All mainstream media eyes are NOT on Israel anymore. The vaccination world champion has disappeared from the headlines. Why?
In Israel, the number of those testing positive for SARS-Cov-2 has exploded, and this, it could be written, despite the fact that in Israel about 63% of the population is fully vaccinated.
Criteria that vaccines must meet
It looks more like cases are exploding BECAUSE the majority of Israelis are at least doubly vaccinated against SARS-CoV-2. Not only does vaccination seem to increase their susceptibility to infection, it also seems to create more virulent variants of SARS-CoV-2.
In March 2017, Andrew Read and David Kennedy published a paper in the Proceedings of the Royal Society B titled “Why does drug resistance readily evolve but vaccine resistance does not?” (See appendix at end)
In the paper, they develop three necessary conditions, they give three criteria that vaccines must meet in order for viruses or bacteria not to succeed in escaping vaccine-induced protection and spawning more virulent and dangerous variants:
- Vaccines must not attack only a small part of the virus or bacterium, they must stimulate the production of a variety of different antibodies in the immune system.
- Vaccines MUST prevent vaccinated individuals from becoming infected, prevent a virus or bacterium from replicating in vaccinated individuals as a result, and prevent it from being passed on by vaccinated individuals.
- Vaccines MUST NOT be used during an epidemic.
The current mass vaccination and the vaccines used in it violate each of the three criteria. What we are seeing in Israel or the UK is nothing more than the consequence of this.
To argue this, a little change of scenery.
Are you familiar with Marek’s Disease? Marek’s Disease is a disease caused by a herpes virus.
Marek’s Disease is usually fatal for those who contract it.
Marek’s Disease is transmitted in dust particles that are spread through the feathers of usually chickens.
Marek’s Disease has killed millions of chickens.
This changed when a vaccine against Marek’s Disease was introduced in 1970. The virulence of the herpes virus seemed to be broken, and the number of cases dropped dramatically. Until Marek’s Disease resurfaced and necessitated a new, modified vaccine. In 1983, the new vaccine was approved. Then, in the early 2000s, the third vaccine, again altered. The herpes virus that causes Marek’s Disease has apparently been able to change so that it was no longer recognized by vaccines. One pathway by which the virus accomplished this feat was described by Andrew Read and a number of co-authors in a 2015 paper published on Plos One.
The title of the paper, “Imperfect Vaccination Can Enhance the Transmission of Highly Virulent Pathogens.” In this paper, Read et al. (2015) show that a vaccine that does not prevent vaccinated individuals from becoming infected, allows the virus to replicate in vaccinated individuals and be passed on by vaccinated individuals, and mutates into far more virulent, far more dangerous variants. Their study population: chickens. Vaccinated chickens that had contracted Marek’s Diesase spread many more far more virulent variants of the virus than did unvaccinated, diseased chickens. Vaccinating the chickens obviously resulted in Marek’s Disease not only not being suppressed, but improved in its virulence, transmissibility and spreadability.
One of the criteria of useful vaccination is injured
Rapidly mutating viruses in particular, such as RNA viruses, present vaccines with almost insoluble problems. If an RNA virus replicates ONCE, then on average one replication error, one mutation, occurs per 10,000 nucleotides. SARS-CoV-2 consists of about 30,000 nucleotides. The problem is compounded by the high replication rate of viruses, which can result in several billion virus particles in the blood after only a few days.
The high rate of replication and mutation is the reason why the genetic pool that makes up a virus is very diverse, for example, consisting of countless different genomes of SARS-CoV-2. But the high mutation rate is only one problem that RNA viruses provide for vaccines. In most cases, the effect of vaccines wears off over time. For vaccines against COVID-19, different studies arrive at a duration of action of 60 to 180 days. After 6 months at the latest, the protective spook is over.
It has long been known that vaccine protection fades. Accordingly, researchers have attempted to respond. One form of response is acellular vaccines. Acellular vaccines carry only a fragment of the virus, such as part of the spike protein.
Acellular vaccines were developed in connection with vaccination against pertussis. Pertussis is caused by a bacterium, Bordetella pertussis. The first vaccine approved against Bordetella pertussis was an inactivated vaccine that caused a number of side effects, including epileptic seizures. Back then, in the 1990s, researchers were concerned about few side effects. Today, in the age of mass vaccination hysteria, millions of side effects are no longer worth mentioning.
Acellular vaccines carrying a question element of the virus were approved for pertussis in the late 1990s and were able to eliminate the known side effects. At the cost of new, unexpected consequences: Vaccine protection disappeared over time, and a whooping cough epidemic in the U.S. and elsewhere was one of the consequences.
This “side effect” of vaccination against whooping cough, the whooping cough epidemic brings scientists from the Netherlands on the plan:
Their revolutionary idea: the epidemic is the result of vaccination: vaccination has INCREASED the virulence of Bordetella pertussis. The revolutionary idea, which people do not like to talk about, especially today, has another uncomfortable side effect: it has been proven to be correct:
In this paper, Lam et al. (2014) show that a variant of Bordetella pertussis has become predominant that no longer contains the protein “pertactin” but has replaced it. The vaccine developed against Bordetella pertussis targeted the immune system to this very protein, just as COVID-19 vaccines now target the human immune system to the spike protein. Then in 2017, the U.S. CDC confirmed that the U.S. is almost exclusively home to variants of Bordetella pertussis that do NOT contain pertactin.
No one doubts that the result of the study by Lam et al. (2014) is a consequence of vaccination. Vaccination against whooping cough has caused the bacterium that causes whooping cough to mutate in a way that renders the vaccine ineffective. The requirement that vaccines create a diverse army of antibodies is a direct result of such findings, to preclude the possibility that a virus can easily pull itself out of the vaccine affair by making a few mutations. In the development of COVID-19 vaccines, this knowledge was wiped off the table.
What is true for bacteria is even more true for viruses
Hepatitis B is a virus that causes liver damage. A vaccine against hepatitis B, which elicits an immune response that directs the human immune system to a hepatitis B surface antigen, was approved in the U.S. in 1989. Just one year later, there were the first reports of fully vaccinated individuals contracting hepatitis B. Just as there are reports today of fully vaccinated people contracting COVID-19.
A number of studies conducted primarily in Taiwan have attributed vaccine failure to the same phenomenon: a variant of hepatitis B that no longer contained the antigen to which vaccines have targeted the human immune system. Ergo, heptatitis B was no longer recognized by the vaccinated immune system. In the period from 1984 to 1999, researchers were able to show, the proportion of hepatitis viruses that no longer contained the antigen relevant to the vaccine increased from 7.8% to 23.1%, as a direct result of vaccination.
Prevnar 7 is a vaccine developed to eliminate streptococci, streptococci that are responsible for pneumonia or meningitis. The problem: There are about 90 serotypes of Streptococcus pneumoniae. Prevnar7 targets seven of them, believed to be the most harmful. The question that usually arises in such a context: What happens to the 70+ remaining serotypes?
William P. Hanage and Marc Lipsitch, both of Harvard University, among others, have answered that question.
Prevnar7 was very efficient against the seven serotypes. They were almost completely eliminated. However, other serotypes, especially 19A, took their place. The result was the same as before vaccination: widespread illness from pneumonia caused by streptococci. The response to this development: Prevnar13. Prevnar13, a result of the same logic at work again today in trying to fill the gaps in first-generation COVID-19 vaccines with frantically concocted booster shots, added 19A to the list of 13 target serotypes.
Result: same. 19A was eliminated. Other serotypes took its place. In a paper published in 2017, authors led by Marc Lipsitch and William P. Hanage conclude that once again, Prevnar13 is able to eliminate the 13 addressed serotypes, meanwhile a number of other serotypes take the place of those eliminated and continue to cause pneumonia and meningitis. Twice the Prevnar vaccine has led to the pathogen “Streptococcus pneumoniae” being completely changed, its population exchanged.
And while vaccination with Prevnar7 and Prevnar13 administered to children can at least claim that the incidence among children has decreased, results from England and Wales show that this decrease has been bought with an increase of corresponding cases among the elderly. Clearly, vaccinated children are better able than unvaccinated children to spread Streptococcus pneuomiae in a vaccine-optimized variant that is better able to infect adults.
That vaccines alter the population of a pathogen has long been known. Either the change occurs by allowing the virus to mutate blithely in the organism of vaccinated individuals, or it occurs by allowing variants of the virus that escape the vaccine to become predominant variants.
Both forms of evolution of viruses cannot be prevented when viruses mutate too rapidly to be eliminated. The mass vaccinations that are currently taking place, which violate all three of the above criteria (1) vaccines must induce a diverse immune response, (2) must prevent infection, replication, and spread of the virus from or by those vaccinated, and (3) must not be used in times of virulent epidemic, are a means of not only amplifying but focusing all of the problems associated with vaccines to have produced some sort of super-bug, super-virus in the end.
The vaccines that are currently being used are part of what is known as a “leaky vaccine.” Leaky vaccines protect against severe disease within limits, but do not prevent infection, let alone replication and spread of the virus by vaccinated individuals. The consequences are more or less dramatic: Such vaccines allow viruses to replicate and mutate in the organism of the vaccinated.
The result is the consequence we described at the beginning of this article in relation to the research of Andrew Read: Virulence of the virus increases. Vaccines fail. Vaccinated individuals evolve into superspreaders. That vaccines against COVID-19 have this consequence, that has already been empirically demonstrated. When virulence increases, the frequency of infection increases among both vaccinated and unvaccinated people.
We are currently living in a great experiment in people
Whether those responsible will be held accountable by future generations is an open question. That the current vaccination mania is a recipe for health catastrophe, on the other hand, does not seem to be an open question.
In 2012, Andrew Read and Vicky Barclay showed that a “leaky” malaria vaccine that did not prevent infection with, replication of, and spread of Plasmodium, the single-celled parasite that causes malaria, but at best protected against severe disease, produced new variants of true super-parasites, parasites that were even faster at killing red blood cells and even faster at replicating.
Vaccination protects, you say. Not always, we say. Especially not if the vaccines violate the three criteria mentioned at the beginning. COVID-19 vaccines violate each of the three criteria.
Why does drug resistance develop easily but not vaccine resistance?