Vaccinated People are Eight Times more likely to be infected with the South African Variant

Yes, you read that correctly. People in Israel who have been given two doses of the Pfizer mRNA ‘vaccine’ are eight times more likely to become infected with the B.1.351 variant of SARS-CoV-2 than unvaccinated individuals according to a study published just a few days ago.

Here, we performed a case-control study that examined whether BNT162b2 vaccinees with documented SARS-CoV-2 infection were more likely to become infected with B.1.1.7 or B.1.351 compared with unvaccinated individuals. Vaccinees infected at least a week after the second dose were disproportionally infected with B.1.351 (odds ratio of 8:1)

But that’s not all. The dominant variant of SARS-CoV-2 in Israel is B.1.1.7, the so called ‘Kent variant’, alleged to be more transmissible and more deadly than the previous dominant variants of the virus. Vaccinees were also disproportionately likely to become infected with B.1.1.7 for a week or two after the first dose and even a week after the second, so they were actually more vulnerable to Covid during that period than those who received no vaccine. This might explain the sharp rise in ‘Covid deaths’ very soon after vaccination, observed in many countries throughout the world.

So, the pro-vaxx fanatics might say ‘Well, yeah, a few people die and stuff after getting the vaccine, but those who don’t die get protected, so it’s all OK in the end’. Er, no. Because, in Israel, those people who made it through two doses without getting seriously sick or dying ‘with Covid’, were still as likely to get infected with the dominant variant of SARS-CoV-2 as the unvaccinated!

No statistically significant difference was observed in the rates of B.1.1.7 infection in FE [fully vaccinated, more than a week after second dose] cases versus unvaccinated controls (odds ratio [OR] of 6:4, one-sided exact McNemar test p=0.38), but a significantly higher proportion of B.1.351 was observed in FE cases vs. unvaccinated controls (OR of 8:1, one-sided exact McNemar test, p=0.02).”

So what the flying f**k is the point in a healthy, non vulnerable person (who is highly unlikely to get severe symtoms from a SARS-CoV-2 infection) getting ‘vaccinated’ against Covid if it makes no bloody difference at all as regards their likelihood of becoming infected with the dominant circulating strain? Also, if, by getting ‘vaccinated’, it makes them initially more vulnerable to the dominant circulating variant and a lot more vulnerable, even after two full doses, to getting infected with a rare variant which might in future become more prevalent, then what, pray to God, is the point? I can’t see it. You’re putting yourself at greater risk by getting an experimental ‘vaccine’ than you are by relying upon your own natural healthy immune system. Not only that, you are signalling to your government that they can push you around and tell you what to put inside your own body. That is an extremely dangerous thing to do, as we are about to find out, as the Israelis have already found out.

Would you believe it though, one of the authors of this study has gone on Twitter to promote her work, saying that it is actually justification for mass vaccination? What? In which Universe? Down which rabbit hole? On the other side of which hyper-dimensional Wormhole?

That last tweet just really kills me. It’s basically saying ‘Follow the science (our science) – get vaccinated!’ I expected a lot better from Israeli scientists. A lot better.

13 comments

  1. “The SA variant does not spread”…except in vaccinated Individuals. So please have the vaccine.

    I suppose these people have degrees, but you have to wonder how they got them.

    Liked by 1 person

  2. Jaime, off topic, but could you have a look at this?

    Click to access acs_2020041718295959.pdf

    I like the plain English in the discussion and conclusion

    “Many references in the IPCC reports refer to the forcing of increased IR radia- tion on the temperature. This factor is much discussed [19] [20]. Our results show that the formulas used by IPCC Equation (1a) and Equation (1b) should give very large temperature changes. The values expected from the Stefan- Boltzmann law are much lower, but even these values were not detected in our warming curves. So the idea that backscatters from CO2 is the main driver of global temperature increase might be wrong.”

    And

    “The change in observed backscatter radiation should give us a measurable temperature increase of 2.4 to 4 K by using the Stefan Boltzmann law. But we only observe a very slight temperature increase due to CO2 backscatter. This in- dicates that heating, due to IR backscatter from CO2, is much less than what is assumed from the Stefan Boltzmann law or from the forcing Equation (1a) and Equation (1b). “

    I think these guys are in big trouble, career-wise.

    Liked by 1 person

    1. Geoff, I’ve read through the paper now and it appears they went to great lengths to eliminate any possible sources of heat loss in the apparatus which could explain the very puzzling lack of warming in the rear chamber, even though they demonstrated that back-scattering of IR was clearly taking place when the front chamber was filled with CO2. They come to the conclusion that the temperature of the air in the back chamber is solely a function of the heating of the plate and effectively zero heating effect comes from the increased back-scattering of IR from the front chamber. This simple experiment, if repeatable and demonstrated conclusively to be technically and theoretically competent, completely destroys the Tyndall GHG theory. I wonder why it hasn’t been given much prominence?

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      1. It seems odd to me, but I couldn’t see any obvious problems. There was some heating engineer who used to claim that back radiation resulted in a standing wave with no energy transferred, or something along those lines. May have to reassess my Luke-warmer status.

        Liked by 1 person

  3. I don’t think this study evaluated the absolute risk of getting infected by B.1.351 (or any other variant in the population at large). It assessed the breakdown by variant type in those with breakthrough infections (ie post vaccination) and compared that with the breakdown in those not vaccinated. If a vaccine is known not to be as effective against B.1.351 you would expect this variant to represent a larger percentage of the variants found in breakthrough infections.
    To give the concept some made-up numbers: Say the unvaccinated population has a 1 in 10 chance of infection and of those infected 1 in 10 would be with variant X. Now imagine the vaccinated population has a 1 in a hundred chance of infection and of those infected half would get variant X.
    In a group of 10 000 unvaccinated people 1000 would get the infection and 100 of those would have variant X.
    In the vaccinated group of 10 000 only 100 would get the infection, but 50 of those would have variant X.
    So, if you did a study only looking at those who got the infection and had a sample of 100 vaccinated and 100 unvaccinated, the unvaccinated 100 would be expected to contain 10 with Variant X. The vaccinated group of 100 would contain 50 with variant X – this variant would be 5 times more common in the vaccinated group even though the absolute risk of getting variant X is 0.5% in the vaccinated group and 1% in the vaccinated group.

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  4. Russell,

    Having read through the paper, I don’t think you are correct. The study compared the absolute rick of being infected with SARS-CoV-2 with reference to the vaccinated and the unvaccinated. They assessed this absolute risk for two variants: B.1.1.7 and B.1.351.

    The recently vaccinated have a significantly greater chance of testing positive compared to those unvaccinated. An earlier PHE study found the same effect:

    “Individuals aged >=80 years vaccinated with BNT162b2 prior to 4th January, had a higher odds of testing positive in the first 9 days after vaccination (odds ratio up to1.48, 95%CI 1.23-1.77)”

    “Comparison was to unvaccinated as the baseline group”.

    ttps://khub.net/documents/135939561/430986542/Early+effectiveness+of+COVID+vaccines.pdf/ffd7161c-b255-8e88-c2dc-88979fc2cc1b?t=1614617945615

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    1. Hi Jaime,

      It would not be possible with this study design to asses absolute risk of infection by any variant of SARS-COV- 2, the reason being that there is no data with which to form a denominator for such an assessment:
      Risk in the “exposed” (in this case the vaccinated) = cases that arise in the exposed divided by the sum of those exposed who became infected PLUS those exposed who did not become infected. This study, while described as a “case-control” study is not actually a case-control study in the normal sense of the word – it is more a cross-sectional study. The “cases” and “controls” were all people who became infected. Therefore the vital part of the denominator in calculating risk (those who did not become infected) is absent.
      To calculate relative risk between the vaccinated and the unvaccinated you would also need to have the above data for the unvaccinated (ie the number that became infected AND the number who did not).

      In assessing the the risk of smoking as a cause of lung cancer it doesn’t help to know how many smokers get lung cancer if you don’t know how many don’t get lung cancer. And if you want to know whether smoking is causally significant you also need to know how many non-smokers get lung cancer AND how many don’t.

      An analogy to illustrate what this study attempted would be this: imagine going to a dermatology clinic and asking the patients whether or not they use a sun blocker. You then get the diagnoses for the unblocked and the blocked groups. You find that the unblocked group consists of equal numbers of psoriasis sufferers and skin cancer sufferers, while the blocked group consists of 90% psoriasis sufferers and 10% skin cancer sufferers. There are two possibilities: either sun blocker causes psoriasis or sun blocker prevents skin cancer but fails to prevent psoriasis. The known body of dermatology would suggest the latter. Likewise in the study in question, it is more likely that the study shows the failure of the vaccine to prevent B.1.135 infection than that the vaccine causes B.1.351 infection.

      (Note the line in the original article that says: “Our study design was not intended to deduce vaccine effectiveness against either variant, since we observe VOCs conditioned on infection, and do not measure absolute infection rates in the vaccinated or control population.)

      Regards,

      Russell

      Liked by 1 person

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