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I'd imagine a lot. Most A&Hers are basically boomers even though they're like 1/3 their ageMakes you wonder how many Kiwis are pro-life....
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I'd imagine a lot. Most A&Hers are basically boomers even though they're like 1/3 their ageMakes you wonder how many Kiwis are pro-life....
Why is natural immunity + vaccine supposed to be better than natural immunity? Why is this supposed to be more persuasive than what I'd originally linked?Vaccination offers longer, stronger immunity, says virologist Sabra Klein.
Interview by Brian W. Simpson | MAY 28, 2021
Misconceptions about COVID-19 vaccines abound. Some common ones: If you’ve had COVID-19, you don’t need the vaccine. Wrong. It’s better get naturally infected than to get vaccinated. Wrong.
Virologist Sabra Klein, PhD ‘98, MS, MA, says an immense amount of data collected in a short time have made clear the safety and effectiveness of vaccines and the limited immunity that comes from being infected with the SARS-CoV-2 virus. Klein is co-director of a new National Cancer Institute Center of Excellence that seeks to understand more about the diversity of immune responses and how sex, age, and other factors lead some people to have longer lasting immunity than others.
In the following Q&A, the Molecular Microbiology and Immunology professor explains the nitty gritty of vaccines, coronavirus infections, and how to best protect yourself. Spoiler alert: Klein is a big vaccine fan.
If someone has had COVID-19, why should they get vaccinated? Don’t they already have immunity?
If you’ve been infected, you have some protection. But that immunity has limits. The biggest limit is that it doesn’t last as long as we would like it to.
Studies have shown that people who have been infected can benefit significantly from vaccination. It gives them a strong, lasting immunity boost. After receiving the first dose of the Pfizer or Moderna vaccine, they have immunity levels comparable to those of uninfected people who have received their second dose.
We’re still trying to better understand why immunity lasts longer for some people than others. Underlying factors like obesity or age appear to play a role in how long immunity lasts.
How long does immunity last from being infected? From vaccination?
Immunity from natural infection starts to decline after 6 to 8 months. We know that fully vaccinated people still have good immunity after a year—and probably longer.
Why is it that the vaccine leads to better immunity than natural infection?
The honest truth is, we don’t know. The immune system of people who have been infected has been trained to target all these different parts of the virus called antigens. You’d think that would provide strongest immunity, but it doesn’t. The Pfizer or Moderna vaccines target just the spike protein—the part of the virus that is essential for invading cells. It’s like a big red button sitting on the surface of the virus. It’s really sticking out there, and it’s what our immune system sees most easily. By focusing on this one big antigen, it’s like you’re making our immune system put blinders on and only be able to see that one piece of the virus.
Does the severity of infection make a difference in immunity? If I had a terrible case of COVID-19 infection, will I have stronger immunity?
Absolutely. My lab here at the Bloomberg School and others have shown that people who were hospitalized, who were really sick with COVID, in many cases are believed to have greater immunity than people with less severe disease. But again, that immunity may be declining. So, even if you had a more severe case, you still should plan to get vaccinated.
Let’s talk about variants of the coronavirus. Do vaccines also provide better protection against them?
The good news is that the current vaccines recognize these variant viruses and induce excellent immunity against them. For people who were previously infected and have high immunity, they have will have pretty good recognition of these variants, but you don’t really know your level of immunity against a specific variant or how degraded your immune response may be. You might actually be susceptible to reinfection with one of these variants. You just can’t predict it.
So, rather than flipping a coin, get vaccinated.
Some people say they would rather be infected naturally than get vaccinated. Others say they’re worried about vaccine side effects. What would you tell them?
Vaccines are tested for their safety in ways that we could never do with a natural viral infection. A lot of what’s referred to as side effects are the precise things that we experience to a greater degree when we are infected: fever, headache, malaise, gastrointestinal issues, etc. With infection, you don’t know how bad it’s going to be. By not getting vaccinated, you’re rolling the dice. You may become severely ill. You may have to be hospitalized. You may die.
There’s also the risk of long COVID. I know a teenage girl who got COVID before the vaccines were available. She didn’t have a lot of symptoms, but now she has all of the symptoms of long COVID. A year later, she is trying to maintain a somewhat normal teenage life with profound fatigue. She has never recovered fully from having COVID.
What about vaccines if you’re pregnant?
At this stage, there is no reason for a pregnant woman not to get vaccinated. We know that pregnant women are at increased risk for more severe outcomes from COVID-19. They’re more likely to be hospitalized than nonpregnant women. And we know the vaccines are safe. They’re effective. And they can, at least, reduce the severity of disease among pregnant women, resulting in improved or normal pregnancy outcomes. This idea that someone who’s pregnant should roll the dice and risk getting infected rather than getting vaccinated is not a good decision.
Brian W. Simpson, MPH ’13, is editor-in-chief of Hopkins Bloomberg Public Health magazine and Global Health NOW and director of editorial at the Bloomberg School.
We’re Zeroing In On the ‘Holy Grail’ of COVID-19 Immunity
Katherine J. Wu
There’s no good way of measuring whether your vaccine worked—yet.
When Kishana Taylor welcomes her twins into the world this December, she’ll be pretty confident that they won’t be carrying the virus that causes rubella, an infection that can be disastrous in infants. Thanks to a vaccine she received as a child, Taylor, a virologist at Carnegie Mellon University, is still immune to the pathogen decades later.
She was able to confirm that in June through a simple test that searched her blood for antibodies that recognize the rubella virus, and then added them up. If her antibody counts were above a certain level, called a correlate of protection, she and her babies would be considered well shielded from disease. “You are considered immune with a titer of 9.9 to rubella,” she tweeted last month, referring to her antibody levels. “My titer? 116. I love my immune system sometimes.”
The term correlate of protection doesn’t exactly roll off the tongue, but it’s one of the sexiest concepts in the field of vaccinology. Correlates are biological benchmarks—measurements of a single immune molecule or cell—that can show that a vaccine is achieving its desired effect. With a correlate in hand, researchers can confirm how well a shot is working and identify the rare individuals in whom it doesn’t take; they can suss out the need for boosters and fast-track the development of new vaccines. At their most powerful, correlates of protection boil down the complexities of an immune response to a single value—one that can confidently affirm that a person won’t get infected or seriously sick. “It’s kind of a magic number,” Ali Ellebedy, an immunologist at Washington University in St. Louis, told me. “It’s the big holy grail,” Emory University’s Sri Edupuganti says. “It’s what we dream about,” Cornell’s Sallie Permar told me last month.
In recent weeks, the correlate community has been buzzing louder than ever. Scientists are on the cusp of confidently defining some correlates of protection against symptomatic disease for the COVID-19 vaccines. If confirmed, these correlates could revolutionize the way we tackle SARS-CoV-2 immunization: Vaccine makers testing a new inoculation may no longer need to follow tens of thousands of people for many months to test their product’s protection. Instead, they could inject just a few hundred people, snag some drops of blood, and see if the elusive correlate is met. That’s how we tee up new flu vaccines every year without the rigmarole of gargantuan clinical trials.
But for all their apparent simplicity, correlates of protection are devilishly hard to come by. Try as researchers might, capturing the oomph of vaccine-induced immunity in one number—or several—isn’t always possible. Even as scientists chase them, correlates are a reminder of just how inscrutable our own bodies can be.
Even our best vaccines start out as educated guesses. Researchers study people who have recovered from a particular infection, and then try to cook up an inoculation that will prompt protection that’s similar to or better than natural immunity. What ends up entering people is simple—a harmless pantomime of the pathogen. But it leads to a tortuously complex response that marshals the immune system’s many defensive players, including antibodies, B cells, T cells, and more.
Finding a correlate means cleaving a single variable out of this mess to act as an envoy for the rest of the immune system. That’s a heavy lift for a single cell or molecule, especially when people react in such different ways to the same pathogen. And not all immune responses can be easily measured. Some of the vaccines we’ve been using for decades still don’t have a concrete correlate, including the shots for mumps, rotavirus, and tuberculosis.
That probably won’t be the case for the COVID-19 vaccines. Since the pandemic’s early days, experts have had their eye on neutralizing antibodies, sometimes nicknamed “neuts,” which can glom on to the outside of viruses and block them from entering cells. Neuts that recognize the coronavirus teem in the bodies of people and laboratory animals that have successfully fought off coronavirus infections. The molecules’ disease-fighting powers have made them the workhorses of antibody-based treatments, such as convalescent plasma and monoclonals. Levels of these neuts also soar after vaccination, and seem especially high in people who don’t come down with COVID-19 after getting all their shots. By now it’s clear that neut numbers do correspond pretty well with protection—the more neuts someone has, the more likely it is that they’re safe from disease. “As far as I’m concerned, the data are clear,” Stanley Plotkin, a vaccine expert at the University of Pennsylvania, told me. “Neutralizing antibodies are it.”
Establishing that this trend exists, though, isn’t the same as zeroing in on a cutoff for protection, above which most vaccinated people would likely be guarded from illness. “We know lower neutralizing titers predict more infection,” Taia Wang, an immunologist at Stanford, told me. “What we’re looking for now is a little more precision.” To suss out a more specific set of numbers, researchers need to repeatedly sample the blood of shot recipients, some of whom have to get sick so researchers can get a sense of what falls below the threshold they’re looking for. “The more breakthroughs you have, the easier it is to determine,” Katy Stephenson, a physician and vaccine expert at Beth Israel Deaconess Medical Center, in Boston, told me. A great irony of vaccinology is that it’s easier to define the success of a vaccine that’s prone to regularly fail—one of the only downsides of our extraordinary shots.
Another hurdle that correlate chasers need to clear is a lack of consistency across vaccine trials, which were conducted at different times in different populations using different inoculation recipes, different criteria for defining COVID-19 severity, and different brands of antibody tests. Aggregating and analyzing all the evidence to produce one unifying correlate requires some serious statistical gymnastics.
Read: COVID-19 vaccine makers are looking beyond the spike protein
By now, though, enough people have been vaccinated, and enough blood samples drawn, that preliminary numbers are starting to emerge. One group of researchers in the United Kingdom has proposed a correlate of protection against COVID-19 for AstraZeneca’s vaccine; two others, one in Australia and another in the United States, have taken a stab at pinpointing measurements that will hold true across several different shots, including the three available to Americans. (Representatives from Moderna, Pfizer, and Johnson & Johnson told me that they didn’t yet have their own correlates to report, but were continuing to investigate.)
But the case isn’t closed. “We have some strong leads, but I would not say we have a correlate yet,” Holly Janes, a biostatistician at the Fred Hutchinson Cancer Research Center, in Seattle, told me.
While neuts have certainly hogged the spotlight so far, they could still be unseated by another molecule or cell. And even if neuts are the real deal, having one correlate doesn’t preclude defining another that captures an additional element of the immune system. Flu vaccines, for instance, seem to come with a bunch of measurable metrics of success, some of which are still being confirmed in research labs. Other, non-neutralizing antibodies exist, and their levels also seem to ratchet up in lockstep with COVID-19 vaccine efficacy.
Many researchers are hoping for more data on T cells, immune cells that support the production of antibodies or annihilate virus-infected cells on their own. Compared with antibodies, T cells are fragile, reclusive, and a pain to measure, Smita Iyer, an immunologist at UC Davis, told me. But they seem fundamental to the success of well-established vaccines, including those for chicken pox and tuberculosis. Against the coronavirus, T cells are known to pick up the protective slack when neuts and other antibodies fail. “There’s not only one immune response that protects you, which is good,” Florian Krammer, a vaccine expert and virologist at the Icahn School of Medicine at Mount Sinai, told me. “If one fails, another can take over.” That redundancy is great for us, but frustrating for researchers looking for a simple portrait of protection.
Things could get even thornier. As is the case with any vaccine, the success of a COVID-19 shot hinges on a multitude of factors—including the strength of the immune system it’s bolstering, the mutability of the virus it’s counteracting, and the exact ingredients in the shot itself. Kids, whose immune systems are still finding their footing, might need correlates of their own; so might older adults and immunocompromised people, whose immune systems are less easily marshaled by vaccines. The numbers we settle on could also vary among vaccine brands because different shots rile up different subsets of immune cells.
Then there’s the biggest wild card of all: the coronavirus itself. It’s continuing to splinter into new variants, some of which have already revealed themselves to be quite capable of dodging certain antibody-based defenses. A neut level that keeps us safe from Alpha won’t necessarily thwart Beta or Delta to the same extent. (There’s at least good news on T cells, which are much harder to stump with mutations—another reason these cells are looking so attractive to some scientists.) “We’re starting to get numbers now, but there are going to be asterisks because of the variants,” Lisa Gralinski, a virologist at the University of North Carolina at Chapel Hill, told me. Because correlates take so long to determine, “whatever number we come up with today is really talking about the past,” Stephenson, of Beth Israel, said. SARS-CoV-2 will always mutate far faster than humans can conjure new correlates. We may well end up with an entire menagerie of correlates against COVID-19, each tailored to its own combination of population, variant, and vaccine. (And that’s all just in the realm of blocking COVID-19 disease; stopping asymptomatic infection would require its own set of correlates as well.)
Read: Delta is driving a wedge through Missouri
But the mere possibility of hitting protection pay dirt is reason enough to keep plugging away. Having a strong correlate of protection against COVID-19 would allow researchers around the world to more quickly bring new vaccines to market in countries where they are sorely needed. A correlate would also give scientists the chance to monitor the natural wane of immune responses and deploy boosters that could rapidly buoy those defenses, if need be. It could act as a guidepost for new shots that fight specific variants before they outsmart the jabs we already have.
The need for correlates is so urgent, the FDA has already gambled that antibodies are the answer: In recent guidance, the agency noted that it would consider green-lighting updated, variant-specific versions of vaccines if they’re able to prompt the production of adequate levels of neuts. It’s a hastier move than some researchers would like. But with variants such as Delta surging amid a largely unvaccinated global population, the shortcut offered by these correlates has never been more appealing. The big hope, researchers told me, is that COVID-19 vaccines will be able to follow in the footsteps of flu shots, which are reformulated seasonally to keep pace with the strains du jour. Vaccine makers can debut new vaccines by simply checking inoculated people’s blood for the telltale markers of protection, rather than waiting to see how these individuals fare against the virus itself.
Spinning the idea of correlates into a personal guarantee of immunity is tempting, especially with antibody tests so readily available. But correlates are just that—correlates, patterns gleaned from large groups of people. Levels of certain immune fighters could track with protection against disease without being directly responsible for our vaccines’ success on a person-by-person basis. “We’re talking about measurements that apply better to populations than to individual people,” Plotkin said.
Some correlates can be tested in individuals, such as in the case of the rubella-antibody test that Taylor took in June, after discovering she was pregnant. But these tests don’t offer absolute certainty. Every trend will have exceptions—some people whose SARS-CoV-2 antibody levels are bonkers-high may still end up getting sick; others with low titers will stay safe. Antibody stocks, after all, naturally dwindle over time, but the body retains the ability to replenish them. Thresholds aren’t hard lines between unprotected and protected; everyone always carries some relative risk, especially amid a pandemic this devastating. “There are no sharp edges in biology,” Iyer told me. Correlates, while useful, can’t actually encompass everything our immune systems are capable of. Without the right amount of nuance, they risk making black-and-white out of a situation that operates entirely in shades of gray.
The geocentric model of our solar system was the only model that was considered correct and accepted among many people of many cultures for centuries (read 99% of scientists). This includes authoritative figures such as the Catholic church and scientists of that time. However, as we all know thanks to the astute observations and publications by Copernicus, Kepler, and Galileo that we know for a fact the Earth is not the center of the solar system. This is probably the highest profile and most well known instance of where the majority/status quo ended up being wrong.Yeah, you really think scientists in China and Russia wouldn't want to be the ones to be the beacons of truth down the lines? Instead, you're gullible enough to believe the 99% of scientists would be corrupted, but the 1% of scientists totally couldn't be corrupted as easily (which is completely retarded, even by your standards) and you also don't think that some scientists in China or Russia, with backing from their government, wouldn't want to be world-wide heroes to expose the covid fraud? All because there's some medical journals in the US and Europe?
You are seriously deluded and really, really bad at logic
Do you got any sources to back this up, or is this just conjecture? From what I've seen, this specific topic has actually been studied and the results indicate that the opposite is true. Natural immunity has been shown to be more virus-specific, while vaccine-induced immunity has been shown to be much broader and encompassing of variants.Natural immunity gives someone a varying set of antibodies, so they will be able to fight off subsequent versions even if there’s been quite a bit of change.
"Wane's fast" is a little subjective in this case. It's true that infection produces long-lasting (at least 8 months) natural immunity, more so for severe Covid than mild Covid.The vaccine seems to give an initial strong protection that wanes fast. It also gives a very narrow antibody response so that when the virus changes it’s less effective.
"Don't work very well" is also quite subjective, and relative. They seem to work quite well if your goal is to not get severely sick or die.But that pool of people who were vaccinated, are not so sick but are shedding at normal rates are hosts who incubate and create a selection pressure to evade the vaccine.
In a nutshell, the vaccines don’t work very well. They are at best a mild prophylactic and at worst creating conditions that favour vaccine evading mutations.
I’ll need a reference for that. I disagree for two reasons. One: When you get a natural infection your body sees the virus. It attacks amd creates antigens to pretty much every bit of protein in that virus. So it’ll be antibodies to one protein and different bits of it, and not only the spike but the nucleocapsid, etc. The mRNA injections are one subunit of spike - so there are fewer bits of protein to even create antibodies TO. Except the human cells it’s sticking out of (oh dear…) SARS patients still have antibodies 17 or whatever years on. Classical immunisation gives the body an inactive virus to look at so it’s going to make a diverse antibody set, but mRNA is literally one subunit as a target. It cannot possibly create a more diverse response.Natural immunity has been shown to be more virus-specific, while vaccine-induced immunity has been shown to be much broader and encompassing of variants.
39% for delta, according to Israel. Bear in mind that number is likely to be an overestimate of ALL cases as many people don’t bother to report mild symptoms.
See I just don’t believe their numbers, for two reasons. Firstly, they’re testing amd counting the vaccinated and unvaccinated differently. Vaccinated, you get a lower sensitivity test, so you’re less likely to get a positive anyway and those positives aren’t even counted unless the patient is in critical care or thereabouts level of illness, or death. That fudges the numbers HUGELY. The second reason is that other countries don’t see that. Israel and the UK are seeing totally different numbers. Why?While we still need a formal study, the Surgeon General says that 97% of hospitalizations for Covid-19 are among the unvaccinated,
You wouldn’t expect it to. It requires distinct serotypes in many models (see dengue.) covid will get there, but at the moment we just have minor strain divergenceAntibody-Dependant Enhancement) has not yet been observed with Covid.
Compared to the alternatives? What does that even mean, it’s not quantitative. We don’t know everything that triggers ADE, and we certainly don’t know enough to say we can design around it. They mean they’ve designed the antibodies to a conserved sequence I think.compared to the alternatives.
That’s not a justification though. It’s just kicking the can - that time will pass regardless and it’s highly unethical to have ‘yeah in a while but whatever’ as an excuseThere were still some concerns, but those are considered to be years off.
No it’s not. You’re confusing the effects on the individual with the effects on the selection pressure in the population as a whole. If person A gets vaccinated, they’re probably not going to get very sick. So they can host a more virulent strain and still be walking around spreading. Person B unvaccinated will be immune naive and may feel bad from that strain, so will be more likely to stay home. Imagine a mixed population of people who have either steel toecaps or sandals . They all have to carry cannonballs around at all times (we are sadistic in our thought experiments.) on day one, everyone has the same weight. But every day, each person drops the cannonball on their neighbours foot or their own in a coin toss, 50:50 chance. If their foot doesn’t break, they get 2 kg added to the cannonball they carry tomorrow. Those with steel toecaps will end up more likely to be carrying heavier balls. When they drop them on those with sandals, feet break. The steel toecap wearers benefit themselves at the expense of the population as a whole.Furthermore, as established, the people who do get infected with Covid despite being vaccinated almost entirely end up with mild to no symptoms. This is the opposite of what you'd expect if the virus was evolving within vaccinated individuals.
I gave a reference. The natural immune response doesn't typically create a dozen different antibodies, rather it's more likely to create a single hyper-fitting antibody type.I’ll need a reference for that. I disagree for two reasons. One: When you get a natural infection your body sees the virus. It attacks amd creates antigens to pretty much every bit of protein in that virus. So it’ll be antibodies to one protein and different bits of it, and not only the spike but the nucleocapsid, etc. The mRNA injections are one subunit of spike - so there are fewer bits of protein to even create antibodies TO. Except the human cells it’s sticking out of (oh dear…) SARS patients still have antibodies 17 or whatever years on. Classical immunisation gives the body an inactive virus to look at so it’s going to make a diverse antibody set, but mRNA is literally one subunit as a target. It cannot possibly create a more diverse response.
Another study found 88% protection for the Pfizer, and 67% for AstraZeneca. I do not know the reason for the wide variation.39% for delta, according to Israel. Bear in mind that number is likely to be an overestimate of ALL cases as many people don’t bother to report mild symptoms.
This sounds like more conjecture. The topic of ADE with Covid 19 and other coronaviruses has been researched. According to the study:No it’s not. You’re confusing the effects on the individual with the effects on the selection pressure in the population as a whole. If person A gets vaccinated, they’re probably not going to get very sick. So they can host a more virulent strain and still be walking around spreading. Person B unvaccinated will be immune naive and may feel bad from that strain, so will be more likely to stay home. Imagine a mixed population of people who have either steel toecaps or sandals . They all have to carry cannonballs around at all times (we are sadistic in our thought experiments.) on day one, everyone has the same weight. But every day, each person drops the cannonball on their neighbours foot or their own in a coin toss, 50:50 chance. If their foot doesn’t break, they get 2 kg added to the cannonball they carry tomorrow. Those with steel toecaps will end up more likely to be carrying heavier balls. When they drop them on those with sandals, feet break. The steel toecap wearers benefit themselves at the expense of the population as a whole.
The individual can benefit from something that harms the whole, until a balancing pressure/pressures is applied. The vaccinated not getting sick is not the metric used to look at how virulent the virus is
Furthermore, ADE is much more likely to appear where mutation rates are high. Mutation rates are much higher (PDF) in non-vaccinated populations than vaccinated ones.Vaccines with a high theoretical risk of inducing pathologic ADE or ERD include inactivated viral vaccines, which may contain non-neutralizing antigen targets and/or the S protein in non-neutralizing conformations, providing a multitude of non-protective targets for antibodies that could drive additional inflammation via the well-described mechanisms observed for other respiratory pathogens. However, it is encouraging that a recent assessment of an inactivated SARS-CoV-2 vaccine elicited strong neutralizing antibodies in mice, rats and rhesus macaques, and provided dose-dependent protection without evidence of enhanced pathology in rhesus macaques74. Going forward, increased vaccine studies in the Syrian hamster model may provide critical preclinical data, as the Syrian hamster appears to replicate human COVID-19 immunopathology more closely than rhesus macaque models75.
This has not happened, we have not observed any ERD in humans.Should it occur, ERD caused by human vaccines will first be observed in larger phase II and/or phase III efficacy trials that have sufficient infection events for statistical comparisons between the immunized and placebo control study arms.
Even if it somehow turns out we were just 'kicking the can'. Kicking the can gives us what we didn't have: Time.That’s not a justification though. It’s just kicking the can - that time will pass regardless and it’s highly unethical to have ‘yeah in a while but whatever’ as an excuse
Yes, that’s what viruses do. The selection pressure is therefore for lower virulence and increased spread over time. Like every other pandemic in history. More mutations isnt an issue, its what the environmental selection pressure does with them that counts. A billion strains selected for lower virulence isnt an issue - two strains selected for immune evasion is. Mutation is the raw material for evolution - the direction of evolution is dictated mainly by the selection pressure. Survival of the fittest.Not developing a vaccine is what would likely have lead to even more mutant strains.
All of the variants thus far have mutated within unvaccinated populations.
The trials did not have sufficient infection events. I was tangentially involved in this and they ended up having to go to Brazil to get patients because infection rates were falling off. The statistical power of the trials was insufficient. Also the phase II work was minima to say the least.This has not happened, we have not observed any ERD in humans
No this is variation within the antibodies within one small bit - the RBD. It’s not able to give antibodies to the nucleocapsid or any other viral components. The epidemiology is tentatively showing this too - those with prior confirmed infection seem to be falling ill at lower rates to those vaccinated.I gave a reference. The natural immune response doesn't typically create a dozen different antibodies, rather it's more likely to create a single hyper-fitting antibody type.
Mind providing some of the sources for your claims?Yes, that’s what viruses do. The selection pressure is therefore for lower virulence and increased spread over time. Like every other pandemic in history. More mutations isnt an issue, its what the environmental selection pressure does with them that counts. A billion strains selected for lower virulence isnt an issue - two strains selected for immune evasion is. Mutation is the raw material for evolution - the direction of evolution is dictated mainly by the selection pressure. Survival of the fittest.
The trials did not have sufficient infection events. I was tangentially involved in this and they ended up having to go to Brazil to get patients because infection rates were falling off. The statistical power of the trials was insufficient. Also the phase II work was minima to say the least.
No this is variation within the antibodies within one small bit - the RBD. It’s not able to give antibodies to the nucleocapsid or any other viral components. The epidemiology is tentatively showing this too - those with prior confirmed infection seem to be falling ill at lower rates to those vaccinated.
Russia is a geopolitical adversary of the American government, however, it's really not in their best interest to sabotage their own situation because they've implemented same kind of approaches (including QR-code passes for vaxxed) as the West. By hurting the narrative of THE BIG FLOO, the Russian government is robbing itself of an excellent excuse to keep doing more nefarious shit that they've been doing since the beginning of 2020.Russia = enemies
Stop feeding the goddamn trolls so they'll go back to their provaxx thread and stay there.I'm a retard, yeah. Never pretended to be a smart person.
But yeah, your obstinate refusal to:
acknowledge the carpet politics that scientific community has impacts what scientists can and can't say
peer pressure in the scientific community
paints you as a bigger retard.
You can also look at how various countries handled pandemic response and remarkable number of countries as an excuse to limit citizen freedoms.
Yeah, you're a retard.
Yes, that's definitely going to persuade them not to come. Much like the rest of leftists these days, if you don't give them a time of day and just keep to yourself, they're still going to go and shit on your floor, because they hate you that much.Stop feeding the goddamn trolls so they'll go back to their provaxx thread and stay there.
Post information related to the vaccines, that is what this thread is for. If you try and convince the anti-vaxx tards of anything they will scream the same shit over and over.Yes, that's definitely going to persuade them not to come. Much like the rest of leftists these days, if you don't give them a time of day and just keep to yourself, they're still going to go and shit on your floor, because they hate you that much.
Well I can’t about the trials, that’s proprietary but it should all be documented if you want to go dig up the CSRs (I do hope they’re public, if not that’s not a good look.) The rest is in any epidemiology or basic biology textbook you care to open. Evolution uses the raw material of variation within a population coupled with natural selection. The mutations are just the fuel. The direction the thing goes depends on the terrain. Peppered moths for example - constant mutation, get darker in polluted areas becasue the tree bark they hide in is darker and lighter ones get eaten so darker ones reproduce more. In cleaner areas, that pressure is gone so lighter ones camouflage against bark and darker ones get eaten. There’s no difference in the mutation number and it wouldn’t matter if there was - what matters is the rounds of selection in each generation that dictates the gene pool in the next. If you spray painted the trees bright orange, you’d end up with orange moths eventually. Vaccinated people select for mutations that spread in the vaccinated. Unvaccinated people select for mutations that are milder and spread faster but make people less sick. If you vaccinate someone they don’t get as sick, so they can carry a ‘worse’ mutation and spread it more. Effectively you’re removing the ‘selection pressure of sickness behaviour’ if you want to read up on it more.Mind providing some of the sources for your claims?
"You can't believe what those dirty Russian haxors are saying because we've always beenI don’t buy the narrative that Russia = enemies, therefore all Russian scientific and media output is for the purpose of subverting American stability, therefore Russia cannot have their own political aims like stabilizing and controlling their own population with the same lies as the American government. It’s silly to say “oh well if your government is lying to you surely their SWORN ENEMY RUSSIA would be Opposite Day from them?!”
All the variants of concern thus far had arisen before widespread vaccines were available.Not developing a vaccine is what would likely have lead to even more mutant strains.
All of the variants thus far have mutated within unvaccinated populations.
ADE =/= vaccine pressured evolution.As for your point on selection pressure, this is a topic that has been considered, but vaccine-pressured evolution (Antibody-Dependant Enhancement) has not yet been observed with Covid.
Oh yes. Pharma patents start when the molecule is discovered and shown. They’re about 14-15 years usually, and in that time you need to do trials and market and make money (a trial can cost up to billions, most are tens to hundreds of millions.) When a pharma company has a drug that works but is out of patent, they can do something called ‘evergreening.’ This is often done by creating a new formulation, extended release, new dosage types or shoving a nitrogen on, or by reversing the chirality of an irrelevant bit (basically take an irrelevant part and mirror image it.) they did it with efexor (venlafaxine.) first they made an extended release, then I think they patented a breakdown molecule or something as Pristiq. It stops or allows legal challenge to generics makers and keeps the prices high. Remember that when you are being told about how they only have your best interests at heart. The guy in the lab who spent his life finding an inhibitor for a certain molecule may be in it for the curing of people, but the marketing and money men are in it for money. And political lobbying access. I think (please correct me if I’m wrong that there’s a link between Pfizer and Reuters, the news agency as well. Either one of the C suite is in Reuters’s board or vice versa. So not only is it money and power, it’s media control to shape social engineering.Wait this is a thing?
James C Smith from their board of directors is also the chairman of the Thomson Reuters Foundation, a charity under the Thomson Reuters media conglomerate group which trains journalists and provides legal expertise, amongst other things.I think (please correct me if I’m wrong that there’s a link between Pfizer and Reuters, the news agency as well. Either one of the C suite is in Reuters’s board or vice versa. So not only is it money and power, it’s media control to shape social engineering.