Blacks living in the US were more affected by the virus but blacks in Africa were less affected => it had nothing to do with the genes (the effect was most likely caused by vitamin D deficiency).
No. It's not one or the other. It's both.
White Europeans' ACE2 receptors have the highest binding affinity for the spike protein in the virus (that is also created by the vaccines). It's an ethnic bioweapon targeting Whites. It isn't targeting blacks. Niggers are in the middle in terms of vulnerability. The title of this post is bullshit.
Ashkenazi jews' ACE2 receptors have the lowest binding affinity for the spike protein, leaving them less likely to get severe disease than any other ethic group. I"m going to go ahead and guess that's not a cohencidence given kikes' proclivity to poison/genocide Whites throughout history..
It's also true that vitamin D helps, but it's also true that it was meant as a bioweapon to kill White Europeans (and South Asians).
The ACE2 receptor binding affinity for the spike protein may play a role, but only a small one. The amount of ACE2 receptors plays a bigger role (smokers have many more than non-smokers but are protected by nicotine), and the amount of TMPRSS2 molecules on the cell surface is the most important factor because the virus cannot enter the cell without it.
To target a virus for one group without affecting another, the targeted DNA must be exactly known. SARS-2 was not meant to kill (the spike protein is dangerous but the virus had no payload) but for data collection. They used the PCR tests to collect billions of DNA samples and now they have all the information needed to attack targeted groups.
The ACE2 receptor binding affinity for the spike protein may play a role, but only a small one.
I've referenced in this tic-toc idiot clip many times. Specifically, ashkenazi jews have a far higher frequency of the K26R variant which inhibits binding of the spike protein. The difference in calories per mol is substantial and when we're talking about exponential replication, it's relatively safe to assume these differences in binding affinity would translate into exponential differences in disease progression and viral replication, as well as the toxicity of the spike protein created from mRNA vaccines.
What evidence do you have that this difference is "a small one"?
The amount of ACE2 receptors plays a bigger role (smokers have many more than non-smokers but are protected by nicotine), and the amount of TMPRSS2 molecules on the cell surface is the most important factor because the virus cannot enter the cell without it.
Again, what evidence do you have to support this claim that the "amount of ACE2 receptors plays a bigger role"?
To target a virus for one group without affecting another, the targeted DNA must be exactly known. SARS-2 was not meant to kill (the spike protein is dangerous but the virus had no payload) ...
The original variant was far more dangerous, and the spike protein from the original variant was equally nasty. I know several elderly but healthy people who caught it before it was amplified by the jew media, and it nearly killed all of them. All still have adverse health effects from their illness in Q1 2020.
It wasn't meant to kill as a primary function, but the "vaccine"'s delivery mechanism (lipid nanoparticles) were meant to attack reproductive organs. This was evidenced by the leaked Japanese FISA request from Pfizer - their own study of their own vaccine showed the lipid nanoparticles concentrating in the ovaries of rats.
...but for data collection. They used the PCR tests to collect billions of DNA samples and now they have all the information needed to attack targeted groups.
Entirely possible, but a change of subject.
Genuinely looking forward to substantiation of your various claims above, although I suspect your apparent advanced knowledge of the topic increases the chances you work for the DOD, a pharma company, or mossad...
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