Your post doesn’t dispute my point.
A study produced by those affiliated to Didier Raoult, the French gobshite who pushed hydroxychloroquine.
The term “scaremongering” has been used ad nauseum throughout this pandemic and in the vast bulk of cases those who have used it have been talking bollocks.
In this case, the use of the term “scaremongering” is entirely appropriate.
Are the vaccines fully tested like all the others that everyone is happy to take like MMR etc?
Can you say they’re fully safe?
Whats the risk/return for a teenager in your view?
No vaccine is ever 100% fully safe. They’re extremely safe compared to the alternative.
I’ve no interest in debating the merits of vaccines that are proven to work with a zombie.
Are they FDA approved mate?
Obesity is due to eating too much, I don’t think $1.50 a day difference in the cost of food is the issue.
Smacks of “I’m Alright, Jack”. Cost is very much an issue for a lot of people when it comes to what they eat. As is convenience. And convenient, unhealthy foods tend to be cheaper.
Anyway, none of that is relevant to how to escape a pandemic. You cannot make obese people healthy in weeks.
Nothing is proven mate.
We’ll know what the craic is next April or May.
People will probably be on their 4th booster by then though. But sure, its crazy to even question it going by the national media narrative.
You don’t have any answers re these vaccines, the people jabbing the public don’t either in fairness.
I sincerely hope it goes well as the likes of Pfizer etc arent going to be held accountable either way.
Their indemnified sure as you know. Ideal for them.
A New Antibody-Dependent Enhancement Hypothesis
By Derek Lowe 16 August, 2021
Here’s another post that I will regret writing, but a great many people have asked me about a new preprint that brings up the possibility of antibody-dependent enhancement with the current vaccines and the Delta variant. To be frank, some of the people promoting this seem to be rooting for the virus, just so long as it humiliates their enemies and proves their own positions to be correct, but there are a lot of honestly worried people out there who are wondering what this paper means. So let’s look at it, with an eye to lessons for evaluating such papers in general.
The authors are building on another recent paper (Li et al.) on neutralizing and non-neutralizing antibodies against the current coronvirus. The preprint version of that one came out in February, and the final version went online in June. That work appears to be very solid, and represents a great deal of effort, so let’s discuss it for a bit before returning to the preprint above. In it, the authors isolated antibodies from human patients that target the receptor-binding domain (RBD) and others that target the N-terminal domain (NTD). They found using in vitro assays that both neutralizing and (especially) non-neutralizing antibodies that bound to the NTD showed antibody-dependent enhancement in cell infection. This took place partly through a well-known ADE pathway involving the Fc-gamma receptor, which allows for infection of macrophages, and this was indeed the main mechanism seen with ADE of the earlier (2003) SARS virus. It should be noted, though, that these seem to use different subtypes of the Fc-gamma receptor, so they’re not completely identical. And there were other cellular ADE events that were Fc-receptor-independent, though a mechanism that has not yet been worked out.
But the Li et al. paper went on to demonstrate that this does not seem to happen in animal models for these SARS-CoV-2 antibodies. Indeed, antibodies that showed ADE in the cell culture models still protected primates from viral replication when they were challenged by the actual virus. Three of the 36 monkeys in the study had increased lung inflammation compared to controls, but still had decreased viral replication, which makes it likely not ADE (which depends on viral infection being worse) but some sort of effect of antibody treatment that is not mediated by virus. None of the animals that got the highest doses of antibodies, for example, showed any of these effects.
And the authors note that if antibody treatment led to ADE in humans, then it would have been seen in the convalescent serum trials and in its clinical usage. But it was not. Convalescent serum was not very beneficial in the end, but it was definitely not harmful. The paper also points out that the vaccine trials and the use of the vaccines in clinical practice have led to no signs of ADE, either. So ADE in cells for SARS-CoV-2 does not seem to translate to animal models of infection, and nothing of the sort has so far been observed in the (huge) human population.
Perhaps that’s why I haven’t been sent so many copies of the Li et al. manuscript, but rather this new one (Yahi et al.) I think it’s the title as well, which is an eye-catcher: “Infection-enhancing anti-SARS-CoV-2 antibodies recognize both the original Wuhan/D614G strain and Delta variants. A potential risk for mass vaccination?” The authors build on the earlier paper and make comparisons to the protein sequence of the Delta variant. They believe that the antibodies identified in the Li et al. paper as causing ADE in cell assays cause the Delta variant NTD to be more tightly bound to the membrane of human cells through an interaction with cell-surface lipid rafts, and they speculate that the balance between neutralization and infection enhancement, while favorable for earlier strains of the coronavirus, is tipped the other way for the Delta variant (thus the title of the paper, and this its rather bizarre Figure 2). About that title, while we’re on it – I’m not completely sure why they reference mass vaccination risks and not risks posed by previous infection by non-Delta strains, because I would have to think that the same concerns would apply.
This one is not a very long paper, and there’s a good reason for that – it contains no experimental data. The postulated binding enhancement via lipid rafts is completely a molecular modeling result, and has not been demonstrated in actual cells. Their computations are explained in more detail in another paper, where you can see that the authors believe that it’s the kinetics of the lipid-raft interaction that may drive transmissibility of various viral strains.
I have no comment on that per se, but I do have to note that modeling-only conclusions about large protein binding events have to be confirmed by experimental data before they can be taken seriously. There are a great number of things that look plausible in such simulations that do not translate to reality. To illustrate that, here is a paper from the same three authors, again completely based on molecular modeling, that goes into a detailed mechanistic explanation of how azithromycin and hydroxychloroquine work together as an effective therapy against the coronavirus. The azithromycin binds to the RBD, you see, while the HCQ is affecting the conformation down at the lipid-raft-binding part of the NTD (this one’s also lipid-raft-centric). That latter interaction is the subject of this earlier paper. The problem is, these two drugs together (or separately) are not actually an effective therapy for coronavirus infection, a fact that the earlier papers’ citations of the work of Didier Raoult cannot overcome. It is a detailed calculated hypothesis to explain something that does not, in fact, exist.
This is a constant danger with simulations. Readers who have not encountered much molecular modeling are often (and understandably) impressed by the graphics and tables that appear with such work, but if you’ve been involved with actual experimentation you’ve seen many, many examples of such hypotheses that turned out to be built on air. Confusing the graphics with reality is a constant danger for all of us.
And in my view, the Yahi et al. paper is not aligned with reality. They do work in a line about how “ although the results obtained so far have been rather reassuring. . . ” with a reference to the Li et al. paper, but they should also refer to the massive amount of real-world evidence now available. We have hundreds of millions of people who have been vaccinated to produce antibodies against the non-Delta coronavirus protein domains and are who are now being exposed to the Delta variant. To reiterate, there is (to the best of my knowledge) no evidence whatsoever of ADE in this situation. In fact, we see the opposite: people who have been vaccinated are far less likely to become infected with the Delta variant, and if they become infected, they are far less likely to experience severe disease. These trends have been seen over and over in different populations, and they are the exact opposite of what you would see if ADE were operating. If the mechanism proposed by Yahi et al. were happening in the real world, then we should see higher Delta infection rates among vaccinated people, with more severe disease. We are not. We are seeing the reverse. The vaccines simply do not appear to be causing ADE, no matter how many reasons one might be able to spin for them to do so.
In short, get real.
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Real world evidence emphatically disproves what they are saying.
Also, they are affiliated to Raoult and have themselves pushed hydroxychloroquine, so to call them “respected” is a serious case of poetic licence.
On this forum, David Icke and his affiliates are “respected” by a number of posters.
But not by non-amoebas.
So maybe they’re “respected” in that sense of the word.
“Science” for clicks.
Don’t get me wrong @Cheasty , I’m not saying vaccines will cause major hassle. But long term effects even if its for a small percentage of young healthy people - needs to be looked at in depth.
I do have serious reservations though on how effective these so called 1G jabs are going to be. Numbers from Israel point to them being not great at all once you go past 6 months or the summer here potentially.
Real world evidence is that people who are vaccinated are getting infected with the Delta variant, and hospitalizations of previously vaccinated are increasing. How the fuck would Derek Lowe or anyone else know how many vaccinated are getting infected when the CDC are not reporting it? Time will tell who is right or wrong, but it is normal for scientists to disagree, that’s how science progresses.
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None of that in any way backs up the hypothesis of the authors of that paper. Real world evidence demolishes it. What is happening has been consistently predicted since the start of the year by the more clued in observers like ISAG.
More transmissible variants come from Covid spreading widely. A poster named Sid Waddell on YBIG was warning back in May 2020 that Covid could mutate into a more damaging form, while seven months later you were calling the emergence of Alpha - which happened well before vaccinations had started - “a load of bollocks”.
Vaccines are not 100% effective, are not claimed to be, and never were claimed to be.
How did Sid Waddell propose preventing Covid spreading in India where the Delta variant emerged? A country with 200 million living in slums, and where it is now estimated from antibody testing 2/3 of the population have been infected. Should they have issued a work from home order?
The reality is there is no way to stop this virus spreading as it is airborne, you may as well stand on the Salthill promenade and try and stop the breeze. The other reality which is a biological fact is that as vaccination rates increase, the selective pressure on the virus is to mutate faster to evade vaccine antibodies. This will happen, and we will be faced with many more variants.
Incessant lying doesn’t help your cause. What I said in December was that there was no scientific evidence that the Alpha variant was more virulent than prior strains, that was true then and is still true. There is some evidence that the Delta variant is more virulent, as in hospitalizations of the age groups infected, but it is not translating into a higher death rate.
Real world evidence of ADE would be higher numbers of vaccinated individuals getting infected and getting ill. Let’s see how it plays out, but to dismiss it out of hand as Lowe does is foolhardy, wouldn’t be the first time an expert has been wrong during this pandemic. One of the most disturbing aspects of this pandemic is the politicizing of science, and the left and right are both guilty of it. It’s very easy find scientists that agree with your position. Nobody has been more wrong than Independent SAGE with their doomsday projections for the UK after it’s recent opening.
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Shouldn’t Texas and Florida be right at the top of that if it went by population? Second and third biggest states respectively?
What in the good fuck happened in Rhode Island? That’s the 44th biggest state. Sid must be very upset with the governor there
Deaths per million of population.
Ah. I stand corrected. Texas and Florida should be WAY out in front so
NY and NJ were riddled right at the start, back when there was serious death toll
Iirc you can only compare those states to bordering states or to New Zealand.
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Italy was riddled at the start too and they’ve since been overtaken by many countries in Europe. It stands to reason that NY and NJ would be too, especially if the policies in Texas and Florida are as bad as certain people are making out