Almost every organ had high levels, almost. Almost total infestation. Almost like someone injected it!
Boosters push and more explained at bottom.
“The first-ever postmortem study of a patient vaccinated against COVID-19 has revealed that viral RNA was found in every organ of the patient’s body, meaning that the vaccine is either ineffective or the coronavirus actually spreads faster in vaccinated individuals.”
Both. But more Latter. And more fatal. I already covered the jabbed dead versus normal. Jabbed are literally more likely to die from it. MSM is hiding this and going on about symptoms. Dead people have reduced symptoms, can confirm.
“A previously symptomless 86-year-old man received the first dose of the BNT162b2 mRNA COVID-19 vaccine. He died 4 weeks later from acute renal and respiratory failure. Although he did not present with any COVID-19-specific symptoms, he tested positive for SARS-CoV-2 before he died. Spike protein (S1) antigen-binding showed significant levels for immunoglobulin (Ig) G, while nucleocapsid IgG/IgM was not elicited. Acute bronchopneumonia and tubular failure were assigned as the cause of death at autopsy;
however, we did not observe any characteristic morphological features of COVID-19.
Postmortem molecular mapping by real-time polymerase chain reaction revealed relevant SARS-CoV-2 cycle threshold values in all organs examined (oropharynx, olfactory mucosa, trachea, lungs, heart, kidney and cerebrum) except for the liver and olfactory bulb. These results might suggest that the first vaccination induces immunogenicity but not sterile immunity.”
So to save 86 year-olds, for like, six months, we need to damage all young adults and children? Fucking locusts. Are the Bad Boomers in power pushing this a Biblical plague? Maybe the jab itself is more Boomer Doomer than the wild virus.
It makes sense the liver would be clear because the liver’s function is clearing that shit but finding it in the heart? Goner. Dead man walking. Kidney? Suggests liver moved it there. Cerebrum? Yep, zombie.
Maybe the liver pushed it out of the liver, and back into the bloodstream, infecting the brain?
Old people and some heavily disease-burdened (like STDs) have thin blood brain barrier.
The cerebrum or telencephalon is the largest part of the brain containing the cerebral cortex, as well as several subcortical structures, including the hippocampus, basal ganglia, and olfactory bulb. In the human brain, the cerebrum is the uppermost region of the central nervous system.Wikipedia
All we need is psychosis and they’re literal zombies. Maybe the psychotic break happens later, once it’s really stewed in the brain juices for a while. It’s written off as dementia in old people so may already be happening. Maybe they get a form of terminal agitation in addition. I do actually know my stuff. When it’s in the basal ganglia you are absolutely screwed. That’s motor control. It’s in the hippocampus possibly explaining the terminally stupid decision to get a second one. It’s damaging memory then, which suggests senility symptoms oncoming. I wonder if it’s more likely to kill small or large amygdala people faster. Likely smaller.
What is the overall effect of this death stick? Advanced cellular senescence? Meaning the average age of death would be those with least lifespan left, presently seen, but that will just keep getting younger and younger and younger. Logan’s Run modRNA mod? So a basic model we assume their remainder lifespan is cut in half.
Does this help pension plans and national debt?
Well assuming 80 is lifespan (slightly shorter in men, who are dying faster from this…)
then a 60yo would die at 70,
a 50yo would die at 65,
a 40yo at 60,
a 30yo at 55,
a 25yo at ~50.
a 20yo at <50,
a 10yo at 45
a 5yo at 40 … etc. Down to school age.
Nobody would die before 35 except anomalies. Do we see this? Why try to deny those unless pattern?
Anomalous deaths would be acute advanced senescence. Intention may be largely chronic.
They can blame global warming.
So, yes. That’s very neat. A lot of younger fertile people getting it would die around menopause/manopause. Hence, perfect economic efficiency is achieved. The aging (genetic void) population dies off as soon as reproduction is achieved. We’d need at least ten years to see if average lifespan has gone down (80 to 70). Assuming this simple model. Younger Boomers and Gen Xers are the ones to watch. A reversal of lifespan is unprecedented. This is the slowest kill model and explains the push until 2023*. We’ll begin to notice by then en masse. This is why new techs need a decade PLUS of human trials. They look at lifespan.
*MPs love the book Nudge.
Has the NHS guaranteed treatment for genomic ‘vaccine’ damage? No. Nobody is talking about this.
Experimental subjects are considered consenting adults, so may not be eligible for NHS treatment.
Add in a sterilising effect especially in men, STD transmission, and the guidestones would be about right.
If that basic of the most basic models is correct, then the kids currently injected will die shortly after their feckless parentals.
Remember, saving the NHS also means fewer old people burdening it like lampreys. They could come out later and thank you for your willing participation, since you did technically save the NHS – by dying younger.
Experiments are permitted to legally deceive you, so long as they debrief you. In 2023.
By accelerating aging population, that’s very eugenic technically but deeply wrong re family. Surplus of orphans. Pedo paradise. Adult IQ would be higher (and GDP shoot up) since the morons would’ve happily skipped along for the euthanasia, children in tow.
The average age is 80-something now because they have no remainder, so it becomes weeks, not years. It fits.
And there’s no known time limit on shedding those synthetic SPs, secondhand smoke-like. At a certain uptake, society may be fumigating itself. Birth rates already have tanked. We may need a leper colony. They could be lifelong biohazards. They could easily test their exhalation at different points post-experimental injections. PE majors have a tube you breathe into, they could easily do it. The fact they don’t means they know the result would make them hated. Could be like the Island 2005 film.
The basal ganglia are a group of subcortical nuclei, meaning groups of neurons that lie below the cerebral cortex. The basal ganglia is comprised of the striatum, which consists of the caudate nucleus and the putamen, the globus pallidus, the subthalamic nucleus, and the substantia nigra The basal ganglia are primarily associated with motor control, since motor disorders, such as Parkinson’s or Huntington’s diseases stem from dysfunction of neurons within the basal ganglia. For voluntary motor behavior, the basal ganglia are involved in the initiation or suppression of behavior and can regulate movement through modulating activity in the thalamus and cortex. In addition to motor control, the basal ganglia also communicate with non-motor regions of the cerebral cortex and play a role in other behaviors such as emotional and cognitive processing.
If it retarded them, I doubt any of us would notice.
An earlier coronavirus vaccine paper: why boosters and well, all of this really
Vaccines against infectious bronchitis of chickens (Gallus gallus domesticus) have arguably been the most successful, and certainly the most widely used, of vaccines for diseases caused by coronaviruses, the others being against bovine, canine, feline and porcine coronaviruses. Infectious bronchitis virus (IBV), together with the genetically related coronaviruses of turkey (Meleagris gallopovo) and ring-necked pheasant (Phasianus colchicus), is a group 3 coronavirus, severe acute respiratory syndrome (SARS) coronavirus being tentatively in group 4, the other known mammalian coronaviruses being in groups 1 and 2. IBV replicates not only in respiratory tissues (including the nose, trachea, lungs and airsacs, causing respiratory disease), but also in the kidney (associated with minor or major nephritis), oviduct, and in many parts of the alimentary tract–the oesophagus, proventriculus, duodenum, jejunum, bursa of Fabricius, caecal tonsils (near the distal end of the tract), rectum and cloaca (the common opening for release of eggs and faeces), usually without clinical effects. The virus can persist, being re-excreted at the onset of egg laying (4 to 5 months of age), believed to be a consequence of the stress of coming into lay. Genetic lines of chickens differ in the extent to which IBV causes mortality in chicks, and in respect of clearance of the virus after the acute phase. Live attenuated (by passage in chicken embryonated eggs) IBV strains were introduced as vaccines in the 1950s, followed a couple of decades later by inactivated vaccines for boosting protection in egg-laying birds. Live vaccines are usually applied to meat-type chickens at 1 day of age. In experimental situations this can result in sterile immunity when challenged by virulent homologous virus. Although 100% of chickens may be protected (against clinical signs and loss of ciliary activity in trachea), sometimes 10% of vaccinated chicks do not respond with a protective immune response. Protection is short lived, the start of the decline being apparent 9 weeks after vaccination with vaccines based on highly attenuated strains. IBV exists as scores of serotypes (defined by the neutralization test), cross-protection often being poor. Consequently, chickens may be re-vaccinated, with the same or another serotype, two or three weeks later. Single applications of inactivated virus has generally led to protection of <50% of chickens. Two applications have led to 90 to 100% protection in some reports, but remaining below 50% in others. In practice in the field, inactivated vaccines are used in laying birds that have previously been primed with two or three live attenuated virus vaccinations. This increases protection of the laying birds against egg production losses and induces a sustained level of serum antibody, which is passed to progeny. The large spike glycoprotein (S) comprises a carboxy-terminal S2 subunit (approximately 625 amino acid residues), which anchors S in the virus envelope, and an amino-terminal S1 subunit (approximately 520 residues), believed to largely form the distal bulbous part of S. The S1 subunit (purified from IBV virus, expressed using baculovirus or expressed in birds from a fowlpoxvirus vector) induced virus neutralizing antibody. Although protective immune responses were induced, multiple inoculations were required and the percentage of protected chickens was too low (<50%) for commercial application. Remarkably, expression of S1 in birds using a non-pathogenic fowl adenovirus vector induced protection in 90% and 100% of chickens in two experiments. Differences of as little as 5% between the S1 sequences can result in poor cross-protection. Differences in S1 of 2 to 3% (10 to 15 amino acids) can change serotype, suggesting that a small number of epitopes are immunodominant with respect to neutralizing antibody. Initial studies of the role of the IBV nucleocapsid protein (N) in immunity suggested that immunization with bacterially expressed N, while not inducing protection directly, improved the induction of protection by a subsequent inoculation with inactivated IBV. In another study, two intramuscular immunizations of a plasmid expressing N induced protective immunity. The basis of immunity to IBV is not well understood.
Serum antibody levels do not correlate with protection, although local antibody is believed to play a role.
Adoptive transfer of IBV-infection-induced alphabeta T cells bearing CD8 antigen protected chicks from challenge infection. In conclusion, live attenuated IBV vaccines induce good, although short–lived, protection against homologous challenge, although a minority of individuals may respond poorly. Inactivated IBV vaccines are insufficiently efficacious when applied only once and in the absence of priming by live vaccine. Two applications of inactivated IBV are much more efficacious, although this is not a commercially viable proposition in the poultry industry.
However, the cost and logistics of multiple application of a SARS inactivated vaccine would be more acceptable for the protection of human populations, especially if limited to targeted groups (e.g. health care workers and high-risk contacts). Application of a SARS vaccine is perhaps best limited to a minimal number of targeted individuals who can be monitored, as some vaccinated persons might, if infected by SARS coronavirus, become asymptomatic excretors of virus, thereby posing a risk to non-vaccinated people.
Looking further into the future, the high efficacy of the fowl adenovirus vector expressing the IBV S1 subunit provides optimism for a live SARS vaccine, if that were deemed to be necessary, with the possibility of including the N protein gene.