Coronavirus

[Mr._Clark]

Right. But, with you wearing a mask, the cougher wearing a mask, and the exchange rate of air in the cabin, the risk is very minimized.

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As you may have noticed from my prior post "In March a Vietnamese businesswoman with a sore throat and a cough boarded a flight in London. Ten hours later, she landed in Hanoi, Vietnam; she infected 15 people on the flight, including more than half of the passengers sitting with her in business class."

My take on this is that the circulation and filtering in aircraft is well short of 100% effective.

I have no doubt that masks are at least somewhat effective, but I would not be comfortable relying on masks in this situation.

You are of course entirely free to be comfortable in this hypothetical.

 

[flyboylr45]

Regardless of any articles, my initial reply was to the statement that the air in airplanes is re-circulated. It is not. Anything outside that scope is beyond my expertise and I don't claim to know more or less.

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[cpp]

Air is not re-circulated in an airplane. Air is always going out the outflow valves and new air from the PACKS gets pumped into the cabin. The entire cabin air is exchanged every 2-3 minutes.

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Hey thanks that's good to know,. I found this " Most aircraft cabin air is "carefully controlled" and completely changed 20 to 30 times per hour with recirculation systems that blend some fresh air with up to 50 percent recycled of cabin air that pass through HEPA filters on “most modern aircraft,” according to the World Health Organization "., So I guess that's better than nothing,.

So , its hoping that the people setting in your area, wear their mask and are in "good health".

 

[GO-NAD!]

It looks like we're going to roll the dice up here - in order to maximize the number of first doses of vaccine administered, we will be delaying second doses.

A behind-the-scenes look at why Canada delayed 2nd doses of COVID-19 vaccines | CBC News

 

[cpp]

It looks like we're going to roll the dice up here - in order to maximize the number of first doses of vaccine administered, we will be delaying second doses.

A behind-the-scenes look at why Canada delayed 2nd doses of COVID-19 vaccines | CBC News

I sure hope they know what their doing . I read this March 6, 2021 "" "The decision is not based on evidence. It's really based on an extrapolation of the evidence," said Brad Wouters, executive vice-president of science and research at the University Health Network in Toronto "

https://www.cbc.ca/news/health/canada-covid-19-vaccine-delay-risk-1.5939134

 

[Swerd]

It looks like we're going to roll the dice up here - in order to maximize the number of first doses of vaccine administered, we will be delaying second doses.
A behind-the-scenes look at why Canada delayed 2nd doses of COVID-19 vaccines | CBC News

I sure hope they know what their doing . I read this March 6, 2021 "" "The decision is not based on evidence. It's really based on an extrapolation of the evidence," said Brad Wouters, executive vice-president of science and research at the University Health Network in Toronto "

https://www.cbc.ca/news/health/canada-covid-19-vaccine-delay-risk-1.5939134

It's probably alright if the 2nd dose of any of the Pfizer, Moderna, or AstraZeneca vaccines is delayed. Most vaccines in existence are able to immunize people with the first dose, and increase that immunity with a second dose, even after a long delay. I'd be surprised if those SARS-CoV-2 vaccines were different.

All the people on the clinical trials of the Pfizer or Moderna vaccines got a 2nd dose after either 3 weeks (Pfizer) or 4 weeks (Moderna), because those companies were interested in completing their trials as fast as possible. As a result, there is presently no clinical data that directly answers the question, 'how long can the 2nd dose be delayed?' We do have scientific data that indicates a longer time between dose 1 and dose 2 is alright. But in the US, the FDA wants to see clinical data from large numbers of people.

In the USA, these vaccines were given Emergency Use Authorizations (EUA) to begin public vaccinations as soon as possible. Because the US FDA is deliberate and cautious, it will not authorize deviating from those clinical trial dose schedules until enough time has passed to remove the emergency status and grant full authorization. Right now, I forget how long that will take, but I believe it will happen within the year.

 

[TLS Guy]

It looks like we're going to roll the dice up here - in order to maximize the number of first doses of vaccine administered, we will be delaying second doses.

A behind-the-scenes look at why Canada delayed 2nd doses of COVID-19 vaccines | CBC News

That is a smart move. So you join the UK and Germany in that plan. Models clearly show that plan puts the pandemic behind you the quickest, and UK real world data is starting to confirm that.

 

[TLS Guy]

I sure hope they know what their doing . I read this March 6, 2021 "" "The decision is not based on evidence. It's really based on an extrapolation of the evidence," said Brad Wouters, executive vice-president of science and research at the University Health Network in Toronto "

https://www.cbc.ca/news/health/canada-covid-19-vaccine-delay-risk-1.5939134

That is half true. The Phase III trial of the Oxford vaccine did spacing of 30, 60 and 90 days. The 90 day spacing produced the best immune response. It was not unreasonable to extrapolate that this would hold true for the mRNA vaccines also. I think that was a low risk gamble compared to the alternative.

 

[TLS Guy]

It's probably alright if the 2nd dose of any of the Pfizer, Moderna, or AstraZeneca vaccines is delayed. Most vaccines in existence are able to immunize people with the first dose, and increase that immunity with a second dose, even after a long delay. I'd be surprised if those SARS-CoV-2 vaccines were different.

All the people on the clinical trials of the Pfizer or Moderna vaccines got a 2nd dose after either 3 weeks (Pfizer) or 4 weeks (Moderna), because those companies were interested in completing their trials as fast as possible. As a result, there is presently no clinical data that directly answers the question, 'how long can the 2nd dose be delayed?' We do have scientific data that indicates a longer time between dose 1 and dose 2 is alright. But in the US, the FDA wants to see clinical data from large numbers of people.

In the USA, these vaccines were given Emergency Use Authorizations (EUA) to begin public vaccinations as soon as possible. Because the US FDA is deliberate and cautious, it will not authorize deviating from those clinical trial dose schedules until enough time has passed to remove the emergency status and grant full authorization. Right now, I forget how long that will take, but I believe it will happen within the year.

Way to deliberate and cautious. We have lots of the AstraZeneca waiting to roll out in the US. Now the EU is begging that vaccine be sent to them. More doses of the Oxford vaccine have been put into peoples arms and in more countries around the world than any other vaccine. There is now abundant evidence from everywhere it has been deployed, that it is effective and safe. It is unconscionable for the FDA not to release this vaccine for US distribution, especially with craziness going on in a lot of states.

In Carver county just south of here (next county) we have a serious outbreak of the UK variant. Like in the UK mass spread started from a school. we could really use that vaccine now. The FDA are indulging in the worst pedantic bureaucratic practices.

 

[cpp]

That is half true. The Phase III trial of the Oxford vaccine did spacing of 30, 60 and 90 days. The 90 day spacing produced the best immune response. It was not unreasonable to extrapolate that this would hold true for the mRNA vaccines also. I think that was a low risk gamble compared to the alternative.

I thought that was only for the AstraZeneca vaccine

 

[TLS Guy]

I thought that was only for the AstraZeneca vaccine

The Oxford vaccine was the only one with data on a 90 day spacing interval. The UK extrapolated that data to the mRNA vaccines, Pfizer and Moderna.
That was not an unreasonable bet, and risk, in my view, and it does seem to be paying off. We are now getting 90 days away from the start of that program and will have real data very soon. I will be surprised if the bet they made was not a good one.

 

[Irvrobinson]

More doses of the Oxford vaccine have been put into peoples arms and in more countries around the world than any other vaccine.

How is this possible when the AZ vaccine is not available in the US, yet the US has administered nearly a third of the doses worldwide, and Chinese vaccines are big players?

COVID-19 vaccine doses administered by country worldwide 2023 | Statista

As of March 20, 2023, over 13 billion COVID-19 vaccine doses had been administered worldwide. China had administered the most vaccinations in total.

www.statista.com

To add my non-expert opinion about the US situation, I like the fact that the FDA is being so careful. I'm a huge supporter of vaccines, but I prefer rigorous science to guesses when someone wants to shoot something into my body.

 

[TLS Guy]

How is this possible when the AZ vaccine is not available in the US, yet the US has administered nearly a third of the doses worldwide, and Chinese vaccines are big players?

COVID-19 vaccine doses administered by country worldwide 2023 | Statista

As of March 20, 2023, over 13 billion COVID-19 vaccine doses had been administered worldwide. China had administered the most vaccinations in total.

www.statista.com

To add my non-expert opinion about the US situation, I like the fact that the FDA is being so careful. I'm a huge supporter of vaccines, but I prefer rigorous science to guesses when someone wants to shoot something into my body.

The answer is licensing.

The Oxford vaccine is bein produced at two large sites in the UK, in Belgium, by Advent Sri in Italy, and above all by the huge factory of the serum institute at Pune India. There is also a large factory in the US making it, which has agreed to produce 300,000,000 doses. This factory is producing at speed, but US approval is slowed as the FDA halted the US phase three trial for about three months, over one case of transverse myelitis that was due to MS and not the vaccine. The UK halted the trial for about a couple of days. So this vaccine will go to the FDA sometime next month.

The factory at Pune is now thought to account for half the worlds supply and is hoping to produce 1.2 to two billion doses this year.

Pfizer is in 69 countries, and AstraZeneca in 58. Next is Moderna in 30. However at least 3 billion doses of the AstraZeneca vaccine are scheduled to be produced this year. This vaccine has the greatest penetration in the third world. The UK is monitoring the quality of the vaccine from the Pune factory, and have just complete an inspection.

This article shows the relative penetration of vaccines around the world.

 

[Irvrobinson]

The answer is licensing.

Licensing doesn't account for the discrepancy between your claim, that the AZ vaccine is in more arms than any other, and the data I posted a link for.

 

[Mr._Clark]

This article does not have a lot of new information but it seems to be quite well-written.

>>>Like all viruses, SARS-CoV-2 will continue to evolve. But McLellan believes that it has a limited number of moves available. “There’s just not a lot of space for the spike to continue to change in ways that allow it to evade antibodies but still bind to its receptor,” he said. “Substitutions that allow the virus to resist antibodies will probably also decrease its affinity for ACE-2”—the receptor that the virus uses to enter cells. Recently, researchers have mapped the universe of useful mutations available to the spike’s receptor-binding area. They’ve found that most of the changes that would weaken the binding ability of our antibodies occur at just a few sites; the E484K substitution seems to be the most important. “The fact that different variants have independently hit on the same mutations suggests we’re already seeing the limits of where the virus can go,” McLellan told me. “It has a finite number of options.” . . .

Confronting the variants, we should be cautious but hopeful. They are a worrying development but not a devastating blow. Every coronavirus vaccine available in the U.S. appears likely to prevent the more concerning consequences of infection—severe illness, hospitalization, death—even for the new variants. (In South Africa, where B.1.351 dominates, Johnson & Johnson’s vaccine prevented a hundred per cent of COVID-19 deaths a month after inoculation.) Vaccinated people, therefore, should feel confident in the protection they’ve gained, and in the knowledge that booster shots, should they become necessary, can quickly be developed and approved. Even for those who have been inoculated, the risk of illness has not been, and may never be, eliminated—but it remains vastly lower than it was before vaccination, despite the new variants in our midst.<<<

What the Coronavirus Variants Mean for the End of the Pandemic

The virus is mutating—but we can still beat it, one vaccination at a time.

www.newyorker.com

 

[Mr._Clark]

I think I just found an article that will get both TLS Guy and swerd fired up (for completely different reasons)(Feel free to rip on this Moore guy, I'm just funn'in with ya)

>>>John Moore, a professor of microbiology and immunology at Cornell University’s Weill Cornell Medical College in New York, isn’t so sure. He says that while the way the body forms an immune response to SARS-CoV-2 is still not very well understood, there are “so many bread crumbs that say neutralizing antibodies are what matters.” The T-cell and B-cell responses, which may be triggered by other proteins, could play a role, he says, but it is antibodies that are critical, and they form in response to the spike protein. “The S protein is the only target for neutralizing antibodies, so there is not a lot of choice,” he says. . . .

“Resistant viruses arise under certain circumstances, and one of them is undervaccination,” Moore says. He also worries about extending the time between doses, as the U.K. has done (it is waiting 12 weeks between doses in order to give first doses to as many people as possible). That’s because there is no data from the Pfizer and Moderna vaccines on how long the immune response from the first dose lasts beyond the first four weeks. His concern is that if a virus finds a host with some immune response, but not enough to totally wipe it out and prevent replication, it puts selective pressure on the pathogen to find successful mutations.<<< (emphasis added)

As mutant COVID variants multiply, the hunt is on for a 'universal' kill-all vaccine

Some scientists think vaccines could be created that would stand up better to the dreaded South African variant, as well as other future strains. Not everyone agrees it's possible.

fortune.com

 

[Swerd]

This article does not have a lot of new information but it seems to be quite well-written.

Yes, it's well written. And as you said, there is little new info. It's a good summary for those people who are new to or baffled by immunology. (That would be most of us.)

>>>Like all viruses, SARS-CoV-2 will continue to evolve. But McLellan believes that it has a limited number of moves available. “There’s just not a lot of space for the spike to continue to change in ways that allow it to evade antibodies but still bind to its receptor,” he said. “Substitutions that allow the virus to resist antibodies will probably also decrease its affinity for ACE-2”—the receptor that the virus uses to enter cells. Recently, researchers have mapped the universe of useful mutations available to the spike’s receptor-binding area. They’ve found that most of the changes that would weaken the binding ability of our antibodies occur at just a few sites; the E484K substitution seems to be the most important. “The fact that different variants have independently hit on the same mutations suggests we’re already seeing the limits of where the virus can go,” McLellan told me. “It has a finite number of options.” . . .

I agree with most of the thinking in this article, that are limits to number and kind of mutations that the S protein can endure before it looses affinity for ACE-2.

But that brings up something we must not forget. The virus doesn't care that it binds to ACE-2, as long as it finds a way inside of a cell. There are many other cell-surface proteins other than ACE-2 that, if the right mutations occur, might allow that to happen. Although that seems like a long-shot, we can't rule it out as a possibility.

 

[Swerd]

I think I just found an article that will get both TLS Guy and swerd fired up (for completely different reasons)(Feel free to rip on this Moore guy, I'm just funn'in with ya)

>>>John Moore, a professor of microbiology and immunology at Cornell University’s Weill Cornell Medical College in New York, isn’t so sure. He says that while the way the body forms an immune response to SARS-CoV-2 is still not very well understood, there are “so many bread crumbs that say neutralizing antibodies are what matters.” The T-cell and B-cell responses, which may be triggered by other proteins, could play a role, he says, but it is antibodies that are critical, and they form in response to the spike protein. “The S protein is the only target for neutralizing antibodies, so there is not a lot of choice,” he says. . . .

“Resistant viruses arise under certain circumstances, and one of them is undervaccination,” Moore says. He also worries about extending the time between doses, as the U.K. has done (it is waiting 12 weeks between doses in order to give first doses to as many people as possible). That’s because there is no data from the Pfizer and Moderna vaccines on how long the immune response from the first dose lasts beyond the first four weeks. His concern is that if a virus finds a host with some immune response, but not enough to totally wipe it out and prevent replication, it puts selective pressure on the pathogen to find successful mutations.<<< (emphasis added)

As mutant COVID variants multiply, the hunt is on for a 'universal' kill-all vaccine

Some scientists think vaccines could be created that would stand up better to the dreaded South African variant, as well as other future strains. Not everyone agrees it's possible.

fortune.com

This article brings out the controversial nature of immunologists. They are often divided into different and opposing camps of thought. For example, the division between the B-cell immunologists (the antibody guys) and the T-cell immunologists. Which infectious disease is fought by which arm of the immune system is an age-old debate. If I can generalize, most (but not all) bacterial infections are countered by B-cells and antibodies; and most (but not all) viral infections are countered by T-cells. What little we know about tumors that can be killed by the immune system indicates that T-cells are more important. But that's a broad generalization that isn't always true. It's safer to say both immune system arms work together.

Polio for example. The initial Salk vaccine worked best at raising antibodies directed against polio virus particles. The Sabin vaccine, the oral vaccine that came along after the Salk vaccine, worked best at raising potent T-cell responses directed against virus infected cells. But both vaccines were effective against the disease caused by this virus.

Even though I was not formally educated as a true immunologist. I tend to agree with the T-cell guys. But there are certainly plenty of examples that support antibodies over T-cells, the opposite, or both.
Many real immunologists disagree with each other. So much so, that it's hard for a non-immunologist like myself to understand things.

So, when I read what that guy Moore said, I was inclined to ignore most of what he says, but I cannot say with certainty that he is all wrong.

In general, I liked the New Yorker article better than the Fortune article.

 

[Mr._Clark]

This is interesting:

>>>Solving a Genetic Mystery at the Heart of the COVID-19 Pandemic . . .

In a paper published in mBio, lead author Russell Neches and his colleagues show that ORF8 evolved from another coronavirus protein called ORF7a, and that both proteins have folds similar to that of a human antibody. This finding helps to explain how the virus avoids immune detection and is able to escalate into a severe infection in some hosts.

“By exploring the structural and functional characteristics of ORF8, and using supercomputers to look at the genomes of over 200,000 viruses, we discovered a striking and highly unusual evolutionary strategy,” said co-author Nikos Kyrpides, a computational biologist at the DOE Joint Genome Institute (JGI). “Amazingly, it seems that within the SARS clade, the gene encoding ORF7a is used as a ‘template’ gene, remaining stable, with a duplicate copy of this gene evolving to a point almost beyond recognition.” SARS-CoV-2 arose and exploded into a pandemic when a SARS strain’s duplicate ORF7a gene happened to mutate leading to a new protein (which we now call ORF8) that gave it the ability to interfere with immune cells.

According to the team, a similar event occurred in the SARS-CoV strain that caused the SARS epidemic in the early 2000s. In that instance, a copy of the ORF7a gene split into two, resulting in ORF8a and ORF8b proteins.<<<

Solving a Genetic Mystery at the Heart of the COVID-19 Pandemic

Computational biologists dig into the origins of a mysterious protein unique to the SARS-CoV-2 lineage

newscenter.lbl.gov

 

[Mr._Clark]

This article brings out the controversial nature of immunologists. They are often divided into different and opposing camps of thought. For example, the division between the B-cell immunologists (the antibody guys) and the T-cell immunologists. Which infectious disease is fought by which arm of the immune system is an age-old debate. If I can generalize, most (but not all) bacterial infections are countered by B-cells and antibodies; and most (but not all) viral infections are countered by T-cells. What little we know about tumors that can be killed by the immune system indicates that T-cells are more important. But that's a broad generalization that isn't always true. It's safer to say both immune system arms work together.

Polio for example. The initial Salk vaccine worked best at raising antibodies directed against polio virus particles. The Sabin vaccine, the oral vaccine that came along after the Salk vaccine, worked best at raising potent T-cell responses directed against virus infected cells. But both vaccines were effective against the disease caused by this virus.

Even though I was not formally educated as a true immunologist. I tend to agree with the T-cell guys. But there are certainly plenty of examples that support antibodies over T-cells, the opposite, or both.
Many real immunologists disagree with each other. So much so, that it's hard for a non-immunologist like myself to understand things.

So, when I read what that guy Moore said, I was inclined to ignore most of what he says, but I cannot say with certainty that he is all wrong.

In general, I liked the New Yorker article better than the Fortune article.

Here's a paper that may be more to your liking. As I understand it, the study (albeit involving a small number of patients) shows a correlation between a large numbers of T cells early in an infection and mild disease and the opposite with regards to neutralizing antibodies. It's interesting that one patient did not test positive for neutralizing antibodies but nevertheless cleared the virus, whereas two patients with high levels of neutralizing antibodies early in the infection had severe disease (one died).

>>>We interrogate the dynamic changes of virological and immunological parameters in 12 patients with symptomatic acute SARS-CoV-2 infection from disease onset to convalescence or death. We quantify SARS-CoV-2 viral RNA in the respiratory tract in parallel with antibodies and circulating T cells specific for various structural (nucleoprotein [NP], membrane [M], ORF3a, and spike) and non-structural (ORF7/8, NSP7, and NSP13) proteins. Although rapid induction and quantity of humoral responses associate with an increase in disease severity, early induction of interferon (IFN)-γ-secreting SARS-CoV-2-specific T cells is present in patients with mild disease and accelerated viral clearance. . . . The temporal association of functional SARS-CoV-2-specific T cell appearance with reduced length of infection suggests that T cells play an essential role in the control of SARS-CoV-2 infection. . . . The most robust functional T cell response was detected in patients with mild symptoms who cleared the virus early, whereas for example, in the patient with severe disease who succumbed to infection, we could only detect a weak and monospecific IFN-γ-secreting cell response at 26 days after symptom onset . . . The opposite scenario was observed for antibodies. The two most severe COVID-19 patients studied here showed the most rapid and robust ability to achieve peak virus neutralization, and the overall quantities of SARS-CoV-2-specific antibodies were higher in severe than in milder COVID-19 cases. These data confirm the numerous observations that have linked virus-specific antibody production and B cell hyperactivation with increased disease severity. Because of the significant link between early induction of T cells and shorter duration of the infection, the demonstration of the early induction of ORF7/8-specific cellular immunity can be of particular significance in viral control. . . . It remains difficult to explain why ORF7/8-specific T cells were preferentially detected during the acute phase of infection. . . . the direct association of early induction of IFN-γ-producing SARS-CoV-2-specific T cells with faster viral clearance and milder disease observed here supports the growing evidence of the protective role of T cells in SARS-CoV-2 infection . . . <<< (citations omitted)

Early induction of functional SARS-CoV-2-specific T cells associates with rapid viral clearance and mild disease in COVID-19 patients

Virus-specific humoral and cellular immunity act synergistically to protect the host from viral infection. We interrogate the dynamic changes of virol…

www.sciencedirect.com