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No you agree in fact.Disagreed
Alternative fact. The alternate for disagree is agree.
Welcome to the leftovers of Trump world.
Again.
If you were vaccinated and WANTED to get infected what would you do.
No mask, go into crowded places with antivax spreaders with 1000X the viral load as the old strain.
Breathe deeply as people come and go. The vaccine has worked enormously well so far. That is the truth right now.
I already have a friend that is a breakthrough in SA. She went to a bachelorette party involving staying in the same room and riding around in the same limo with two girls who felt very sick. She tested positive and has gotten over what she describes as a slight head cold that she went in to get tested for after finding out about the two girls.
The vaccine WORKED. But the inconvenience of having to miss work. Thank you antivaccers.
No you agree in fact.Disagreed
Alternative fact. The alternate for disagree is agree.
Welcome to the leftovers of Trump world.
Keep up the science bashing.
He's got a firm grasp on mutations
"During the first ten months of the pandemic, high waves of infectious cases that occurred in overcrowded areas (e.g., slums, favelas, highly populated cities,..) affected by the pandemic may have caused immune pressure on viral infectiousness, especially upon re-exposure of previously asymptomatically infected individuals. It is possible that such events have been driving natural selection and enhanced circulation of more infectious, S-directed immune escape variants. The higher and more widespread the viral infectious pressure, the higher the likelihood that previously asymptomatically infected subjects become re-exposed to the virus at a point in time where their ers of low affinity, S-directed Abs are still high enough to compete with their natural, polyreactive Abs for binding to the circulating Sars-CoV-2 lineage (see Fig. 1; in previous contributions, I have explicitly explained why S-specific Abs have higher affinity for S protein than natural IgMs, which bind to virus surface-expressed motifs through multivalent interactions). Consequently, enhanced infectivity rates could lead to a transient increase of the susceptibility of younger age groups (< 60-65 years) to Covid-19 disease and may, therefore, raise morbidity and hospitalization rates in these age groups (as is currently observed in many European countries as well as in the US). So, the higher and more widespread the viral infectious pressure, the more productive the breeding ground for more infectious variants and the higher the likelihood for natural selection of certain S-directed immune escape variants (i.e., such that evolved mutations capable of resisting suboptimal immune pressure on viral infectiousness). Immune escape variants that are selected because of their capacity to overcome such immune pressure exhibit a higher level of infectiousness. This is how high infectivity rates facilitate breeding of increasingly infectious viral variants. During the first year of the pandemic, several of such ‘more infectious’ immune escape variants have emerged (e.g., alpha (2), beta, gamma, delta).
Depending on the remaining protective effect provided by natural Abs, younger and healthy age groups, and children in particular, may not even show any symptoms at all, even though dominant circulation of more infectious variants (e.g., delta variant) is now substantially increasing the risk of repeated exposure. This already explains why Covid-19 disease in the non-vaccinated is primarily observed in young, middle-aged adults. Since younger age groups are generally better protected by natural, poly-reactive Abs, cases of severe disease in these groups are rather rare. The severity of the disease in these subjects is thought to depend on the time point of re-exposure after their previous infection (i.e., the shorter thereafter, the higher the concentration of blocking S-specific Abs, the higher the likelihood for contracting more severe disease).
Because both, binding of natural CoV-nonspecific Abs to Sars-CoV-2 and binding of Sars-CoV-2 to the Ace-2 entry receptor is mediated by multivalent interactions, it is reasonable to assume that the blocking effect of natural, CoV-nonspecific Abs on the interaction between the Ace-2 receptor and a given Sars-CoV-2 lineage primarily depends on the functional concentration of these natural Abs. This would already explain why, under normal cir stances (i.e., if not suppressed by S-specific Abs), young and/ or healthy individuals can effectively deal with all Sars-CoV-2 viral variants. The higher the affinity of S for Ace-2 (i.e., the higher the level of intrinsic viral infectiousness) and the older the age group, the lower the residual (i.e., non-suppressed) functional capacity of natural Abs.
In contrast, vaccinal Abs are directed at a limited set of S-derived Sars-CoV-2 motifs (i.e., epitopes primarily comprised within the receptor-binding domain [RBD] of the S protein). Hence, very few mutations within this limited set of epitopes will already substantially diminish the affinity of vaccinal Abs for binding to Sars-CoV-2. This, however, does not apply to S-specific Abs acquired upon recovery from natural Covid-19 disease as those are directed at a much broader and diversified spectrum of B cell epitopes. This would already explain why more infectious Sars-CoV-2 variants more readily escape from vaccinal S-specific Abs than from naturally acquired S-specific Abs and also why we are now seeing more and more breakthrough disease cases with the more infectious delta variant in vaccinees whereas young and/ or healthy individuals or previously symptomatically infected people (provided seronegative for S protein (3)) remain largely protected from Covid-19 disease.
Molecular epidemiologists conclude that, because of the steadily increasing S-directed immune pressure exerted by the human population, circulating variants are now increasingly evolving mutations that drive resistance to S-specific Abs, especially to those recognizing immunodominant epitopes that are situated within the RBD and N-terminal domain (NTD) of the S protein. It is highly unlikely that naturally acquired S-specific Abs are responsible for this immune pressure as people who recover from Covid-19 disease only cons ute a relatively small subset of the population and mount Abs against a much broader and more diversified panel of S-derived epitopes. Given the nature of the vaccinal Abs and the large vaccine coverage rates in most countries, there can be no doubt that the steadily increasing population-level immune pressure found to be exerted on RBD, for example, is caused by vaccination of large masses of people (in a previous contribution, I have expressed my astonishment about the fact that these brilliant scientists didn’t even mention ’mass vaccination’ at all as a potential cause of the massive increase in S-directed immune pressure; (see my recent contribution: 'Why the ongoing mass vaccination experiment drives a rapid evolutionary response of SARS-CoV-2'). This evolution is, of course, extremely worrisome. Whereas progressing convergent evolution towards increased resistance against functional, S-specific Abs elicited by the vaccine may not necessarily further increase the affinity of the virus for the Ace-2 receptor (and hence, not commonly cause more disease in young and healthy individuals), it is reasonable to assume that such evolution will rapidly raise the number and severity of disease cases in the vaccinated part of the population. This is because growing VI escape will cause vaccinees to lose their vaccine-mediated immune protection while having their natural, CoV-nonspecific natural Abs suppressed by high ers of long-lived, S-specific vaccinal Abs (4). It is reasonable to assume that, as a general rule, the level of suppression of natural, CoV-nonspecific Abs will increase with increasing strength (adjuvantation!), frequency and coverage rate of booster immunizations (including 2nd generation vaccines!).
Vaccinal S-specific Abs cannot outcompete S-specific Abs from previously symptomatically infected individuals for binding to viral variants due to multivalent B-cell epitope recognition by the naturally primed immune system. On the other hand, immunity acquired upon recovery from natural Covid-19 disease is very robust and has repeatedly been reported to be capable of dealing very effectively with a diversified range of antigenic variants upon re-exposure (including variants of concerns; VoCs). Non-antigen (Ag)-specific innate immune adjuvantation enables epitope spreading and is, therefore, likely to contribute to broad immune recognition. Naturally acquired immunity is, therefore, an almost ‘invariant’ component to herd immunity. It is, however, uncertain whether binding of S-specific Abs from previously symptomatically infected individuals to circulating VI-escaping viral variants could render these individuals more susceptible to Ab-dependent enhancement of disease (ADE)."
And you completely missed his point on the variants.
"The interactions described above allow to understand how mass vaccination on a background of enhanced viral infectiousness (pandemic!) engages both, the vaccinated and unvaccinated population to expedite natural selection and adaptation of immune escape variants harboring additional, RBD-associated mutations which increasingly inhibit VMI. This is to say that mass vaccination campaigns conducted during a pandemic of more infectious variants will precipitate resistance of more infectious Sars-Cov-2 variants to S-based Covid-19 vaccines.
The more ‘more infectious’ variants expand and dominate and the more these variants are subject to vaccine-mediated immune selection pressure, the more rapidly the beneficial effect from mass vaccination (i.e., reduction of viral transmission and prevention of disease) will be replaced by a growing failure of the vaccines to protect the vaccinees and of the vaccinees to protect the unvaccinated. This evolution is currently expedited by relaxation of infection-prevention measures, including more frequent contacts among healthy individuals. More frequent contacts between asymptomatically infected vaccinated and non-vaccinated subjects (5) will only promote breeding of new variants that are both, more infectious and more readily escape from vaccine immunity (e.g., lambda variant)."
68.7% of 18+ are fully vaccinated in Bexar county.
So you're making the argument that more people SHOULD be vaccinated and people SHOULD get boosters. That's a far cry from your earlier suggestion that vaccinations don't matter.
You supposed pro-vaxxers sure have a strange way of advocating for vaccinations.
The old and sick should get shots just like flu shots. But should be optional like flu shots. If they wanna die up to them.
Basically the startegy.should be.EXACTLY like flu shots. (For adults)
You CAN be infected with the delta variant and be vaccinated and have few if any symptoms.
Your cases were cases in the hospital? The goal is to keep people out of the hospital and from getting really ill. This still may be difficult if you get a large dose of virus at once with ANY vaccine.
I don't think the government should compel vaccines either, at least not yet. But I'm okay with businesses doing it, and I'm definitely okay with shaming the absolute out of the unvaccinated and everyone who enables them.
This isn't the flu yet.
Im ok with all this. But it seems forced vax passport is imminent. Which is crazy given recent findings.
Should the vaccine for Diphtheria, Pertussis, and tetanus be mandatory for school children?
Should any vaccine be mandatory for ANY population of people who can get vaccinated?
Are those emergency approved vaxes?
NO.
They are not emergencies because people are vaccinated.
Why are you trying to compare DTAP which has been around for decades to an experimental vaccine?
Quit trying to pretend the vaccine is unsafe and you took the needle up the ass.
We know better, we have more numbers than for any of those others now.
In Bexar County, the vaxxed are <5% of hospitalizations.
Because you calling it experimental NOW is trying to pretend like it is harmful and does not work which is patently FALSE.
Yes think this.
We have the data numbskull. If the data undergoes a giant change, we change protocol and methods.
Quit trying to pretend the vaccine is dangerous and does not work.
Some kids have very bad reactions to the aforementioned vaccine as well.
Just very few.
It is 100% experimental now, that is not even up for debate. I never said it didn't work. We already know it is harmful to certain populations now the question is how harmful and what harms show up years down the road.
Discussing mandatory vaccines and trying to compare DTAP to the Covid vaccine is absolutely re ed.
You wont admit this heater.
You will find some case, somewhere with a person has a bad reaction. No .
Our immune systems ARE NOT all the same. There is genetic variation among people and there are people getting bad tainted vaccinations when the numbers of vaccinations is enormous.
Total misunderstanding of probability and numbers so you go find that case in the guise that it is widespread.
No it is not because it has been tested at a much higher rate than any of those other vaccines now.
YOU are hung up on the word experimental because of the speed at which it was made, thats your problem.
Well the vaccine is OUT dumb and we can follow it with MUCH, MUCH larger numbers of test subjects than the others.
What is your problem? Its not the time it takes for testing if the vaccine has already been tested... what do you not get here?
YOu should have had a louder voice during the phase which it was tested on paid volunteers. And it was rushed THEN because it was a huge problem. It has worked. What do you NOT get?
Yeah.
Pulling the basic Darrin again.
Darrin and Snakeboi want everyone to be infected now since their unsanitary asses got the rona immediately after it hit Bexar County.
And they want everyone to get as huge a load of virus as possible because like every Trump now they just want to watch the world burn.
Put hater in that group under both administrations.
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