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...
I had to collect the knowledge about C19 because I barely survived the first months of 2020 and doctors knew nothing at that time. I've found NAC that protected my blood vessels, bromhexine that lowered the amount of TMPRSS2, and vitamin D that prevented the cytokine storm.
Thanks. The study measured electrostatic attraction, but that's only affects the chances of binding after a spike protein contacts an ACE2 receptor. If it is already there, it will try again until success. After binding, the virus has a long way to go to enter the cell, there are many factors at play.
The study shows a lower electrostatic attraction for Africans than for Europeans. C19 was almost non-existent in Africa and heavily affected Europeans, so it seems that the electrostatic attraction can explain a lot. But Africans in the US were twice as much affected as Whites, so there must be other factors that are even more important.
the "vaccine"'s delivery mechanism (lipid nanoparticles) were meant to attack reproductive organs. This was evidenced by the leaked Japanese FISA request from Pfizer
They pumped mice full of that stuff to see where it accumulates, so they can look closer at these places. We'll never know what they have found in humans. The viral vector vaccines (AstraZeneca, ..) have similar side effects as the mRNA vaccines but don't use nanoparticles.
The vaccines are a different beast than the virus, even if they use the same spike protein, because the spike protein alone is dangerous without binding to ACE2 receptors. Also, most vaccine side effects are caused by the immune reaction (two types of clotting, for example). In theory, the virus can cause these immune reactions too, but it seems that the immune system is able to sort dangerous antibodies out when there is an infection, and it cannot do that in a vaccine-induced pseudo infection.
(post is archived)