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What's the opinion of the experts on here? Is this journalistic exaggeration, or are we risking everything by changing the double vaccination schedule?nsaspook said:
What's the opinion of the experts on here? Is this journalistic exaggeration, or are we risking everything by changing the double vaccination schedule?nsaspook said:
That's a nice approach, but as we have seen that doesn't work well.Even rolling out the vaccine at all when there is so much transmission occurring is far from ideal, he said, suggesting it would have been safer to beat down the amount of virus in circulation before beginning the vaccine deployment.
PeroK said:What's the opinion of the experts on here? Is this journalistic exaggeration, or are we risking everything by changing the double vaccination schedule?
The virus itself is known to cause only partial (? weak, maybe?) immunity: sometimes with very low antibody levels. Compared to - guess only! - 20% of the population having 'natural' unreliable immunity; 6% having artificial 60% immunity or 3% having 95% immunity... Well, the difference does not feels really dramatic.PeroK said:...are we risking everything by changing the double vaccination schedule?
Sorry, I can't understand what you are saying here.Rive said:The virus itself is known to cause only partial (? weak, maybe?) immunity: sometimes with very low antibody levels. Compared to - guess only! - 20% of the population having 'natural' unreliable immunity; 6% having artificial 60% immunity or 3% having 95% immunity... Well, the difference does not feels really dramatic.
I think the high number of copies (=> high number of mutations) racing to re-infest that 20% is a far more worse problem.
It's good enough to protect almost everyone for at least ~9 months, because double infections are still incredibly rare. They do happen, but not at a level where they would be relevant for the pandemic. In particular, the protection from getting the disease itself is far better than 95% over the observable time range.Rive said:The virus itself is known to cause only partial (? weak, maybe?) immunity: sometimes with very low antibody levels.
Sorry, but you do not know that. There is no widespread random and regular PCR testing amongst the already infected.mfb said:double infections ... do happen, but not at a level where they would be relevant for the pandemic.
From the article:PeroK said:Sorry, I can't understand what you are saying here.
The virus itself known to be unreliable when it's about antibody levels after an infection. Compared to the virus (which is lacking any quality management standards, as it seems) the vaccine is actually far more reliable (again: it's about antibody levels).if you wanted to make a vaccine-resistant strain, what you would do is to build a cohort of partially immunized individuals in the teeth of a highly prevalent viral infection
When I was studying the research on immunity months ago, it was thought that antibodies might not last long, but T-memory cell immunity was likely to be pretty reliable and long lasting. I haven't kept up on research since then, except that the vaccines were found to also trigger T-cell immunity. Does anyone know the current knowledge about this issue?Rive said:Sorry, but you do not know that. There is no widespread random and regular PCR testing amongst the already infected.
The only thing actually known is that reinfections which are bad enough to be tested again are rare.From the article:
The virus itself known to be unreliable when it's about antibody levels after an infection. Compared to the virus (which is lacking any quality management standards, as it seems) the vaccine is actually far more reliable (again: it's about antibody levels).
So if somebody is worrying about new strains, then he should look for the growing number of already recovered patients first because at this point they are a far more 'beefy' population of interest for the virus (which were left to grew into a 'healthy' gene pool already, ready for some drifting to occur).
The situation is not good, but the vaccine and its usage is just a very minor part of it.
Rive said:So if somebody is worrying about new strains, then he should look for the growing number of already recovered patients first because at this point they are a far more 'beefy' population of interest for the virus (which were left to grew into a 'healthy' gene pool already, ready for some drifting to occur).
These findings carry a potentially important message for SARS-CoV-2 vaccines. Most current vaccine candidates are focusing on spike protein as the immunizing antigen, but natural infection induces broad epitope coverage in T-cells. It will be essential to understand the relation between breadth, durability and quality of T-cell responses and resulting protective immunity with SARS-CoV-2 vaccines and natural infection.
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It would be a public health and “trust-in-medicine” nightmare with potential repercussions for years - including a boost to anti-vaccine forces - if immune protection wears off or antibody-dependant enhancement develops and we face recurrent threats from COVID-19 among the immunized. Data correlating clinical outcomes with laboratory markers of cell-mediated immunity, not only with antibody responses, after vaccination or natural infection with SARS-CoV-2 or other betacoronviruses may prove critically valuable, particularly if protective immunity fades or new patterns of disease emerge.
Antibody-based drugs and vaccines against severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) are being expedited through preclinical and clinical development. Data from the study of SARS-CoV and other respiratory viruses suggest that anti-SARS-CoV-2 antibodies could exacerbate COVID-19 through antibody-dependent enhancement (ADE). Previous respiratory syncytial virus and dengue virus vaccine studies revealed human clinical safety risks related to ADE, resulting in failed vaccine trials. Here, we describe key ADE mechanisms and discuss mitigation strategies for SARS-CoV-2 vaccines and therapies in development. We also outline recently published data to evaluate the risks and opportunities for antibody-based protection against SARS-CoV-2.
Well, that is protection.Rive said:Sorry, but you do not know that. There is no widespread random and regular PCR testing amongst the already infected.
The only thing actually known is that reinfections which are bad enough to be tested again are rare.
Regarding the worries linked above it's just not good enough. No conclusive information about cold-like reinfections, while the 'no significant amount of reinfections' kind of responses are just too commonplace. That's just very bad kind of guesswork around an important issue.mfb said:Well, that is protection.
As far as I know that's around the field of 'colds'. While it does imply that you get - well: just a cold - it will not actually prevent you get that cold. So this kind of 'protection' would likely kind of allow the virus to coexist in the human population.Jarvis323 said:...T-cells give long lasting and cross-reactive protection...
We have been following the discussions and news reports about reducing the number of doses, extending the length of time between doses, changing the dose (half-dose), or mixing and matching vaccines in order to immunize more people against COVID-19. These are all reasonable questions to consider and evaluate in clinical trials. However, at this time, suggesting changes to the FDA-authorized dosing or schedules of these vaccines is premature and not rooted solidly in the available evidence. Without appropriate data supporting such changes in vaccine administration, we run a significant risk of placing public health at risk, undermining the historic vaccination efforts to protect the population from COVID-19.
...
We know that some of these discussions about changing the dosing schedule or dose are based on a belief that changing the dose or dosing schedule can help get more vaccine to the public faster. However, making such changes that are not supported by adequate scientific evidence may ultimately be counterproductive to public health.
We have committed time and time again to make decisions based on data and science. Until vaccine manufacturers have data and science supporting a change, we continue to strongly recommend that health care providers follow the FDA-authorized dosing schedule for each COVID-19 vaccine.
Ygggdrasil said:This is anecdotal evidence...
The paper describes findings from 24 patients hospitalized at University of Miami Tower or Jackson Memorial Hospital with COVID-19 who developed severe acute respiratory distress syndrome. Each received two infusions given days apart of either mesenchymal stem cells or placebo.
Researchers found the treatment was safe, with no infusion-related serious adverse events.
Patient survival at one month was 91% in the stem cell treated group versus 42% in the control group. Among patients younger than 85 years old, 100% of those treated with mesenchymal stem cells survived at one month.
If live attenuated vaccines are off the table, then how could other types of vaccines achieve long-lasting protection? According to Le Vert, the answer lies in aiming vaccines at antigens within the SARS-CoV-2 virus. His company, Osivax, is developing a vaccine candidate that consists of nanoparticles carrying copies of internal Covid-19 antigens.
“We believe that targeting internal antigens such as the nucleocapsid presents an advantage over surface antigens as they have a much lower mutation rate,” said Le Vert. He added that an immune T-cell response against these internal antigens could protect against both current and future strains of Covid-19.
“If these mutation trends persist and increase with the worldwide spread of the virus, we believe that the vaccines targeting the spike surface antigen might have limited efficacy.”
Furthermore, Le Vert pointed out that mutations in surface proteins on the SARS-CoV-2 virus could even cause some vaccines to exacerbate the infection. This can happen via a phenomenon known as antibody-dependent enhancement, where certain antibodies stick to the virus incorrectly and make it even better at infecting cells.
Gottlieb cited experimental evidence from Bloom Lab, and explained 501.V2 does appear to partially escape prior immunity. It means that some of the antibodies people produce when they get infected with Covid, as well as the antibody drugs, may not be quite as effective.
“The new variant has mutated a part of the spike protein that our antibodies bind to, to try to clear the virus itself, so this is concerning,” Gottlieb said. “Now, the vaccine can become a backstop against these variants really getting more of a foothold here in the United States, but we need to quicken the pace of vaccination.”
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“It really is a race against time trying to get more vaccine into people’s arms before these new variants become more prevalent here in the United States,” said Gottlieb.
Where did it all go wrong, one wonders?Astronuc said:In the NY Times, "California has an oxygen shortage for patients as it sees a surge in Covid cases. Los Angeles County’s EMS agency issued guidelines for emergency workers to use the “minimum amount of oxygen necessary” to keep patients’ oxygen saturation level at or just above 90%."
Apparently, emergency medical technicians (EMTs) have been told not bring suspected COVID-19 patients to the some hospitals because there is no room. I think I heard a statistic that 1 or 4 persons in LA county are infected.
Indeed.PeroK said:Where did it all go wrong, one wonders?
They don't want to end up like the other places.OmCheeto said:Scotland is included, as I heard the other day that they were going into full shutdown for the rest of the month. Which, from the shape of the graph, still has me confused.
You're from a country where the President would rather pretend that COVID doesn't exist, so I can see how you would be confused by a government that takes pro-active measures based on scientific modelling and epidemiology. I know that might be hard to accept, but it does happen!OmCheeto said:Scotland is included, as I heard the other day that they were going into full shutdown for the rest of the month. Which, from the shape of the graph, still has me confused.
“Researchers at the Centers for Disease Control and Prevention are monitoring all emerging variants of the coronavirus, including in 5,700 samples collected in November and December,” according to Jason McDonald, a spokesman for the agency. “To date, neither researchers nor analysts at C.D.C. have seen the emergence of a particular variant in the United States,” he said.
Among the variants circulating in the U.S. are B.1.1.7, first identified in Britain and now driving a surge and overwhelming hospitals there. The variant has been spotted in a handful of states, but the C.D.C. estimates that it accounts for less than 0.5 percent of cases in the country so far.
Another variant circulating at low levels in the U.S., known as B 1.346, contains a deletion that may weaken vaccines’ potency. “But I have seen nothing on increased transmission,” said Michael Worobey, an evolutionary biologist at the University of Arizona who discovered that variant.
That variant has been in the United States for three months and also accounts for fewer than 0.5 percent of cases, so it is unlikely to be more contagious than other variants, according to a C.D.C. scientist who spoke on condition of anonymity because he was not authorized to speak about the matter.
All viruses evolve, and the Coronavirus is no different. “Based on scientific understanding of viruses, it is highly likely there are many variants evolving simultaneously across the globe,” Mr. McDonald, of the C.D.C., said. “However, it could take weeks or months to identify if there is a single variant of the virus that causes Covid-19 fueling the surge in the United States similar to the surge in the United Kingdom.”
Carl Zimmer contributed reporting from New Haven and Noah Weiland from Washington D.C.
morrobay said:R0 question: If one infected person infects two in one infection period and those two infect two and those four infect two then after three infection periods there are 2^3 new infections at third infection period. But the total infections are 14. So is the R0 considered 2. Or: (R0)^3 = 14. And 3(logR0)=log14. Then logR0 = .382 . R0=2.4 ?
Just looking at the math without all the epidemicall variables . Then the R0 like I stated above and you also , is the number of people one infected person transmits infection to in an infection period . Given 3 infection periods ( 12 days/4 day infection period) So three infection periods .Then starting with #1 two infections, #2 four infections , and those four newly infected infect two each. So 8 new infections or 14 total. How does this correspond to e^R0 t. With three infection periods and the R0 in my example being 2. Then the newly infected would be 2^3 or the total for three periods equaling 14. So plugging in: y = e^2*3 = 403 ?bhobba said:R0 is the number one person infects each time period and in simple models is considered constant. Roughly it gives a simple differential equation dy/dt = R0*y, y the number infected. The solution is e^(R0*t). It is rough for a number of reasons eg I took it as linear between each period in deriving the differential equation,
Thanks
Bill
The person in charge of managing the hell out of the operation is Jeff Zients, who served as chief performance officer under President Barack Obama and led the rescue of HealthCare.gov. In a Saturday briefing with journalists, Zients broke the plan down into four buckets. Loosen the restrictions on who can get vaccinated (and when). Set up many more sites where vaccinations can take place. Mobilize more medical personnel to deliver the vaccinations. And use the might of the federal government to increase the vaccine supply by manufacturing whatever is needed, whenever it is needed, to accelerate the effort. “We’re going to throw the full resources and weight of the federal government behind this emergency,” Zients promised.
Most elements of the plan are surprising only because they are not already happening. Biden’s team members intend to use the Federal Emergency Management Agency to set up thousands of vaccination sites in gyms, sports stadiums and community centers, and to deploy mobile vaccination options to reach those who can’t travel or who live in remote places. They want to mobilize the National Guard to staff the effort and ensure that strapped states don’t have to bear the cost. They want to expand who can deliver the vaccine and call up retired medical personnel to aid the campaign. They want to launch a massive public education blitz, aimed at communities skeptical of the vaccine. They’re evaluating how to eke out more doses from the existing supply — there is, for instance, a particular syringe that will get you six doses out of a given quantity of Pfizer’s vaccine rather than five, and they are looking at whether the Defense Production Act could accelerate production of that particular syringe and other, similarly useful goods.
Is it? It isn't clear to me that it is or should be better. That article is very heavy on opinion and very light on facts, even mis-matching key facts so that the picture of the current situation isn't clear. I've read a bunch of articles about the current situation and still don't think I've seen a clear reason why the roll-out has been so slow or why the current approach should be failing (and not just in the US -- most Western countries seem to be having trouble). So let's start with that.BillTre said:Here is a NY Times opinion article on how the approach of there Biden administration will differ from that of the Trump administration WRT dealing with the Corona virus.
Looks like an improvement to me.
https://www.healthline.com/health-news/why-the-covid-19-vaccine-rollout-is-so-slowHowever, the distribution of vaccines has gotten off to a slower-than-expected start, with millions of doses distributed to states but sitting unused in freezers.
It's a major pandemic so I favor an all-hands-on-deck apprach and x+1>x, so it is trivial to say that that's "better", but I don't see why it should have been necessary so far to achieve the goal. It looks to me like our existing capacity should already have vastly outperformed the goal.Set up many more sites where vaccinations can take place. Mobilize more medical personnel to deliver the vaccinations.
That's pretty vague. How does the government do that and how long does it take?And use the might of the federal government to increase the vaccine supply by manufacturing whatever is needed, whenever it is needed, to accelerate the effort.
Here's the mismatch:russ_watters said:Is it? It isn't clear to me that it is or should be better. That article is very heavy on opinion and very light on facts, even mis-matching key facts so that the picture of the current situation isn't clear.
On its own, this doesn't tell us anything at all about any sort of problem because we don't know where the remaining 19 million doses are. If they're expired and in a trash can, that's a failure. If they're in a refrigerator to be administered tomorrow or in shipping a shipping container on a truck, then they're somewhere in the supply chain and there isn't necessarily an issue. And maybe more have been vaccinated if there is a lag in reporting the vaccinations. But the numbers are as of January 15, so we can say that the total shipped is below the roughly 35 million that should have been administered by now. So it would seem that too few have shipped (even fewer if you consider that they couldn't pre-stage the vaccine and only started shipping the day after approval). So, what is causing that bottleneck?According to data from the Centers for Disease Control and Prevention, of the roughly 31 million doses that have been sent out, about 12 million have been used.
morrobay said:Then the newly infected would be 2^3 or the total for three periods equaling 14. So plugging in: y = e^2*3 = 403 ?
russ_watters said:That article is very heavy on opinion and very light on facts, even mis-matching key facts so that the picture of the current situation isn't clear. I've read a bunch of articles about the current situation and still don't think I've seen a clear reason why the roll-out has been so slow or why the current approach should be failing (and not just in the US -- most Western countries seem to be having trouble). So let's start with that.
Yes, I know. Doesn't mean I need to be happy abou/agree with the value of such a low quality source.BillTre said:Well, it is an opinion article (as I clearly labeled it).
I don't know what you mean by that. What data are you referring to? That sounds vaguely like conspiracy theory.However, I think the main issue is that data stream of US government info on the corona virus has been corrupted and the data are not dependable.
This is likely also true with Florida data.
I expect different numbers to become available a week or two.
russ_watters said:I don't know what you mean by that. What data are you referring to? That sounds vaguely like conspiracy theory.
Late last week, Chicago mayor Lori Lightfoot — typically cautious on COVID-19 policy — raised some eyebrows after calling for restaurants and bars to reopen "as soon as possible."
Her logic: The current COVID-19 surge has been primarily fueled by at-home gatherings and parties, and if people are going to gather regardless of what any stay-at-home order dictates, state and local governments should try to provide spaces where at least some mitigation efforts will be taken.
...
Despite the ban, California has had one of the worst winter COVID-19 surges in the country, which begs the following question: Is it possible that shutting down outdoor dining made the state's surge even worse?Dr. Monica Gandhi, an infectious disease expert at UCSF, believes it's highly likely.
"We won’t be able to know the exact percentage it drove, but I would say closing outdoor dining certainly did not help and likely hindered efforts to avoid a surge," she said. "It shut down in early December, and things did not get better from there; things actually got worse. Restrictions should be about understanding the human condition and keeping places that are safe open. Those of us who argue for a harm reduction approach have the same goal as the lockdownists: We want to reduce transmission, but we understand the human condition and the need to be with people."
Well, fair enough, but I thought we were in a narrowly focused discussion of the vaccine roll-out. I'm not real interested in case rates for this discussion either.BillTre said:But, I will make predictions:
I expect these things will begin to happen within a couple of weeks. Some maybe faster, some slower.
- the numbers of vaccines produced will be revised down
- estimates of numbers (cases, deaths, hospitalizations) associated with the corona virus, will be changing (but this could (will?) be attributable to changes in calculations)
- the federal vaccine back-up supplies will be shown to have been vastly over-estimated and over-hyped
- weird reasons for not doing obvious things will be revealed (some will involve corruption ($'s))
Check back with that latency.
I have, to a large extent, come to be not be so interested in all the corona virus numbers, because I think there are too many problems with them.
Besides the normal causes of uncertainty and differences between states...
Thanks, The compound interest formula, final=initial (1+%)^n is exactly how I am solving for the R0 from initial and final infections: 17(R0)^6 = 231. Then (R0)^6=13.58 and 6(logR0) = log 13.58. therefore log R0 =.1888 so R0 is 1.54 I just am asking if this is valid for solving R0. Note 6 infection periods from 24 days/4 day max.infectious period from initial infection.bhobba said:It's in deriving the differential equation. The time period you used is discreet. To get the differential equation let us say the time period is a day. To get to an infinitesimal time period you assume during that one day it is linear (it isn't really but it is a simplifying assumption). The detail is using a one day R0, the increase over 1 day is R0*y where y is the current number of cases. Making the simplifying assumption it is linear, over half a day it is R0*1/2*y, over an infinitesimal period dt it is R0*dt*y. So you get after an infinitesimal time period of dt the increase, dy, is R0*dt*y. So one gets dy/dt = R0*y. Why it does not give your numbers is in deriving the equation we assume it is linear during that one day period. It isn't really, so you do not get the same numbers as your discreet calculation. You could get the R0 (R0') over an infinitesimal period from solving e^(R0') = 1+R0 or R0' = Ln(1+R0). That would be a more refined model. Ln = Log to base e. It still will not give your discreet values because you are assuming a continuous infection rate instead of a discreet one. It would have been better to express your infection rate in terms of an infinitesimal time period to start with so after dt the new number of infections is y + R0*y*dt. For your 3 days the infinitesimal R0, R0' would be e^(R0'*3) = 1 + R0 or R0' = (ln (1 +RO))/3. This is similar to the concept of force of interest in finance:
https://en.wikipedia.org/wiki/Compound_interest
Thanks
Bill