I would’ve guessed September due to schools and universities. Then there’s the magic bean branding of Poison AZ is worse than Poison PF. The illusion of choice.
So hypothetically we can sue the companies for damage from spike protein shedding, since we didn’t consent to take it into our body. Like trespassing, biochemically.
So good for you, the military in Australia is apparently using ‘task forces’ with the police to hold people down and inject them (chemical rape). I’ve asked for public videos I can link to about this, yet to see anything but it would make sense why Youtube suddenly suspended Sky News Australia. Why now?
Design and Analysis of Shedding Studies for Virus or Bacteria-Based Gene Therapy and Oncolytic Products Guidance for Industry
No pretending they didn’t know, this paper is six years old.
I’ve yet to see any proven limit to the shedding. Rumour has it they may stop after 2-4 weeks post each injection but this is unlikely. We know people have been producing spikes some 5 months later, so I’d wager eternal production that tapers off. This could be a straight AIDs.
See sections VI and also page 15.
“Shedding of such products may be intermittent and unpredictable”.
“higher potential for recombination or reversion in the patient, the shedding pattern and/or what is shed may change”
They’re supposed to already know, among other things:
“The duration of shedding, including the first and last day of shedding, and the peak period(s)”
Page 16 notes they need to study:
“• Whether the shed product was determined to be infectious.”
Watch the cop out:
“Because transmission to untreated individuals is an extremely low probability event,”
that is opinion, not fact
the point of science is checking
“monitoring such individuals for transmission is usually not required during the clinical
development of a product. However, if there is a potential for transmission, additional”
like a gain of function spike? That potential?
“data will be needed to assess that possibility; in which case, we recommend that sponsors
consult with OCTGT in connection with developing a monitoring plan.”
Monitoring. Not stopping. That’s it. And it’s probably why some of them were given placebo and saline. The shedding group?
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.
Self-reported vaccination for the current season was associated with a trend (P < 0.10) toward higher viral shedding in fine aerosol samples; vaccination with both the current and previous year’s seasonal vaccines, however, was significantly associated with greater fine-aerosol shedding in unadjusted and adjusted models (P < 0.01). In adjusted models, we observed 6.3 (95% CI 1.9–21.5) times more aerosol shedding among cases with vaccination in the current and previous season compared with having no vaccination in those two seasons.”
“The association of current and prior year vaccination with increased shedding of influenza A might lead one to speculate that certain types of prior immunity promote lung inflammation, airway closure, and aerosol generation. This first observation of the phenomenon needs confirmation. If confirmed, this observation, together with recent literature suggesting reduced protection with annual vaccination, would have implications for influenza vaccination recommendations and policies.”
“Prior immunity” promotes lung inflammation… Now I wanted to explain this part so that people wouldn’t be misled. Immunity and vaccination are not synonymous, in fact, this study provides the very evidence to prove that vaccinations like the influenza vaccine don’t provide immunity,
herd immunity is also a myth (search bar it)
hence the vaccinated being infected and spread it more. The correct wording should have read that “prior VACCINATIONS promote lung inflammation” as this fact has been shown in animal studies.
This means that when you receive a flu vaccine, elucidated by this study and animal studies, the lungs are damaged. Hence the scientific term/phrase “vaccine-associated enhanced respiratory disease” which in animal studies
has shown that flu vaccinations damage lung tissue of the vaccinated and distort or weaken the natural immunity of the host, person or animal. Could this be just one more reason more people are developing severe lung diseases like COPD or why the rates of asthma in America are increasing in the vaccinated?
The short and simple: The research shows…
The vaccine doesn’t protect one from infection.
That the vaccinated are “shedding”/spreading more virus simply by breathing.
That prior vaccination has weakened the immune systems of those who got the shot.
Individuals who receive the flu vaccine are placing others around them at greater risk than the unvaccinated.
Get the measles vaccine, and you won’t get the measles—or give it to anyone else. Right? Well, not always. A person fully vaccinated against measles has contracted the disease and passed it on to others. The startling case study contradicts received wisdom about the vaccine and suggests that a recent swell of measles outbreaks in developed nations could mean more illnesses even among the vaccinated.
more illnesses even among the vaccinated.
if ‘wisdom’ means marketing lies
When it comes to the measles vaccine, two shots are better than one. Most people in the United States are initially vaccinated against the virus shortly after their first birthday and return for a booster shot as a toddler. Less than 1% of people who get both shots will contract the potentially lethal skin and respiratory infection.
A cold is potentially lethal.
Water is potentially lethal.
Oxygen is potentially lethal.
And even if a fully vaccinated person does become infected—a rare situation known as “vaccine failure”—they weren’t thought to be contagious.
That’s why a fully vaccinated 22-year-old theater employee in New York City who developed the measles in 2011 was released without hospitalization or quarantine. But like Typhoid Mary, this patient turned out to be unwittingly contagious. Ultimately, she transmitted the measles to four other people, according to a recent report in Clinical Infectious Diseases that tracked symptoms in the 88 people with whom “Measles Mary” interacted while she was sick. Surprisingly, two of the secondary patients had been fully vaccinated. And although the other two had no record of receiving the vaccine, they both showed signs of previous measles exposure that should have conferred immunity.
A closer look at the blood samples taken during her treatment revealed how the immune defenses of Measles Mary broke down.
As a first line of defense against the measles and other microbes, humans rely on a natural buttress of IgM antibodies. Like a wooden shield, they offer some protection from microbial assaults but aren’t impenetrable. The vaccine (or a case of the measles) prompts the body to supplement this primary buffer with a stronger armor of IgG antibodies, some of which are able to neutralize the measles virus so it can’t invade cells or spread to other patients. This secondary immune response was presumed to last for decades.
Also a lie.
By analyzing her blood, the researchers found that Measles Mary mounted an IgM defense, as if she had never been vaccinated. Her blood also contained a potent arsenal of IgG antibodies, but a closer look revealed that none of these IgG antibodies were actually capable of neutralizing the measles virus. It seemed that her vaccine-given immunity had waned.
so…, antibody impotence?
assuming she ever had immunity
you just said “vaccine failure”, which means she was NEVER immune, despite being exposed to the vaccine
Although public health officials have assumed that measles immunity lasts forever, the case of Measles Mary highlights the reality that “the actual duration [of immunity] following infection or vaccination is unclear,” says Jennifer Rosen, who led the investigation as director of epidemiology and surveillance at the New York City Bureau of Immunization. The possibility of waning immunity is particularly worrisome as the virus surfaces in major U.S. hubs like Boston, Seattle, New York, and the Los Angeles area. Rosen doesn’t believe this single case merits a change in vaccination strategy—for example, giving adults booster shots—but she says that more regular surveillance to assess the strength of people’s measles immunity is warranted.
there are millions of diseases
If it turns out that vaccinated people lose their immunity as they get older, that could leave them vulnerable to measles outbreaks seeded by unvaccinated people—
but this case literally proves a fully “protected” person can CAUSE it
and if you ask about most outbreaks, “which % of that case group were already vaccinated for it?” they get angry and defensive and usually refuse to answer you
and the MSM doesn’t report it either… huh
which are increasingly common in the United States and other developed countries. Even a vaccine failure rate of 3% to 5% could devastate a high school with a few thousand students, says Robert Jacobson, director of clinical studies for the Mayo Clinic’s Vaccine Research Group in Rochester, Minnesota, who wasn’t involved with the study. Still, he says, “The most important ‘vaccine failure’ with measles happens when people refuse the vaccine in the first place.”