https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7077191/In addition, spike stalk S2 in SARS-CoV-2 is highly conserved and shares 99% identity with those of the two bat SARS-like CoVs (bat-SL-CoVZXC21 and bat-SL-CoVZC45) and human SARS-CoV [11]. Thus, the broad spectrum antiviral peptides against S2 has the potential to be effective treatment [93]
No offense, but he know A LOT more about it than you. The SiriusXM app is free right now. The whole interview would be on there and you might get the context you are looking for. IIRC the part you are referencing was him saying we don't know why it affects some in the at risk demo but not all.AWvsCBsteeeerike3 wrote: ↑May 7 20, 1:59 pmIs there a link to that interview somewhere, my 8 seconds of search only got previous interviews. I was able to find a little bit of the transcript online, but it didn't talk about vaccines.
In the transcript, whichi s blocked at work so I can't post the link (but read on my phone), he didn't come off as well informed. The one thing I'd question is the statement 'we just don't know why' certain groups are targeted by the virus. It's pretty well established that they know precisely how the virus breaks down cells (via the spike attaching to the ACE2 enzyme) and we know the groups he talked about have elevated ACE2 levels. This has been known since march and was well studied prior to Sars-Cov-2 existing because the Cov-2 spike that attaches to ACE2 is same as the Sars-Cov (1) spike that existed in 2002.
That came off as confusing. So, I'll rephrase it. The Sars-Cov-2 virus (causes Covid 19, very prevalent in the world today, big pita) infects cells via the same mechanism that the SARS virus infected cells and that is through an enzyme that has been well studied. And, it's well known those enzymes are more available in certain groups of people.
Here's a link from a study done in 2005 that established the ACE2/SARS connection.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287568/
You can just re-date the study to 2020 and replace SARS-CoV with SARS-CoV-2.Angiotensin converting enzyme 2 (ACE2), the receptor for both the SARS-CoV and the related human respiratory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma. As assessed by immunofluorescence staining and membrane biotinylation, ACE2 protein was more abundantly expressed on the apical than the basolateral surface of polarized airway epithelia. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected.
In short, I'm getting myself all worked up, but how can a doctor speak intelligently about the subject and not know this basic piece of information.
https://www.howardstern.com/show/2020/5 ... ad-summer/stlouie_lipp wrote: ↑May 7 20, 3:08 pmNo offense, but he know A LOT more about it than you. The SiriusXM app is free right now. The whole interview would be on there and you might get the context you are looking for. IIRC the part you are referencing was him saying we don't know why it affects some in the at risk demo but not all.AWvsCBsteeeerike3 wrote: ↑May 7 20, 1:59 pmIs there a link to that interview somewhere, my 8 seconds of search only got previous interviews. I was able to find a little bit of the transcript online, but it didn't talk about vaccines.
In the transcript, whichi s blocked at work so I can't post the link (but read on my phone), he didn't come off as well informed. The one thing I'd question is the statement 'we just don't know why' certain groups are targeted by the virus. It's pretty well established that they know precisely how the virus breaks down cells (via the spike attaching to the ACE2 enzyme) and we know the groups he talked about have elevated ACE2 levels. This has been known since march and was well studied prior to Sars-Cov-2 existing because the Cov-2 spike that attaches to ACE2 is same as the Sars-Cov (1) spike that existed in 2002.
That came off as confusing. So, I'll rephrase it. The Sars-Cov-2 virus (causes Covid 19, very prevalent in the world today, big pita) infects cells via the same mechanism that the SARS virus infected cells and that is through an enzyme that has been well studied. And, it's well known those enzymes are more available in certain groups of people.
Here's a link from a study done in 2005 that established the ACE2/SARS connection.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287568/
You can just re-date the study to 2020 and replace SARS-CoV with SARS-CoV-2.Angiotensin converting enzyme 2 (ACE2), the receptor for both the SARS-CoV and the related human respiratory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma. As assessed by immunofluorescence staining and membrane biotinylation, ACE2 protein was more abundantly expressed on the apical than the basolateral surface of polarized airway epithelia. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected.
In short, I'm getting myself all worked up, but how can a doctor speak intelligently about the subject and not know this basic piece of information.
Typically, I'd defer to medical professionals and acknowledge I know A LOT less. But, that simply doesn't appear to be the case. Those groups have elevated ACE2 levels and that's the answer. Further, to your point, people within an at risk group don't all have identical immune systems which accounts for the different outcomes of individuals within those groups. That's not to say it's 100%, but it's pretty well established that we know how the virus works and we know the importance of immune systems. Granted it's a novel virus, so it's not 100% understood on a granular level like how important copper level in the blood is, but it's understood well enough to know what he says just can't be known.Howard was also curious why the virus wreaks havoc on some people while leaving others asymptomatic.
“It’s a dastardly virus—and I don’t use that word often,” Dr. Agus said. “In New York City, almost 95 percent of patients hospitalized had either obesity, diabetes, or elevated blood pressure. Period. Why does it discriminate against those people? We Just dont know.”
OK. You seem to have the answers. But I'll still defer to his expertise. Maybe it's not as cut and dry as you think.AWvsCBsteeeerike3 wrote: ↑May 7 20, 4:13 pmhttps://www.howardstern.com/show/2020/5 ... ad-summer/stlouie_lipp wrote: ↑May 7 20, 3:08 pmNo offense, but he know A LOT more about it than you. The SiriusXM app is free right now. The whole interview would be on there and you might get the context you are looking for. IIRC the part you are referencing was him saying we don't know why it affects some in the at risk demo but not all.AWvsCBsteeeerike3 wrote: ↑May 7 20, 1:59 pmIs there a link to that interview somewhere, my 8 seconds of search only got previous interviews. I was able to find a little bit of the transcript online, but it didn't talk about vaccines.
In the transcript, whichi s blocked at work so I can't post the link (but read on my phone), he didn't come off as well informed. The one thing I'd question is the statement 'we just don't know why' certain groups are targeted by the virus. It's pretty well established that they know precisely how the virus breaks down cells (via the spike attaching to the ACE2 enzyme) and we know the groups he talked about have elevated ACE2 levels. This has been known since march and was well studied prior to Sars-Cov-2 existing because the Cov-2 spike that attaches to ACE2 is same as the Sars-Cov (1) spike that existed in 2002.
That came off as confusing. So, I'll rephrase it. The Sars-Cov-2 virus (causes Covid 19, very prevalent in the world today, big pita) infects cells via the same mechanism that the SARS virus infected cells and that is through an enzyme that has been well studied. And, it's well known those enzymes are more available in certain groups of people.
Here's a link from a study done in 2005 that established the ACE2/SARS connection.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287568/
You can just re-date the study to 2020 and replace SARS-CoV with SARS-CoV-2.Angiotensin converting enzyme 2 (ACE2), the receptor for both the SARS-CoV and the related human respiratory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma. As assessed by immunofluorescence staining and membrane biotinylation, ACE2 protein was more abundantly expressed on the apical than the basolateral surface of polarized airway epithelia. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected.
In short, I'm getting myself all worked up, but how can a doctor speak intelligently about the subject and not know this basic piece of information.
Typically, I'd defer to medical professionals and acknowledge I know A LOT less. But, that simply doesn't appear to be the case. Those groups have elevated ACE2 levels and that's the answer. Further, to your point, people within an at risk group don't all have identical immune systems which accounts for the different outcomes of individuals within those groups. That's not to say it's 100%, but it's pretty well established that we know how the virus works and we know the importance of immune systems. Granted it's a novel virus, so it's not 100% understood on a granular level like how important copper level in the blood is, but it's understood well enough to know what he says just can't be known.Howard was also curious why the virus wreaks havoc on some people while leaving others asymptomatic.
“It’s a dastardly virus—and I don’t use that word often,” Dr. Agus said. “In New York City, almost 95 percent of patients hospitalized had either obesity, diabetes, or elevated blood pressure. Period. Why does it discriminate against those people? We Just dont know.”
Regardless, everything I've seen, which is granted possibly A LOT less than Agus because I don't follow vaccines, a 6 month timeline seems to at a minimum combine phases, shorten the timelines for observation between phases, and shorten the amount of time given to fine tune the correct dosage. I'm up to date on all vaccines as are my kids, but if they're going to be messing with RNA or creating a traditional vaccine to a type of virus that currently has no vaccines available, and do it in a shortened timeframe, all to cure a virus that in the end will likely have an infection fatality rate of less to well less than 1% for the majority of the demographics, then I'm going to be pretty skeptical.
Sounds...promising.The researchers were able to move swiftly because they had already developed a vaccine candidate for Middle East Respiratory Syndrome (MERS), a virulent respiratory disease caused by another member of the coronavirus family. Last year they showed that the vaccine was safe in people and prompts an immune response that lasts for at least a year. In January, the group began adapting the technique to create a vaccine for SARS-CoV-2, the coronavirus responsible for COVID-19.
...
To create their vaccine, the Oxford team genetically engineered a virus that is harmless in people to carry genetic material from SARS-CoV-2. The virus they chose, which belongs to a family called adenoviruses, causes a common cold in chimpanzees. The researchers modified the virus so that it could not replicate in people; this approach has previously been used to test vaccines for more than 10 different diseases, though none has made it to market.
The COVID-19 vaccine—which the researchers have dubbed ChAdOx1 nCoV-19—includes a gene that codes for the spike-shaped protein on the surface of the virus. Similar proteins are found on other coronaviruses like the ones that cause SARS and MERS, and help the pathogens invade our cells. Studies in animals have shown that antibodies the body produces after being exposed to this protein are key for developing protective immunity, George says.
When people receive the ChAdOx1 nCoV-19 vaccine, their cells will use the instructions in the viral DNA to build this spike protein. By training the immune system to recognize this protein, the vaccine prepares it to spring into action should it ever encounter the actual virus.
Fact of the matter is, there's a reason besides $$$$ why the red tape is there for FDA approval for drugs/vaccines/tests. Science is rarely ever easy and straightforward and evidence based medicine takes time. Expedited approval has its risks for failure and possibly harm.heyzeus wrote: ↑May 8 20, 8:27 amThis is purely anecdotal, so please do take it for what it's worth, and don't consider it authoritative or anything.
But my neighbor, who I like and respect a lot, is a clinical researcher for a pharmaceutical company; she works in drug trials. She has two kids exactly my kids' ages. I asked her when she thinks a vaccine will be widely available, and if she'd feel comfortable giving it to her kids once it is. She expects it'll be a year, and she wouldn't give it to her kids for at least a full year after it hits the market. There are likely going to be problems and almost certainly unforeseen complications with certain medical conditions or other drugs.
