. We extracted from them all the complete S protein sequences and identified point mutations thereof. Six mutations were located on a 14-residue segment (929-943) in the 'fusion core' of the heptad repeat 1 (HR1). Our modeling in the pre- and post-fusion S protein conformations revealed, for three of them, the loss of interactions stabilizing the post-fusion assembly. On May 29th, the SARS-CoV-2 genomic sequences in GISAID were 34,805. An analysis of the occurrences of the HR1 mutations in this updated dataset revealed a significant increase for the S929I and S939F mutations and a dramatic increase for the D936Y mutation, which was particularly widespread in Sweden and Wales/England. We notice that this is also the mutation causing the loss of a strong inter-monomer interaction, the D936-R1185 salt bridge, thus clearly weakening the post-fusion assembly."

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We're about to cross the 500 page mark...
I wanted to say thanks to everybody who made useful & insightful contributions to this epic thread during these epic times. I've learned a lot from y'all
This is not an easy topic to navigate for a variety of reasons, so thanks to all  -  including @Webmaster  for allowing us 3 tries to get it right.


  coach800.thumb.png.5978e83d27f04c984a8b3 Thank You for letting us have this thread - and as others have noted its been a better source of COVID19 info than any news site

 

Stay safe and full speed ahead

FFlogo-3.png.0e332ecfa437937fd7426b9dd0e  FFlogo-3.png.0e332ecfa437937fd7426b9dd0eFFlogo-3.png.0e332ecfa437937fd7426b9dd0e

 

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16 minutes ago, Shanedorf said:


This is not an easy topic to navigate for a variety of reasons, so thanks to all  -  including @Webmaster  for allowing us 3 tries to get it right.


  coach800.thumb.png.5978e83d27f04c984a8b3 Thank You for letting us have this thread - and as others have noted its been a better source of COVID19 info than any news site

 

Stay safe and full speed ahead

FFlogo-3.png.0e332ecfa437937fd7426b9dd0e  FFlogo-3.png.0e332ecfa437937fd7426b9dd0eFFlogo-3.png.0e332ecfa437937fd7426b9dd0e

 

tenor.gif?itemid=8252799

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2 hours ago, JTagg7754 said:

Good News Guy is back to break you from your typical doomer and gloomer!!..... At least potential good news....

Is the virus weakening like it's like brother did many years ago?? It's possible. Also possible it's just a weaker variant that exists. This mutation could potentially lower virulence.

https://www.biorxiv.org/content/10.1101/2020.06.08.140152v1

"#Abstract
The iconic 'red crown' of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is made of its spike (S) glycoprotein. The S protein is the Trojan horse of coronaviruses, mediating their entry into the host cells. While SARS-CoV-2 was becoming a global threat, scientists have been accumulating data on the virus at an impressive pace, both in terms of genomic sequences and of three-dimensional structures. On April 21st, the GISAID resource had collected 10,823 SARS-CoV-2 genomic sequences. We extracted from them all the complete S protein sequences and identified point mutations thereof. Six mutations were located on a 14-residue segment (929-943) in the 'fusion core' of the heptad repeat 1 (HR1). Our modeling in the pre- and post-fusion S protein conformations revealed, for three of them, the loss of interactions stabilizing the post-fusion assembly. On May 29th, the SARS-CoV-2 genomic sequences in GISAID were 34,805. An analysis of the occurrences of the HR1 mutations in this updated dataset revealed a significant increase for the S929I and S939F mutations and a dramatic increase for the D936Y mutation, which was particularly widespread in Sweden and Wales/England. We notice that this is also the mutation causing the loss of a strong inter-monomer interaction, the D936-R1185 salt bridge, thus clearly weakening the post-fusion assembly."

Pre peer review, so take it with a grain of salt. Hopefully it has some merit!

 

Also, 

I asked my wife who is a scientist, but not a chemist or immunologist, to read it. This is her summary:

Viruses from COVID patients all over the world were sequenced (their genetic code was figured out) and the sequences were uploaded to a database. These scientists downloaded all the sequences and looked for mutations to see how the virus changes during person-to-person transmission, and they pulled the updated data again a month later to see what new strains were popping up. They put the sequences into a computer program that modeled the theoretical structure of the virus and, based on what we know about how viruses infect cells, found that the new and more common mutations likely make the virus less stable, and therefore possibly less infectious.

It has some drawbacks, in that they don't compare the sequence data to actual patient outcomes and they don't test the virus on cells - it's all computer modeling at this point.

Edited by WizeGuy
Word choice
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35 minutes ago, WizeGuy said:

Pre peer review, so take it with a grain of salt. Hopefully it has some merit!

 

Also, 

I asked my wife who is a scientist, but not a chemist or immunologist, to read it. This is her summary:

Viruses from COVID patients all over the world were sequenced (their genetic code was figured out) and the sequences were uploaded to a database. These scientists downloaded all the sequences and looked for mutations to see how the virus changes during person-to-person transmission, and they pulled the updated data again a month later to see what new strains were popping up. They put the sequences into a computer program that modeled the theoretical structure of the virus and, based on what we know about how viruses infect cells, found that the new and more common mutations likely make the virus less stable, and therefore less infectious.

It has some drawbacks, in that they don't compare the sequence data to actual patient outcomes and they don't test the virus on cells - it's all computer modeling at this point.

Not sure how old you are or how much you know but isn't this what happened with sars?? It just basically mutated into a common cold type virus? 

 

Edit: and this is very interesting. Thanks for sharing

Edited by JTagg7754
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50 minutes ago, JTagg7754 said:

Not sure how old you are or how much you know but isn't this what happened with sars?? It just basically mutated into a common cold type virus? 

 

Edit: and this is very interesting. Thanks for sharing

Yes, and the same thing happened with Zika. Clinical trials were discontinued because the virus went away.

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