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COVID-19 Pandemic: Transmissions, Deaths, Treatments, Vaccines, Interventions and More...

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I've said this a few times now: short of a cure/vaccine, there's only one "hope" we kind of have for this being a lot less impactful than everyone thinks and that's if the cross-reactivity we've seen in some people unexposed to the virus (based on testing their serum in cell cultures against the new virus and seeing indications of potential antibody and T-cell activity) confers some immunity or at least makes for a much milder infection. There's no way of knowing the answer to this now, though and even if we did, doing these tests require days of work to assess cross-reactivity for one single person (there's no simple "test" for this), so we're very unlikely to ever "know" who might have build in defenses.

Let's try to get this thread back on track a bit...

So, I've mentioned this "cross-reactivity" a few times in the past 2 weeks, but haven't really elaborated on it much yet, other than a post 2 wweks ago (5th link) as it's pretty complex and could easily be subject to errors and misinterpretation. I'm certainly not an expert in immunology, so paging @UMRU here for comment. The first link is to a preprint from a group in Germany first noting this cross-reactivity and the 2nd link is to a peer-reviewed article in Cell (very prestigious journal) from a group from La Jolla, while the 3rd is to today's preprint on a similar topic (but a bit different) from a group in Singapore. The 4th link is to an article in Science about the first two articles, which is easier to follow.

The first two papers discuss how people infected with the new coronavirus (CV2) harbor memory T cells (a subtype of white blood cells which are part of the "adapative immune system" and very important for immunity and vaccines) that target the virus, which likely helps them fight off the virus and recover. That was kind of expected, but the more interesting thing, in some ways, is that both studies also found some (roughly half - small studies) people who had never been infected with CV2 (samples from before 2019) have these cellular defenses, most likely because they were previously infected with other coronaviruses.

The third link was just published as a preprint from a group in Singapore. They found that people who had been exposed to SARS had memory T-cells reactive to CV2 proteins and furthermore that 9 of 18 people never exposed to SARS or CV2 had memory T-cells reactive to CV2 proteins and they think that resulted from previous infections with animal betacoronaviruses.

Obviously, as per the Cell paper and the Berlin paper and per this one, lots to think about with regard to whether and to what extent these findings mean some % of the population may either be immune to or only mildly affected by the novel coronavirus - do these findings help explain why so many people become infected but are asymptomatic? Are there a bunch more people who simply won't become infected by CV2 because of this cross-reactivity? The answer to the last question, in particular, is extraordinarily important to gauging the future impact of the pandemic, since these people wouldn't be showing up as positives in antibody testing of the population, but could significantly reduce the number of people who could become infected (and, of course become ill and/or die). I assume this is going to explode as an area of research.

https://www.medrxiv.org/content/10.1101/2020.04.17.20061440v1
https://www.cell.com/action/showPdf?pii=S0092-8674(20)30610-3
https://www.biorxiv.org/content/10.1101/2020.05.26.115832v1.full.pdf
https://www.sciencemag.org/news/2020/05/t-cells-found-covid-19-patients-bode-well-long-term-immunity
https://rutgers.forums.rivals.com/t...ocial-distancing.191275/page-116#post-4563258
 
I believe health professionals recommended liquor stores stay open so that alcoholics were able to get liquor and not go into withdrawal and need to be hospitalized
I responded to this above.

Maybe I'm overly cynical on this one.
 
Imo the "alcoholic" angle was a cover.

My guess is two considerations were in play here, 1)the general public wants to drink and this was a pacifier of sorts 2)pressure from beer/wine/liquor makes.
Hey, not saying I agree with it but that was the sell.
 
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I think we should get a clear message on why certain decisions on what is allowed to open and why and what is not at this time.

I have not followed his press conferences to know if he does that
No, he doesn't give any reasoning and next to no notice as to when to expect reopenings. It's a major problem.
 
I will say our #'s are getting to the point where Murphy needs to open things up.

We do have to balance the Covid vs economy considerations, and given the graphs vs the toll on the economy, it looks very weighted toward opening.
+1
Absolutely no rational reason not to open up.
 
Do we have to do EVERYTHING around here??:Laughing
Tip of the spear, bitches!:CHOP:

436xsj.jpg
 
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You don't think there is solid science behind the idea that if people are not in close contact that they will not spread the virus?

No I don't think that it is solid science, I think is simplistic science, because you are leaving out a large number of factors such as how long are people in contact, where are they in contact (inside and outside) are they masked or unmasked. When it comes down to effecting peoples lives either through the virus or though economics (that can and will have permanent health effects) we need solid science.

Now I understand that part of the problem in all of this is that we didn't know much about this virus and given we had little knowledge we went for the nuclear option (to be sure). But we need to admit that and stop pretending we knew what we were doing.

 
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Let's try to get this thread back on track a bit...

So, I've mentioned this "cross-reactivity" a few times in the past 2 weeks, but haven't really elaborated on it much yet, other than a post 2 wweks ago (5th link) as it's pretty complex and could easily be subject to errors and misinterpretation. I'm certainly not an expert in immunology, so paging @UMRU here for comment. The first link is to a preprint from a group in Germany first noting this cross-reactivity and the 2nd link is to a peer-reviewed article in Cell (very prestigious journal) from a group from La Jolla, while the 3rd is to today's preprint on a similar topic (but a bit different) from a group in Singapore. The 4th link is to an article in Science about the first two articles, which is easier to follow.

The first two papers discuss how people infected with the new coronavirus (CV2) harbor memory T cells (a subtype of white blood cells which are part of the "adapative immune system" and very important for immunity and vaccines) that target the virus, which likely helps them fight off the virus and recover. That was kind of expected, but the more interesting thing, in some ways, is that both studies also found some (roughly half - small studies) people who had never been infected with CV2 (samples from before 2019) have these cellular defenses, most likely because they were previously infected with other coronaviruses.

The third link was just published as a preprint from a group in Singapore. They found that people who had been exposed to SARS had memory T-cells reactive to CV2 proteins and furthermore that 9 of 18 people never exposed to SARS or CV2 had memory T-cells reactive to CV2 proteins and they think that resulted from previous infections with animal betacoronaviruses.

Obviously, as per the Cell paper and the Berlin paper and per this one, lots to think about with regard to whether and to what extent these findings mean some % of the population may either be immune to or only mildly affected by the novel coronavirus - do these findings help explain why so many people become infected but are asymptomatic? Are there a bunch more people who simply won't become infected by CV2 because of this cross-reactivity? The answer to the last question, in particular, is extraordinarily important to gauging the future impact of the pandemic, since these people wouldn't be showing up as positives in antibody testing of the population, but could significantly reduce the number of people who could become infected (and, of course become ill and/or die). I assume this is going to explode as an area of research.

https://www.medrxiv.org/content/10.1101/2020.04.17.20061440v1
https://www.cell.com/action/showPdf?pii=S0092-8674(20)30610-3
https://www.biorxiv.org/content/10.1101/2020.05.26.115832v1.full.pdf
https://www.sciencemag.org/news/2020/05/t-cells-found-covid-19-patients-bode-well-long-term-immunity
https://rutgers.forums.rivals.com/t...ocial-distancing.191275/page-116#post-4563258

I read the Cell paper in detail last week, but I have only skimmed the other two.

Back in 1770, Dr. Edward Jenner noticed that people exposed to the cow disease, cowpox, did not get sick from smallpox. For this discovery, we credit him with inventing the concept of vaccination. These three papers are suggesting that what worked for Jenner and Cowpox, might also work for this virus. Some people may have already been "vaccinated" by exposure to different strains of coronaviruses - there are now 7 known to infect humans.

This is a very reasonable idea and the data in the Cell paper support this to some degree - but how much? Well our COVID discussion group was not terribly impressed. Why you ask? Well, although they were able to detect some T cell responses in uninfected donors, the response was really, really low. More concerning was that there was no detectable antibody against SARS-2. Antibodies stick around a lot longer than T cells, so that is hard to explain. There are also technical reasons why the interpretation is a bit suspect, but it would take too long to explain.

With that said, it's hard to argue with three papers finding similar results and the idea makes sense. It also makes sense that old people might be more susceptible because the "natural" vaccination they got when they were young might be wearing off.
 
No I don't think that it is solid science, I think is simplistic science, because you are leaving out a large number of factors such as how long are people in contact, where are they in contact (inside and outside) are they masked or unmasked. When it comes down to effecting peoples lives either through the virus or though economics (that can and will have permanent health effects) we need solid science.

Now I understand that part of the problem in all of this is that we didn't know much about this virus and given we had little knowledge we went for the nuclear option (to be sure). But we need to admit that and stop pretending we knew what we were doing.

Science can be both simple and solid.

Murphy and every other governor was starting from this starting point. Now you are right there are complexities along the way, and I certainly don't argue that our governor has made laser precision decisions here, nor do I think all his decisions on which businesses to close or keep open hold up to scrutiny, but the general idea of limiting spread by limiting person to person contact really can't be argued.
 
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Imo the "alcoholic" angle was a cover.

My guess is two considerations were in play here, 1)the general public wants to drink and this was a pacifier of sorts 2)pressure from beer/wine/liquor makers.
Shutting down liquor stores would surely lead to increased suicides. Especially in NJ where beer and wine are not available at most grocery and convenience stores.
 
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Shutting down liquor stores would surely lead to increased suicides. Especially in NJ where beer and wine are not available at most grocery and convenience stores.
I might still argue it was a cover, but I won't, I concede the point.
 
Well, my former company (and current one, as I'm doing some consulting for them, part-time) Merck, finally broke radio silence today. Great to see, as I've been wondering when we would, as I knew we had a few irons in the fire. Anyway, Merck, the 2nd largest vaccine maker, announced it is developing two vaccines for COVID (including one from Themis, whom Merck is buying) and is licensing a phase II drug for COVID. See the excerpt below and the link, which goes into much more detail on the two vaccines.

https://www.statnews.com/2020/05/26...of-two-different-covid-19-vaccines-this-year/

Merck is buying Vienna-based Themis, which is developing an experimental Covid-19 vaccine based on a measles vaccine that could begin human studies soon. It is also partnering with the nonprofit IAVI on the development of a vaccine related to Merck’s existing Ebola vaccine that could enter human studies later this year. And it is licensing an experimental drug from a small company called Ridgeback Biotherapeutics.

“We are committed to making a contribution to the eradication of Covid-19,” Roger Perlmutter, who heads Merck Research Laboratories, the company’s research and development division, said in an interview.

Merck executives see the company’s history of developing vaccines and treatments against infectious diseases as central to its identity, often citing the decision three decades ago to donate a treatment for river blindness as a pivotal moment in the 129-year-old company’s history. But until now, Merck has been conspicuously absent from the efforts to develop a Covid-19 vaccine. It’s not that the company wasn’t working on the problem, Perlmutter said, but that it simply wasn’t ready to speak.

Some more details on what could look like the "afterthought" part of the Merck announcement the other day, relative to the vaccine announcements, but may end up being pretty important. The antiviral drug that Merck has licensed from Ridgeback Biotherapeutics, known as EIDD-2081, which came from the Emory Institute of Drug Development, a small company, that George Painter (famed drug discovery scientist) joined in 2013, shows some amazing activity against all kinds of viruses (including SARS-CoV-2) in vitro and in animals and is about to start phase II clinical trials.

It has shown better activity against the virus in vitro and in animals than remdesivir - both attack the same RNA polymerase enzyme in the virus, but Remdesivir blocks the enzyme so the virus can't replicate, while EIDD-2801 causes the enzyme to make replication mistakes which ead to a catastrophic mutational burden.

Whether it will work well in humans is obviously an open question, but if it does, one major advantage it has over remdesivir is that it's orally bioavailable, so it's available in tablet form, meaning it doesn't need to be dosed by IV in a hospital. One drawback is its potential mutagenicity, although with an acute (5-day dosing), potentially lifesaving application, one would think that wouldn't be a showstopper. It also looks like a relatively simple molecule to make (good chance this would've been my team's project if I hadn't retired), so if it works, I doubt availability would will be a major issue. Stay tuned.

SbzYFGP.png


https://cen.acs.org/pharmaceuticals..._source=LJ&utm_medium=Social&utm_campaign=CEN

https://www.ft.com/content/de7df1ee-c566-4c79-9b3e-9b7d792d424c
 
Some more details on what could look like the "afterthought" part of the Merck announcement the other day, relative to the vaccine announcements, but may end up being pretty important. The antiviral drug that Merck has licensed from Ridgeback Biotherapeutics, known as EIDD-2081, which came from the Emory Institute of Drug Development, a small company, that George Painter (famed drug discovery scientist) joined in 2013, shows some amazing activity against all kinds of viruses (including SARS-CoV-2) in vitro and in animals and is about to start phase II clinical trials.

It has shown better activity against the virus in vitro and in animals than remdesivir - both attack the same RNA polymerase enzyme in the virus, but Remdesivir blocks the enzyme so the virus can't replicate, while EIDD-2801 causes the enzyme to make replication mistakes which ead to a catastrophic mutational burden.

Whether it will work well in humans is obviously an open question, but if it does, one major advantage it has over remdesivir is that it's orally bioavailable, so it's available in tablet form, meaning it doesn't need to be dosed by IV in a hospital. One drawback is its potential mutagenicity, although with an acute (5-day dosing), potentially lifesaving application, one would think that wouldn't be a showstopper. It also looks like a relatively simple molecule to make (good chance this would've been my team's project if I hadn't retired), so if it works, I doubt availability would will be a major issue. Stay tuned.

SbzYFGP.png


https://cen.acs.org/pharmaceuticals..._source=LJ&utm_medium=Social&utm_campaign=CEN

https://www.ft.com/content/de7df1ee-c566-4c79-9b3e-9b7d792d424c
What does this mean:

"...while EIDD-2801 causes the enzyme to make replication mistakes which lead to a catastrophic mutational burden."
 
Remember the time when people were hoarding toilet paper........
Think people now realize they dont sh t anymore than they did prior to covid. Still cannot figure why TP many many other things would do before that
 
There will be a vaccine by March. Things are progressing quicker than expected which was originally middle of summer next year
 
Some more details on what could look like the "afterthought" part of the Merck announcement the other day, relative to the vaccine announcements, but may end up being pretty important. The antiviral drug that Merck has licensed from Ridgeback Biotherapeutics, known as EIDD-2081, which came from the Emory Institute of Drug Development, a small company, that George Painter (famed drug discovery scientist) joined in 2013, shows some amazing activity against all kinds of viruses (including SARS-CoV-2) in vitro and in animals and is about to start phase II clinical trials.

It has shown better activity against the virus in vitro and in animals than remdesivir - both attack the same RNA polymerase enzyme in the virus, but Remdesivir blocks the enzyme so the virus can't replicate, while EIDD-2801 causes the enzyme to make replication mistakes which ead to a catastrophic mutational burden.

Whether it will work well in humans is obviously an open question, but if it does, one major advantage it has over remdesivir is that it's orally bioavailable, so it's available in tablet form, meaning it doesn't need to be dosed by IV in a hospital. One drawback is its potential mutagenicity, although with an acute (5-day dosing), potentially lifesaving application, one would think that wouldn't be a showstopper. It also looks like a relatively simple molecule to make (good chance this would've been my team's project if I hadn't retired), so if it works, I doubt availability would will be a major issue. Stay tuned.

SbzYFGP.png


https://cen.acs.org/pharmaceuticals..._source=LJ&utm_medium=Social&utm_campaign=CEN

https://www.ft.com/content/de7df1ee-c566-4c79-9b3e-9b7d792d424c
Thanks for this update. This is what I come to the thread for. This type of drug is as important if not more important to me than a vaccine. I do t care if I get sick from COVID-19 I just need to know that I can take something that will allow me to not end up in the hospital. I gotta believe we can come up with something like that by the end of the summer.
 
What does this mean:

"...while EIDD-2801 causes the enzyme to make replication mistakes which lead to a catastrophic mutational burden."

It mutates into a form which is not sustainable. Kinda like that Family Guy episode where Stewie makes clones of himself and Brian and they come out all stupid and goofy and spontaneously melt.
 
Thanks for this update. This is what I come to the thread for. This type of drug is as important if not more important to me than a vaccine. I do t care if I get sick from COVID-19 I just need to know that I can take something that will allow me to not end up in the hospital. I gotta believe we can come up with something like that by the end of the summer.
The best chance of a viable safe treatment by summer is Leronlimab. It is 1 of 4-5 treatments in clinical trials now that might have results by mid summer, and has shown prior effectiveness in Trials for AIDS(800 people), with no known adverse side effects. It has 50 of 75 people enrolled in its FDA trial for treatment of mild/ moderate COVID patients, and only 37 of 350 enrolled in its FDA trial for severe/ critical COVID patients as of 3 days ago, but patients enrolled in multiple states, NY, NC , Cal, etc. If the mild / moderate trial finishes enrolling by Monday, June 1, the Company will announce 14 and 28 day mortality results , so by mid June or late June , results will be submitted to the FDA and quick approval might follow. The Company has hired Samsung Pharmaceuticals to ramp up production to 1 million by the end of the year. Leronlimab is injectable and can be given outside of the hospital or early on in ER unlike most other treatments. Right now, since Remdesiver and Hydroxychloroquin have not proven effective, it is the best treatment chance out there right now.
 
Study saying 1 in 7 New Yorker adults had been infected by COVID by the end of March about 10 times higher than official 189K count. Extrapolating they think about 14% of population had it. Latino and African American communities a higher percentage at 30% and 22% percent respectively.

From CNN:

More than 2 million New Yorkers had been infected with Covid-19 by the end of March – about 10 times the official count, according to a new study.

State data, however, shows only about 189,000 cases by the end of March. That means about 1.8 million cases potentially went undetected.

Why cases may have been undercounted:There are several reasons why those cases were not detected, said study coauthor David Holtgrave, dean of the School of Public Health at the University at Albany.

Some infected people may have had no symptoms, or only mild symptoms, and so never went to the doctor, Holtgrave said. Others might have wanted to get tested but couldn’t find a doctor to test them, given the shortage of tests in February and March.

In the study, researchers drew blood from more than 15,000 New York adults and found that about 14%, or 1 out of 7, had antibodies to the virus, which means they had previously been infected. The researchers extrapolated that number to the entire population.

On herd immunity: While the 14% infection rate was higher than previously thought, it’s still not high enough to confer herd immunity, Holtgrave said.

Herd immunity is when a community has a sufficiently high proportion of people who are immune to a disease so that the disease is unlikely to spread. These are the full results of New York's antibody survey, some of which New York Gov. Andrew Cuomo has previously mentioned.

The data also shows that communities of color were disproportionately infected. Among those who had antibodies, 30% were Hispanic and 22% were black, which is higher than their proportions in the New York population.

The study was coauthored by officials at the New York Department of Health, and posted on the pre-print server MedRXiv.org, which means it wasn’t peer reviewed or published in a medical journal.
 
The allowance was to avoid a rush of alchoholics suffering withdrawal - this would alleviate some of the demand on ERs in hospitals.

My wife works in a local hospital. She told me they used to keep alcohol in the safe back in the day if a doctor prescribed it for a patient. Bananas to hear that one. This was like 10 years ago, so not sure what the deal is now.
 
The best chance of a viable safe treatment by summer is Leronlimab. It is 1 of 4-5 treatments in clinical trials now that might have results by mid summer, and has shown prior effectiveness in Trials for AIDS(800 people), with no known adverse side effects. It has 50 of 75 people enrolled in its FDA trial for treatment of mild/ moderate COVID patients, and only 37 of 350 enrolled in its FDA trial for severe/ critical COVID patients as of 3 days ago, but patients enrolled in multiple states, NY, NC , Cal, etc. If the mild / moderate trial finishes enrolling by Monday, June 1, the Company will announce 14 and 28 day mortality results , so by mid June or late June , results will be submitted to the FDA and quick approval might follow. The Company has hired Samsung Pharmaceuticals to ramp up production to 1 million by the end of the year. Leronlimab is injectable and can be given outside of the hospital or early on in ER unlike most other treatments. Right now, since Remdesiver and Hydroxychloroquin have not proven effective, it is the best treatment chance out there right now.
We know you own stock in leronlimab, but at least try to be accurate. Remdesivir, right now, is the only drug I know of showing some modest clinically relevant benefit for COVID patients, as time to recovery was significantly improved in hospitalized patients; mortality was reduced, but not considered statistically relevant. Leronlimab may end up being great, but we don't know that yet, so let's wait for the data. Also, while HCQ certainly does not appear to be effective in hospitalized patients, we should have some good data very soon on its use in mildly ill patients.
 
My wife works in a local hospital. She told me they used to keep alcohol in the safe back in the day if a doctor prescribed it for a patient. Bananas to hear that one. This was like 10 years ago, so not sure what the deal is now.

That was very likely due to punctilious ethanol being regulated by the ATF to allow it to be used for scientific/medical uses without paying the hefty tax. Such users have to account for its usage or else have to pay the tax, so that's why it's kept locked up. Same thing in chemistry labs, but we had ways around that, since we "needed" that pure ethanol for our "experiments" (the ones at our house, where we mixed it with fruit punch at parties to evaluate its effect on our "subjects" lol).

https://www.uab.edu/ehs/images/docs/ss/ss_2006_12_ethyl_alcohol.pdf
 
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