Underreported and essentially invisible within the mainstream news cycles, a critical shortage of ordinary U.S. medicine has been growing and becoming an emergency situation for many families. If rationing kicks in fully, be careful about what you post on social media. Determining allowances based on political ideology is a real concern.
In a general sense the issue is mostly an outcome of the U.S. outsourcing drug ingredient procurement and manufacture to China and India. Many companies in both of those countries have been struggling with operational interruptions as a result of COVID-19. As supplies in the U.S. rapidly dwindle, local news media outlets are now starting to pick up on the issue. WATCH:
(Via Fox Business) – The nationwide shortage of basic antibiotics and critical medications that treat chronic conditions and bacterial infections has become the latest issue to hit the medical world. Consequently, it is forcing many doctors to rely on alternative medicines to treat patients.
“What was once an unthinkable situation—a shortage of basic antibiotics such as amoxicillin and Augmentin to treat ear and skin infections or even medications such as Albuterol to treat asthma—is now a harsh reality,” New York City-based emergency room physician Dr. Robert Glatter told FOX Business.
Even the “shortage of basic medications such as children’s Tylenol—integral to treating fever and mild to moderate pain—is impacting our ability to provide care for our patients,” Glatter said.
Currently, the Food and Drug Administration (FDA) has a list of more than 180 current or resolved drug shortages. He said there have been shortages of antivirals such as Tamiflu, which is used to treat high-risk patients with influenza, as well as diabetic medications such as Ozempic due to the “inappropriate and off-label use” of the medication for weight loss and cosmetic purposes.
Glatter predicted that the drug shortage problem rippling throughout the U.S. could last for at least another year, if not longer.
According to federal health officials, intermittent or reduced availability of certain products can occur for many reasons, including manufacturing and quality problems, delays and discontinuations.
However, Glatter said that the problem is in part because the U.S. is currently facing challenges in obtaining raw materials. For instance, source materials for manufacturing the active pharmaceutical ingredients in the majority of drugs come from China, which is dealing with limited production and output of raw materials involved in pharmaceutical manufacturing due to rigid lockdown measures, Glatter said.
The U.S. is also dependent on India for a significant number of generic medications, but India also relies on China for the raw materials used to produce active pharmaceutical ingredients, he added. (read more)
Data from the Centers for Disease Control and Prevention (CDC) showed that vaccinated and boosted people made up most of the COVID-19 deaths in August. EVERY person I personally know who has had problems from blood clots to being rushed to the hospital was vaccinated. I went to get my hair cut, yes what’s left of it, and the two women there both lost their sons-in-law in their 20s after being vaccinated.
Meanwhile, Fauci, finally under oath, could not name a single study that showed that masks ever worked. Indeed, there were many studies that showed that masks never worked during the 1918 Spanis Flu. Indeed, the CDC even conceded that cloth masks never worked.
Initially, Fauci spoke the truth that masks were useless. All the studies from the 1918 Spanish Flu confirmed that masks never worked and the Washington Postsaid they were “useless.” Everyone knows that the Post is so left they could never walk a straight line. Here is a 2009 study of the 1918 Spanish Flu.
Fauci 2009 Influenza 1918 study
Now the head of Pfizer has refused to testify before the European Parliament. Let’s face the facts. This entire COVID scam was carried out with the full knowledge of those at the very top. It was done for the purpose of creating this Great Reset Agenda. It was being pushed by the WEF and Klaus Schwab for political purposes. Remember how the WEF was telling us it was so great to lock everyone down? And now, they claim the inflation has nothing to do with shortages, but Putin’s invasion of Ukraine. They really think everyone, of the vast majority anyhow, is outright stupid and will believe whatever they say.
These people should be removed from any power and imprisoned for life. Of course, there is no possible justice when the very people apply their laws ONLY to us, and never act in an ethical manner themselves.
On October 7, the Office of Florida’s Surgeon General Joseph A. Ladapo, MD, PhD, issued an announcement recommending “against males aged 18 to 39 from receiving mRNA Covid-19 vaccines.” [link] This created quite a stir as his advice goes against the recommendations of the Centers for Disease Control and Prevention (CDC) and numerous other scientific organizations.
Dr. Ladapo cited a Florida health dept study showing an 84% increase in the incidence of cardiac-related death among males 18-39 years old within 28 days following mRNA vaccination. Immediately Dr. Ladapo became a target by federal officials, big tech and defensive media. {Direct Rumble Link} Dr. Ladapo appeared on Tucker Carlson last night to discuss. WATCH:
.
| Dear friend,I wrote “The Real Anthony Fauci” so that Americans — both Democrat and Republican — can understand Dr. Fauci’s pernicious role in allowing pharmaceutical companies to dictate a COVID-19 response that trampled public health, the global economy, our constitutional rights and all the traditional values of liberalism.Despite the suppression of media coverage, the book became a bestseller.Selling over 1,000,000 copies since the release in November 2021.Spending 17 weeks on the New York Times Best Sellers list.Soaring to #1 on Amazon, over three months.Appearing on Wall Street Journal, USA Today, and Publisher’s Weekly bestseller lists.Instead of fostering transparency and respectful debate, and implementing the traditional, well-established public health strategies for countering pandemics, Dr. Fauci promoted a militarized and monetized response including draconian lockdowns, business closures, coercive vaccination with experimental jabs, and a litany of totalitarian controls that transformed our country into a surveillance state and racked up the world’s highest COVID-19 body count.He then worked with Big Pharma, media and social media titans, and Pentagon and intelligence agencies to vilify and marginalize dissent, punish every attempt at questioning, and to gaslight skeptics. Government worked with media and social media titans to ban books, silence physicians and scientists, and condemn artists, writers, poets, and intellectuals who questioned the unscientific orthodoxies of the medical and biosecurity cartels.CHD has partnered with our friends at Revealed Films to transform my book into a compelling documentary that exposes the corrupt reign of the “nation’s most trusted doctor,” Dr. Fauci and his accomplices in a coup d’etat that almost developed.The documentary will stream for FREE on October 18, 2022.We need your support to be able to conquer the censorship and ensure that millions of people are able to view the film. Together we can get the truth to the masses and reveal the story of “The Real Anthony Fauci.” |
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In truth, Robert F. Kennedy, Jr. Chairman, Children’s Health Defense  |
Link to the site with information on the coming movie
#TrishRegan #Fauci #Fed
Markets are waiting on Jerome Powell’s speech at Jackson Hole this Friday…and any way you slice it, it won’t be good for the economy or for Wall Street. Powell messed up bigtime and the American economy is stuck paying the price. On the bright side, Anthony Fauci is (finally) retiring! Join me for a look at today’s headlines.
Siraj and Jay discuss the CDC admitting to f*cking up the COVID-19 pandemic response, Liz Cheney gets ousted from Congress, developments in the FBI raid of Trump’s home at Mar-A-Lago, and the one-year anniversary after the catastrophic Afghanistan withdrawal. It’s everything that makes you want to drink on Habibi Power Hour.
Exposure of a highly C-19 vaccinated population to monkeypox virus (MPV) spilling over from an animal reservoir promotes asymptomatic human-to-human transmission in susceptible sexual minority communities (SMCs). MPV infection in SMCs could therefore evolve more infectious viral variants that spread to all parts of a highly C-19 vaccinated population and thereby prevent establishment of herd immunity
Increasing numbers of outbreaks of human monkeypox have been reported from across central and west Africa over the last 3-4 decades. Zoonotic infection with MPV in the current setting of limited smallpox vaccination and little orthopoxvirus immunity[1] in several parts of the world renders human populations more susceptible to contracting monkeypox disease. MPV has therefore been considered a well-suited candidate for a global epidemic.
As productive poxvirus infection is mostly symptomatic and viral transmission almost exclusively occurs through close contact with an infected animal or person or via virus-contaminated objects, such as bedding or clothing, it has been generally acknowledged that natural epidemic outbreaks in humans can largely be contained through basic infection-prevention measures (including good hygiene practices). Unless the viral infection rate is high (e.g., in densely populated areas and poor [environmental] hygiene conditions), it is difficult to imagine how MPV could evolve to adapt to the human population, let alone how it could ignite a multi-country epidemic or even a pandemic in countries where MPV is not an endemic zoonosis. Pandemics typically occur with pathogens that cause so-called acute self-limiting infection, meaning that they have the potential to spread asymptomatically before inducing a type of natural immunity that prevents productive infection upon subsequent exposure and, therefore, generates herd immunity. Whereas until recently many still tended to believe that the threat of a globally spread MPV was a myth, cases are now being reported globally (at least in all highly C-19 vaccinated parts of the world) to the extent that WHO has now declared MPV a health emergency of international concern—all of this has happened within just a few months. This does not provide enough time for population-level innate immunity to become sufficiently trained to turn MPV infection, which is typically symptomatic (so-called ‘acute self-limiting viral disease’, ASLVD) into an infection that is predominantly asymptomatic (so-called ‘acute self-limiting viral infection’, ASLVI) and can therefore much more easily spread between people. On the other hand, adaptation of a virus to a new host population never implies natural selection of less infectious viral variants, on the contrary. If neither viral evolution nor immune training is responsible for shifting symptomatic into asymptomatic viral transmission (thereby allowing MPV to spread more efficiently from person-to-person and eventually become a pandemic), other non-evolutionary disease-mitigating influences must be considered. As spread of MPV is now particularly expanding in countries with high C-19 vaccine coverage rate and as ASLVD-enabling viruses that are predominantly transmitted through close contact do not spread rapidly, there must be a link between the type of population-level immunity in highly C-19 vaccinated populations and the rapid expansion in prevalence of MPV cases. It’s also important to note that—so far— MPV disease symptoms in these populations have been rather ‘mild’ and predominantly manifest in individuals from the gay and bisexual male community. This already suggests that sexual contact, especially when the latter is at risk of traumatizing the skin or mucosa (e.g., in case of anogenital intercourses), facilitates symptomatic MPV infection.
While I cannot unambiguously prove this, I strongly believe that the sudden emergence of a significant number of (mild) cases of MPV in highly C-19 vaccinated countries is not purely coincidental but related to enhanced activation of broadly reactive, MHC-unrestricted CD8+ T cells in vaccinees. I have previously reported on how a universal CTL (cytotoxic T lymphocyte) epitope can facilitate elimination of host cells infected with ASLVI- or ASLVD-enabling glycosylated viruses and thereby allow recovery from disease, however without inducing immunologic memory (https://www.voiceforscienceandsolidarity.org/scientific-blog/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment). More specifically, MHC-unrestricted CD8+ T cells that now increasingly prevent C-19 disease in healthy vaccinees are the same as those required to abrogate productive infection with other glycosylated viruses that have evolved reduced susceptibility to our innate immune system[2], including poxviruses (https://www.frontiersin.org/articles/10.3389/fimmu.2021.740223/full).
Given the enhanced immune activation of pathogen-nonspecific CTLs[3] in C-19 vaccinees, MPV infection in C-19 vaccinees is likely to become abrogated at an early stage of productive infection, thereby dampening productive MPV infection and potentially causing asymptomatic/ mild infection in sexual minority communities (SMCs) of a highly C-19 vaccinated population. Consequently, MPV infection may even fail to induce MPV-neutralizing antibodies (Abs) in vulnerable[4], C-19-vaccinated individuals that are immunologically naïve to MPV (i.e., today persons younger than 45 to 55 years of age, depending on the country). However, it is reasonable to assume that asymptomatic MPV infection may elicit short-lived, low affinity anti-MPV Abs in these individuals (as has, for example, been reported in case of asymptomatic infection with SARS-CoV-2 (SC-2; https://www.medrxiv.org/content/10.1101/2020.06.22.20137141v2.full.pdf). As asymptomatic infections promote viral transmission within these minority communities, the infection rate of MPV in this vulnerable subpopulation is likely to grow over time. This rise in viral infection rate will subsequently increase the likelihood for previously asymptomatically infected persons from SMCs to become re-infected while titers of their short-lived, low-affinity anti-MPV antibodies are still relatively high. Binding of such low-affinity, non-neutralizing Abs to the virus is thought to enhance viral infectiousness and could thereby cause a disease outbreak in these communities. It is, therefore, reasonable to expect that the proportion of vulnerable individuals who develop virus-neutralizing Abs (i.e., upon their recovery from MPV disease[5]) in the C-19 vaccinated part of the population will increase over time. However, in vulnerable, non-C-19-vaccinated individuals, trained innate immune cells (i.e., NK cells) are likely to prevent MPV from breaking through this first line of immune defense and would therefore largely prevent priming of virus-neutralizing Abs. For the time being, symptomatic manifestations in highly C-19 vaccinated populations are predominantly mild and mostly occurring in SMCs. This suggests that even in cases of symptomatic infection, viral clearance via innate or adaptive cytolytic immune cells (in the case of non-C-19 vaccinated or C-19 vaccinated, respectively) is still effective enough to prevent more problematic symptomatology in most cases.
Rising virus-neutralizing Ab titers can only prevent monkey disease but not viral infection. Hence, re-exposure to MPV of C-19 vaccinated individuals who are in the process of seroconverting promotes natural selection of more infectious MPV immune escape variants while fostering asymptomatic transmission and thereby contributing to a further rise in viral infectious pressure. Due to the steadily growing infection rate in SMCs of highly C-19 vaccinated populations, the overall MPV-neutralizing Ab response in these communities is likely to exert suboptimal immune pressure on viral infectiousness and can therefore be expected to drive dominant circulation of naturally selected, more infectious MPV immune escape variants. Based on all the above, the enhanced infection rate mediated by asymptomatic transmission of MPV in SMCs of highly C-19 vaccinated populations is likely to increase the probability of adaptive evolution of MPV in these communities. It is, therefore, critical to monitor the selective landscape of MPV as unfolded in SMCs of highly C-19 vaccinated populations in order to verify whether the evolutionary trajectory is shifting towards promoting natural selection and expansion of immune escape variants that are more infectious (as is smallpox virus, for example).
Vaccination of vulnerable groups (SMCs) against MPV is likely to accelerate adaptive evolution of MPV in highly C-19 vaccinated populations and could thereby raise the incidence of (severe) MPV disease in vulnerable subsets of non-C-19-vaccinated individuals and ignite multi-country epidemics of MPV in non-C-19-vaccinated animal and human populations that are immunologically naïve to orthopoxvirus
Several countries are now about to start vaccination campaigns targeted at people who are at risk of contracting monkeypox disease using live attenuated, replication-incompetent smallpox vaccine. Both, individuals from SMCs engaging in high-risk sexual behaviors for MPV infection and close contacts of monkeypox cases (including very young children, pregnant women, elderly or immunocompromised individuals) are eligible for MPV vaccination (https://www.ecdc.europa.eu/sites/default/files/documents/Monkeypox-multi-country-outbreak.pdf). Live attenuated, replication-incompetent orthopox (e.g., smallpox) vaccines prime virus-neutralizing Abs in the vast majority of both vaccinated and non-vaccinated individuals (i.e., individuals < 50y). However, unlike live attenuated replication-competent orthopox vaccines[6], they do not train cell-based innate immunity. There can be no doubt that vaccination in the context of more infectious circulating MPV variants will further promote natural selection and dominant propagation of even more infectious immune escape variants and thereby allow MPV to evolve into a human pathogen exhibiting an even higher level of infectiousness (comparable to smallpox?). This situation is reminiscent of that which has been responsible for driving adaptative evolution of more infectious SC-2 (SARS-CoV-2) variants following C-19 mass vaccination campaigns. The evolutionary dynamics of MPV will only be expedited when vaccine coverage rates grow; they could eventually modify the current mode[7] and course of chain of MPV transmission such as to asymptomatically spread to all parts of a homogenously mixed, highly C-19 vaccinated population. This would increase the risk for C-19 unvaccinated subjects to contract MPV disease, especially for those who are particularly vulnerable to MPV disease because of Ab-mediated enhancement of viral infectiousness or enhanced susceptibility to MPV infection due to risky (sexual) behavior (see further below). Because of asymptomatic transmission, highly C-19 vaccinated populations would serve as a human reservoir of more infectious MPV immune escape variants.
Spill-over of more infectious MPV variants to populations that are immunologically naïve to orthopoxvirus is likely to trigger epidemics of MPV in poorly C-19 vaccinated countries
It is reasonable to assume that populations which do not ‘benefit’ from hyperactivation of cytotoxic CD8+ T cells will become more susceptible to productive infection with new, more infectious MPV variants (https://www.voiceforscienceandsolidarity.org/scientific-blog/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment). This applies, for example, to several different animal populations as well as to human populations in poorly C-19 vaccinated countries (e.g., in Africa). Asymptomatic infections in highly vaccinated C-19 countries are likely to promote spill-over events involving transmission of more infectious MPV variants from these highly C-19 vaccinated human reservoirs to vertebrate animals (possibly even including livestock) and poorly C-19 vaccinated human populations that are immunologically naïve to orthopoxvirus.
Asymptomatic transmission of more infectious MPV variants can also become problematic for the C-19 unvaccinated in highly C-19 vaccinated countries, particularly for C-19 unvaccinated children and vulnerable people (e.g., part of SMCs) who are immunologically naïve to orthopoxvirus.
In young children, rapid re-infection subsequent to previous asymptomatic MPV infection by more infectious MPV variants is likely to entail a rise in cases of Ab-dependent enhancement of MP disease[8] whereas risky sexual behavior renders individuals from SMCs more susceptible to viral infection. One can therefore expect the incidence rate of monkeypox disease to increase in both, non-C19-vaccinated children and SMC members.
Previous vaccination with smallpox (i.e., cowpox) vaccines will likely improve protection from MPV disease in the non-C-19-vaccinated but not in the C-19 vaccinated.
While recall of Abs induced by vaccination against smallpox virus in the past will provide an additional layer of natural immunity in the unvaccinated, repetitive recall of Spike (S)-specific infection-enhancing Abs[9] in C-19 vaccinated individuals by circulating SC-2 variants will allow the latter to outcompete other glycosylated pathogens for internalization into mucosa-resident dendritic cells, thereby reducing or potentially even preventing recall of previously smallpox vaccine-induced Abs. This would imply that older (> 45-50y) C-19 unvaccinated individuals are likely to benefit from their smallpox-vaccination in the past whereas their C-19 vaccinated peers may not. However, as already mentioned, the infection can be expected to be largely asymptomatic/ mild in the vast majority[10] of vaccinated and unvaccinated individuals in highly C-19 vaccinated populations, even in the absence of previous smallpox vaccination.
No child should be vaccinated against monkeypox during this C-19 pandemic
Vaccination with replication-incompetent orthopoxvirus-based vaccines of highly C-19 vaccinated (sub)populations is not only going to drive the expansion of more infectious MPV variants but will also have the same detrimental effect as C-19 vaccines in children: the continuous recall of vaccinal anti-MPV Abs (by circulating, more infectious MPV variants) will keep the innate Abs on the sideline and could thereby predispose the child to immunopathologies[11] (https://www.voiceforscienceandsolidarity.org/scientific-blog/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment).
But even replication-competent smallpox vaccines can put the child’s health at risk. Akin to all other live attenuated & replication-competent vaccines (e.g., childhood vaccines), these vaccines are known to come with a risk of side-effects:
“Health complications can occur after receiving the vaccine, and the risk of experiencing serious side effects must be weighed against the risk of experiencing a potentially fatal smallpox infection. The vaccine may cause myocarditis and pericarditis, which are inflammation and swelling of the heart and surrounding tissues and can be very serious. Based on clinical studies, myocarditis and/or pericarditis occur in 1 in 175 adults who get the vaccine for the first time” (https://www.fda.gov/vaccines-blood-biologics/vaccines/acam2000-smallpox-vaccine-questions-and-answers).
“Potentially life-threatening reactions could occur in 14-52 cases out of every million. According to CDC it is estimated that 1 to 2 people out of every 1 million people vaccinated could die” https://www.cdc.gov/smallpox/vaccine-basics/vaccination-effects.html).
The risk of severe disease may significantly increase when these live attenuated, replication competent orthopoxvirus-based vaccines are administered to C-19-vaccinated children. S-directed Abs are thought to sideline the child’s innate immune Abs and thereby prevent NK cell-mediated innate immune recognition of host cells infected by glycosylated viruses (including pox viruses) [https://www.voiceforscienceandsolidarity.org/scientific-blog/intra-pandemic-vaccination-of-toddlers-with-non-replicating-antibody-based-vaccines-targeted-at-aslvi1-or-aslvd2-enabling-glycosylated-viruses-prevents-education-of-innate-immune-effector-cells-nk-cells]. This may enable live attenuated, replication competent orthopoxvirus (e.g., vaccinia virus) comprised within the vaccine to blow through the child’s first line of immune defense and cause (severe) monkeypox disease.
Stated bluntly, vaccination of young children against MPV is at risk of provoking life-threatening disease.
The vast majority of C-19 vaccinees and C-19 unvaccinated individuals in highly C-19 vaccinated populations develop asymptomatic (or very mild) infection upon exposure to MPV. However, close and disruptive physical contact may promote viral entry through broken skin/ mucosa and is therefore more likely to cause symptomatic infection. Whereas strong training of cell-based innate immunity is likely to prevent productive infection of C-19 unvaccinated persons in highly C-19 vaccinated populations and contributes to herd immunity, hyperactivated cytolytic CD8+ T cells in C-19 vaccinated individuals can only enhance abrogation of productive infection, resulting in substantial mitigation of disease symptoms.
Due to the current advanced stage of the evolutionary trajectory of the C-19 pandemic in highly C-19 vaccinated SMCs, MPV is likely to evolve more infectious/ pathogenic variants. Public health authorities in several highly C-19 vaccinated countries have now started rolling out MPV vaccination campaigns targeted at SMCs. MPV vaccination in the ‘at risk’ groups typically use live attenuated, non-replicating smallpox vaccines. Although these vaccines are much less problematic in terms of vaccine-induced side effects (they have even been approved for use in immunocompromised or immunodeficient people), they can only prevent orthopox (including smallpox) disease—not productive infection. As the type of protection conferred by these vaccines is solely based on the induction of antigen-specific, virus-neutralizing Abs, MPV vaccination programs using this type of vaccines will inevitably expedite adaptive evolution of MPV and hence, further promote dominant circulation of more infectious immune escape variants. Consequently, even small-scale deployment of live attenuated, non-replicating orthopox vaccines targeted at preventing disease in vulnerable individuals are highly problematic in that they have the potential to rapidly turn highly C-19 vaccinated populations into a human reservoir for asymptomatic transmission of more infectious MPV variants to poorly C-19 vaccinated populations that are immunologically naïve to orthopoxvirus. Viral transmission from these reservoirs is therefore at risk of igniting multi-country epidemics in poorly C-19 vaccinated countries while increasing the risk of Ab-dependent enhancement of disease in young C-19 unvaccinated children and individuals at high risk of exposure to MPV (due to risky behavior) living in highly C-19 vaccinated countries.
Given the current epidemiologic situation, mandatory vaccination against monkeypox cannot be justified, regardless of C-19 vaccination status. In C-19 vaccinated populations, current vaccination campaigns will only promote further expansion of more infectious MPV variants. But even in non-C19-vaccinated countries, vaccination is not a reasonable option. This is because poxvirus epidemics do not generate herd immunity sensu stricto[12] and prevention, therefore, of world-wide poxvirus epidemics is only possible when the virus can be eradicated. However, eradication is only feasible provided there are no asymptomatic reservoirs and a global mass vaccination program is conducted with vaccines that are capable of preventing productive infection. The first condition is obviously not fulfilled since highly vaccinated countries now serve as asymptomatic reservoirs for MPV. The second condition cannot be fulfilled either since this would require usage of replication-competent vaccines, ideally in a pre-exposure prophylactic setting (or at least within a few days after suspected exposure). However, even replication-competent smallpox vaccines would not enable protection from productive infection by more infectious MPV immune escape variants for the latter will not be a good match for the vaccinal Abs and could, therefore, expedite propagation of more infectious variants in non-C-19 vaccinated populations too. Furthermore, side-effects caused by the existing replication-competent smallpox vaccines may raise additional concerns in regard of vaccine safety.
Finally, no child should be vaccinated with any of the current C-19 vaccines (https://www.voiceforscienceandsolidarity.org/scientific-blog/intra-pandemic-vaccination-of-toddlers-with-non-replicating-antibody-based-vaccines-targeted-at-aslvi1-or-aslvd2-enabling-glycosylated-viruses-prevents-education-of-innate-immune-effector-cells-nk-cells) and no non-C-19-vaccinated young child should be vaccinated with any type of smallpox vaccines. This is because the replication-competent vaccines may cause (severe) MPV disease in these young children whereas the replication-incompetent vaccines put them at risk of contracting immunopathologies.
In conclusion, no C-19 unvaccinated person should engage in sexual behavior that is at risk of enhancing MPV infectiousness (e.g., anogenital intercourses) or be vaccinated with zoonotic orthopoxvirus types once human-to-human transmission of antigenically shifted (i.e., more infectious) MPV variants is occurring!
The current MPV pandemic is to be considered an indirect consequence of the unfortunate C-19 mass vaccination program and does not yet constitute a public health emergency of international concern. However, each vaccination program that uses non-replicating vaccines targeted at immunologically naïve ‘at risk’ communities to fight ASLVI-enabling glycosylated viruses[13] will expedite the expansion in prevalence of more infectious immune escape viral variants. This is why the MPV vaccination campaigns that are currently kicked off are not only likely to have a detrimental impact on individual health (particularly in C-19 unvaccinated children and vulnerable people) but should also be considered at risk of provoking a true public health emergency of international concern.
However, as far as highly C-19 vaccinated countries are concerned, the evolution of MPV towards establishing an asymptomatic reservoir of more infectious MPV variants is merely a ‘side-effect’ of the ongoing evolutionary trajectory of SC-2 in these countries. I therefore predict that the imminent detrimental health consequences of the C-19 mass vaccination program will soon obviate the need for further speculation on how the MPV pandemic/ multi-country epidemic is going to evolve in industrialized countries and, therefore, in third-world countries.
POSTSCRIPTUM
Vaccination of vulnerable groups against zoonotic influenza virus (MPV) in a highly C-19 vaccinated population will drive adaptive evolution of zoonotic influenza virus and ignite multi-country epidemics in C-19 unvaccinated countries
The immunological mechanisms underlying asymptomatic transmission of MPV from highly C-19 vaccinated populations to immunologically orthopoxvirus-naïve, C-19 unvaccinated individuals or poorly C-19 unvaccinated populations also largely apply to a zoonotic influenza virus. This is to say that vaccination (with a non-replicating zoonotic flu vaccine) of a C-19 vaccinated subpopulation that is at high risk of contracting zoonotic influenza infection is prone to further promoting the expansion of zoonotic flu virus and causing (severe) influenza disease in vulnerable people from the C-19 unvaccinated part of the population.
Which individuals are to be considered vulnerable to zoonotic influenza virus?
Whereas orthopoxviruses originating from various animal species induce cross-neutralizing Abs, influenza viruses from animal species do not induce broadly cross-neutralizing Abs. Individuals who received smallpox (i.e., cowpox-based) vaccines in the past are therefore not prone to developing Ab-dependent enhancement of viral infectiousness upon subsequent exposure to MPV. However, asymptomatic human-to-human transmission of an antigenically shifted influenza variant spilling over from an animal reservoir (e.g., birds) may become particularly problematic in individuals who have previously recovered from productive infection with a common seasonal influenza virus type or who have previously been vaccinated against predominantly circulating influenza virus types (i.e., primarily the elderly and people with co-morbidities are who are otherwise immune suppressed). Zoonotic infection of these individuals with an antigenically shifted viral variant (most likely avian influenza) will likely lead to more and more cases of Ab-dependent enhancement of influenza disease[14] in humans. However, severe disease is unlikely to occur due to trained cell-based innate immunity (in C-19 unvaccinated persons) or cell-based adaptive immunity (in C-19 vaccinated persons). Should public health authorities recommend vaccination of this vulnerable group against the zoonotic influenza virus (most like, avian influenza virus), we will undoubtedly witness circulation of more infectious variants in highly vaccinated populations, resulting in enhanced rates of disease predominantly in C-19 unvaccinated children (because of a higher chance of re-infection shortly after previous exposure) and individuals who have previously been primed with common (seasonal) influenza virus types.
Similar to the epidemic predictions made for MPV, asymptomatic transmission of zoonotic influenza (most likely avian influenza) from highly C-19 vaccinated populations will likely give rise to multi-country epidemics of zoonotic influenza in poorly C-19 vaccinated populations that are immunologically naïve to the transmitted zoonotic influenza virus.
Similar also to the risks associated with MPV vaccination of young children, immunization of young children with any type of zoonotic influenza vaccine is at risk of causing (severe) zoonotic influenza disease (i.e., in the case of replication-competent vaccines) or immunopathologies (i.e., in the case of replication-incompetent vaccines).
In conclusion, no C-19 unvaccinated person should be vaccinated with common (seasonal) or zoonotic influenza virus types once human-to-human transmission of antigenically shifted (i.e., more infectious) influenza variants is occurring!
References
1. Populations aged < 50y have not been vaccinated in the past against smallpox. The smallpox vaccine uses live attenuated, replication-competent cowpox (vaccinia) virus and largely protects against monkeypox disease.
2 Infections with these viruses typically cause acute self-limiting viral disease
3 As the current SC-2 variants are further strengthening their infectiousness, presumably as a result of stronger
binding to the infection-enhancing Abs (https://www.voiceforscienceandsolidarity.org/scientific-blog/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment),
more SC-2 virions are internalized into migrating dendritic cells and thereby contribute to activation of cytolytic
CD8+ T cells
4 For the purpose of this manuscript, ‘vulnerable’ refers to individuals from sexual minority communities (SMCs),
wherein SMCs refer to gay and bisexual male communities engaging in high-risk sexual behaviors for MPV infection
(e.g., anogenital intercourses)
5 Disease in vulnerable, C-19 vaccinated individuals occurs when the virus breaks through the cytolytic immune defense provided by the hyperactivated CTLs
6 Regardless of safety concerns about potential side-effects, live attenuated, replication-competent orthopox
vaccines will not be effective when used in highly C-19 vaccinated populations. This is because elimination of MPV-
infected cells by cytotoxic innate or adaptive immune cells (i.e., trained innate NK cells or CTLs in the non-C19-
vaccinated or C-19 vaccinated, respectively) will largely prevent ‘vaccine take’.
7 Enhanced intrinsic infectiousness could even enable airborne transmission (e.g., via particle/ droplet aerosol) as
in the case of smallpox
8 Re-infection with MPV in the presence of non-neutralizing, low-affinity anti-MPV Abs enhances viral
infectiousness and, therefore, disease in young, C-19 unvaccinated children
9 These Abs are currently making C-19 vaccinees more and more susceptible to productive re-infection with SC-2
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8351274/
10 The additional protective effect of past vaccination with smallpox vaccines might predominantly benefit the
elderly (> 65 y) and vulnerable people.
11 Because of deficient or insufficient education of NK cells to sense virus-associated self-mimicking peptides
expressed on the surface of host cells infected by said ASLVI- or ASLVD-enabling glycosylated viruses
(https://www.voiceforscienceandsolidarity.org/scientific-blog/intra-pandemic-vaccination-of-toddlers-with-non-
replicating-antibody-based-vaccines-targeted-at-aslvi1-or-aslvd2-enabling-glycosylated-viruses-prevents-
education-of-innate-immune-effector-cells-nk-cells ).
12 Herd immunity sensu stricto relates to a level of naturally induced, protective immunity that has been established in the majority of the population and is high enough to protect the remainder of that population by virtue of diminished infectious transmission.
13 Although monkey pox is an ASLVD, it can be considered an ASLVI when spreading in a highly C-19 vaccinated population at this stage of the C-19 pandemic (i.e., due to hyperactivation of cytolytic CD8+ T-cells)
14 This is because the antigenically shifted immune escape variant from the animal reservoir will not properly match
the vaccine-induced Abs.
Geert Vanden Bossche, DVM, PhD General Manager at Voice for Science and Solidarity | The biggest challenge in vaccinology: Countering immune evasion originally published on TS News on Aug. 5, 2022
MIS-C is a disease that may occur in school-age children two to six weeks after infection with SARS-CoV-2 (SC-2) virus. MIS-C is a post-infectious inflammatory condition which typically occurs after asymptomatic/mild SC-2 infection. Some children may need hospitalization because of inflammatory reactions in different organs. While the syndrome can be serious, the absolute risk for MIS-C is very low (about 6.5 per 100 000 person-years) and known to be increased in boys aged 5-11 years with foreign-born parents, asthma, obesity, and life-limiting condition (https://www.thelancet.com/action/showPdf?pii=S2666-7762%2822%2900137-5).
MIS-C mostly resolves within a few days after timely and adequate (immunosuppressive) treatment. As the pandemic evolves and more infectious Omicron (sub)variants are now dominating the scene, MIS-C is occurring less frequently and with diminished severity of disease (https://jamanetwork.com/journals/jama/fullarticle/2792718). This evolution cannot be entirely explained by C-19 vaccination of young children as vaccine coverage rates in this age group are still very low (15% and 3% as recently reported in studies from Israel and the US, respectively; https://jamanetwork.com/journals/jama/fullarticle/2792718; https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciac471/6605071).
It is therefore tempting to speculate that enhanced viral infectiousness and transmission significantly contribute to dampening the incidence rate and severity of MIS-C in young children. This suspicion is supported by a previous study in which the authors speculated that some of the risk factors they identified for MIS-C could be associated with enhanced disease transmission (e.g., in children with foreign-born parents or explaining the shift in age from 12-15 years down to 5-11 years amongst children with MIS-C throughout the pandemic (https://www.thelancet.com/action/showPdf?pii=S2666-7762%2822%2900137-5).
To better understand the origin of the disease, and why children in particular are susceptible to contracting MIS-C, it is important to understand how the child’s innate immune system is educated and trained to combat infections with glycosylated viruses causing acute self-limiting viral infection (ASLVI; e.g., SC-2) or acute self-limiting viral disease (ASLVD).
In young children who have cleared their maternal antibodies (around the age of 6 months), abundantly produced innate (sometimes called ‘natural’) antibodies (Abs) play a critical role in initiating active use of their own immune system. In these children, innate Abs are tasked with recognizing and binding free-circulating self-derived glycan motifs (e.g., decorating foreign-derived [including pathogen-derived] or self-derived proteins) to potentiate[2] the presentation of repetitive patterns of foreign- or self-derived self-mimicking peptides on the surface of autologous somatic cells or antigen (Ag-)presenting cells (APCs). Glycosylation of self-proteins is an important mechanism for inducing T cell-mediated peripheral tolerance[3] and, not surprisingly, mimicked by several pathogens (e.g., glycosylated viruses) as a strategy to subvert the host immune system. As they decorate themselves with self-mimicking patterns of self-glycans, glycosylated viruses (e.g., corona virus [CoV], influenza virus, respiratory syncytial virus [RSV], measles, mumps, rubella, varicella virus,…) can be recognized and captured by innate Abs and thereby contribute to educating the child’s innate immune effector cells (i.e., NK cells).
As the child grows up, the functional capacity of their innate Abs gradually declines so that their immune system can progressively replace the ‘self’-sensing innate Ab capacity by a pool of pre-primed NK cells that can recognize pathogen-derived self-mimicking (i.e., ‘altered self’) motifs on virus-infected or otherwise pathologically altered host cells such as to kill those cells.
For as long as a child possesses an abundant functional capacity of innate Abs, glycosylated pathogens and self-ligands will be complexed by innate Abs to educate NK cells on how to distinguish ‘self’ from ‘non-self’. This is how the innate immune system of the young child is thought to ‘adapt’ to the early-life extra-maternal environment where it must learn to rapidly sense peptide motifs that differ from self-peptides. This would enable NK cells to target and kill autologous host cells that are decorated with such ‘altered self’ peptides (e.g., infected, or otherwise pathologically altered host cells).
Once NK cells are educated, the NK cell training process dictates their functional re-programming (https://www.frontiersin.org/articles/10.3389/fimmu.2018.01869/full). Training is thought to result from epigenetic alterations that are triggered by changes in the SC-2 infectious landscape and generate ‘adaptive’ or ‘memory-like’ NK cells. Adequate training of its first line of immune defense enables the child to mount protective natural immunity against SC-2 (and other glycosylated viruses/ pathogenic agents sharing the same PSMPs[4]) upon future exposure. This can already explain why prophylactic childhood vaccinations using live attenuated virus are very efficient at inducing natural immunity against measles, mumps, rubella, varicella and generating herd immunity−it’s only when they become infected with an antigenically ‘shifted’ (i.e., very different) variant that individuals who acquired natural immunity can still contract disease due to ADEI.
When young and healthy children become infected during an outbreak of a virus with a relatively low reproduction number (R0; e.g., infection with common cold coronavirus [CoV] or seasonal Flu; R0 < 2.5), they almost always develop asymptomatic or very mild infection. However, dominant circulation of more infectious CoV or Influenza virus variants can occasionally provoke cases of severe disease in children. It is reasonable to postulate that enhanced viral infectiousness raises the chance for a person to become re-infected shortly after a previous course of asymptomatic infection. This will increase the likelihood that immature, short-lived Ag-specific Abs[5] of relatively low affinity, which typically develop after asymptomatic/ mild infection, will still be present when that person becomes re-exposed to the virus. Because of their Ag-specificity, these Abs may outcompete the child’s innate polyspecific IgM Abs, which have an even lower affinity for the protein Ag that is responsible for initiation of infection (i.e., spike [S] protein in the case of CoV). Depending on their titer, these non-neutralizing, Ag-specific Abs can therefore prevent or at least diminish binding of innate Abs to the virus. Although these short-lived Abs cannot neutralize the virus, they can bind to it and enhance its infectiousness.
This is particularly problematic in young children as insufficient training of their NK cells prevents effective immune targeting of SC-2-infected cells expressing virus-derived self-mimicking peptides on their surface. NK cells that are largely ‘pathogen-inexperienced’ together with enhanced SC-2 infectiousness would entail enhanced susceptibility of young children to SC-2 infection (i.e., so called ‘Ab-dependent enhancement of viral infectiousness’; ADEI). Hence, re-infection shortly after previous asymptomatic exposure will likely allow the virus to break through the cell-based innate immune system of young children and could potentially cause (severe) disease (https://pubmed.ncbi.nlm.nih.gov/33391280/).
However, as these post-infectious Abs wane rapidly (they are no longer detectable at about 8 weeks), only a limited number of children will become re-exposed to the circulating virus shortly after their previous productive exposure. This already explains why most cases of MIS-C occur between 2 and 6 weeks (on average 4 weeks) after the previous asymptomatic/ mild infection, presumably depending on the titer of the infection-enhancing Abs at the timepoint of re-exposure. It is therefore not surprising to also observe high variability in the severity of MIS-C disease.
After many years of NK cell vaccine research (which I was unable to publish for intellectual property reasons), I determined that the recruitment on MHC class I molecules of PSMPs into ‘non-self’ high-density arrays (situated outside of the MHC class I peptide-binding groove!) is what allows for activation and epigenetic imprinting (i.e., training) of cytotoxic NK cells that are capable of killing host cells that present such PSMPs on their surface (for example as a result of viral infection).
I postulate that strong stimulation by enhanced viral infectiousness could even obviate the need for cumulative triggering of NK cells (so-called ‘training’) in order for NK effector cells to become imprinted with memory. NK cells that have acquired a memory-like phenotype could readily eliminate host cells that are infected with relevant glycosylated pathogens. Enhanced viral infectiousness in the young child could allow productive SC-2 infection even in the presence of innate Abs and thereby enable ‘power training’ of pre-primed NK cells. Even though symptoms could still be mild, productive infection would have the capacity to substitute a single ‘power training’ event for regular, incremental training of functional NK cell responsiveness to pathogen-derived ligands.
As full-fledged NK cell ‘priming’ towards PSMPs would therefore improve with enhanced viral infectiousness, C-19 unvaccinated children (and even some adolescents) who recently contracted mild disease would be equipped with innate immune memory while no longer developing infection-enhancing anti-S Abs (as shown in fig. 1). Alternatively, enhanced viral infectiousness leads to higher viral infection rates and thereby shortens the average time window for a person to become re-exposed after a previous asymptomatic SC-2 infection. A shortened window for re-exposure makes it more likely that the latter occurs in the presence of a relatively high titer of infection-enhancing Abs. It is not unreasonable to assume that the mechanism of naturally induced infection-enhancing Abs is similar to the one previous described for vaccine-induced anti-S Abs−a high enough concentration of these Abs would allow a subset of these Abs to bind to SC-2 virions tethered to dendritic cells and thereby exert a disease-mitigating effect (https://www.voiceforscienceandsolidarity.org/scientific-blog/predictions-gvb-on-evolution-c-19-pandemic + fig. 2).
Based on the rationale explained above, one could easily understand how the prolonged C-19 pandemic and the enhanced frequency of repetitive waves of more infectious variants (e.g., Omicron) is likely to have a ‘power training’ effect on relevant NK cells of young C-19 unvaccinated children developing mild primary infection (i.e., overlapping with abundant functional capacity of innate Abs) or to provide a strong disease-mitigating adaptive immune response in those who recently contracted asymptomatic SC-2 infection. The latter would be protected from severe and even moderate disease by virtue of infection-enhancing Abs and cytotoxic CD8+ T cells, respectively (as illustrated in fig. 2). A further increase in viral infectiousness would not make young, previously asymptomatically infected children more susceptible to disease but rather increase their likelihood to develop productive SC-2 infection and generate effector memory NK cells or further expand those (as shown by the arrows in green in fig. 1).
With this understanding, it is not surprising that the advent of Omicron (sub)variants has led to a rapidly regressing incidence rate and severity of MIS-C (https://jamanetwork.com/journals/jama/fullarticle/2792718).
As the mass vaccination program during this pandemic has led to the dominant circulation of more infectious SC-2 variants, it is not surprising to find that a few, young (C-19 unvaccinated) children contracted MIS-C and even needed hospitalization—this was an extremely rare event at the beginning of the pandemic. However, the mass vaccination program has provided immune escape variants characterized by a higher level of intrinsic viral infectiousness (e.g., of the delta variant) with a competitive advantage. The ensuing higher infection rate in the population (and in households!) therefore came with an additional likelihood for young children to become re-infected shortly after their previous asymptomatic infection. As previously described, the incidence rate of MIS-C is now waning as a result of enhanced innate immune training and mitigation of (severe) disease by more and more infectious SC-2 variants that have now become dominant.
Parents should be adequately briefed about early signs and symptoms of MIS-C (https://www.hopkinsmedicine.org/health/conditions-and-diseases/coronavirus/misc-and-covid19-rare-inflammatory-syndrome-in-kids-and-teens) as the prognosis is very favorable upon timely and adequate treatment. However, the consequences of vaccinating young children with these replication-incompetent C-19 vaccines will be an unforgivable sin that will only lead to hospitalization and mortality rates that dwarf those highest observed for MIS-C (https://www.trialsitenews.com/a/intra-pandemic-vaccination-of-toddlers-with-non-replicating-antibody-based-vaccines-targeted-at-aslvi1-or-aslvd2-enabling-glycosylated-viruses-pr-66e8b959; https://www.trialsitenews.com/a/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment-a212bb47).
Notwithstanding the fact that these vaccines may–FOR NOW (!)–still protect against (severe) disease from SC-2 as well as from other ASLVI- or ASLVD-enabling glycosylated pathogens (https://www.trialsitenews.com/a/vaccination-of-vulnerable-groups-against-monkeypox-virus-mpv-in-a-highly-c-19-vaccinated-population-will-drive-adaptive-evolution-of-mpv-and-ignite-2db3eac6), enhanced adsorption or internalization of more infectious Omicron (sub) variants (e.g., BA.4, BA.5 and BA.2.12.1) onto or into tissue-resident dendritic cells dampens presentation of other, pathogen-derived antigens by these professional APCs while exhausting CD8+ T cells (as illustrated in fig. 2). This is highly likely to diminish the child’s immune defense against a multitude of microbial glycosylated pathogens and prevent peripheral tolerance, thereby putting them at higher risk of contracting immunopathologies (https://www.trialsitenews.com/a/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment-a212bb47).
More importantly, the currently circulating Omicron (sub)variants are already endowed with higher intrinsic virulence that–for now–is still kept in check by the virulence-inhibiting activity of infection-enhancing anti-S Abs (as reviewed in: https://www.voiceforscienceandsolidarity.org/scientific-blog/predictions-gvb-on-evolution-c-19-pandemic). We have already witnessed how more infectious variants developed resistance to potentially infection-neutralizing Abs induced by C-19 vaccines and there is little doubt that more virulent SC-2 lineages will manage a similar ‘trick’ to develop resistance to potentially virulence-‘neutralizing’ Abs (especially since repeated exposure to more infectious circulating Omicron (sub)variants will recall these vaccinal S-specific Abs and thereby ensure sustained immune pressure). When this happens, vaccinated infants and toddlers will be left with an adaptive immune system that does no longer protect them from severe C-19 disease and with NK cells that have not been trained due to prolonged suspension of their education (https://www.trialsitenews.com/a/intra-pandemic-vaccination-of-toddlers-with-non-replicating-antibody-based-vaccines-targeted-at-aslvi1-or-aslvd2-enabling-glycosylated-viruses-pr-66e8b959). Prolonged sidelining of the child’s innate Abs is thought to hamper the functional capability of cytotoxic NK effector cells to sense and target virus-derived, molecular self-mimicking peptides that are expressed on virus-infected host cells. As already reported, lack of innate immune education could dramatically impede the child’s capacity to generate natural immunity to SC-2 in particular as well as other ASLVI- or ASLVD-enabling glycosylated viruses in general (https://www.trialsitenews.com/a/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment-a212bb47).
On the other hand, diminished complexation of foreign glycosylated ligands by innate Abs could render NK cells that lack self-MHC-I inhibitory receptors hyporesponsive to stimulatory receptor activation as a result of their chronic low-level stimulation by self-derived peptides. Because of the resulting diminished threshold of NK cell activation in the periphery, young C-19 vaccinated children would be prone to developing immunopathologies.
However, in the likely event that resistance to potentially virulence-‘neutralizing’ Abs develops, it can be expected that−given the high SC-2 infection rate− C-19 vaccinated infants and toddlers will primarily succumb to Ab-dependent enhancement of severe C-19 disease rather than to severe disease from any other circulating ASLVI or ASLVD or from immunopathology.
Increased SARS-CoV-2 exposure results from dominant expansion of more infectious SC-2 variants, a phenomenon undeniably caused by the C-19 mass vaccination program. As suggested by the results from earlier studies, increased exposure to SC-2 together with a number of predisposing factors renders very few young children susceptible to developing MIS-C following a recent asymptomatic infection (https://www.thelancet.com/action/showPdf?pii=S2666-7762%2822%2900137-5).
There is no doubt that vaccinating children against SC-2 is a colossal blunder and merely places the child at high risk of severe health damage. MIS-C has not only a low incidence (which is further declining) but can also be successfully treated using conventional drug therapy. This contrasts with the protective effect of C-19 vaccination against MIS-C, which is temporary and leaves the young child at high risk of contracting Ab-dependent enhancement of severe disease upon future exposure to new SC-2 variants (which will dominantly emerge as a result of the current population-level immune pressure on viral virulence).
It is critical to understand that the high viral infection rate in highly C-19 vaccinated populations due to mass vaccination, rather than a lack of C-19 vaccination, is responsible for this phenomenon. There is therefore no single scientific rationale for vaccinating children against SC-2−exactly the contrary is true: C-19 vaccination of young children is highly likely to not only provoke a soaring incidence of severe disease and mortality due to immunopathology and other microbial diseases but ultimately also due to SC-2.
Public health authorities are creating the illusion for parents that C-19 vaccines will protect their children, instead of educating them how to recognize early signs and symptoms of MIS-C in order to seek highly effective treatment for their child in due time. In addition, they seem to ignore that preserving natural immunity in young children is critical as it is the key pillar of herd immunity to ASLVIs, including SC-2.
Fig. 1: Upon exposure to more infectious SC-2 variants, young children may develop MIS-C as a result of re-exposure shortly after previous asymptomatic infection. However, as their infectiousness increases, new SC-2 variants may break through the child’s innate Ab-mediated protection and thereby cause mild infection that imprints its NK cells with memory and therefore dramatically boosts the child’s first line of immune defense. Alternatively, more infectious variants enable re-exposure in the presence of higher titers of short-lived infection-enhancing anti-S Abs. In the latter case, young children are protected from severe disease presumably because a subset of anti-S Abs can bind to SC-2 virions tethered to dendritic cells (see fig. 2), thereby inhibiting severe/systemic disease whereas sustained activation of CTLs (as a result of the infection-enhancing capacity of these Abs upon their binding to free virions) further mitigates C-19 disease. Both scenarios may be responsible for the observed reduction in the incidence rate and severity of MIS-C as the pandemic continues to evolve (indicated by “–“ and arrows in blue). Since the pandemic has now evolved highly infectious SC-2 variants (i.e., the new Omicron [sub]variants), viral exposure of young children is more and more likely to readily cause mild infection resulting in NK cell ‘power training’ and further expansion of effector memory NK cells upon a further increase in viral infection rates (indicated by “+” and arrows in green). This may ultimately prevent young children from developing MIS-C all together.
Fig. 2 (from https://www.trialsitenews.com/a/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment-a212bb47):
Acute, self-limiting viral infections that don’t lead to systemic/severe disease (and possibly death) are terminated by M(ajor) H(istocompatibility) C(omplex)-unrestricted, cytotoxic CD8+ T cells that have no memory and the activation of which is triggered by a universal, pathogen-nonspecific Tc epitope comprised within the spike (S) protein. Unless an infected person progresses to developing severe disease, this is what allows a fairly rapid recovery from disease after primary productive infection (and certainly before fully functional virus-neutralizing Abs peak) [according to 2a-2b-2c-2d pathway]. However, rather than stimulating de novo generation of new neutralizing Abs towards variants that escaped the neutralizing activity of vaccine-induced Abs, exposure of vaccinees to these immune escape variants will rapidly boost their declining titers of non-neutralizing, infection-enhancing Abs (those are directed against an antigenic site that is conserved within the N-STD of all SC-2 variants and has therefore a license to commit ‘antigenic sin’ once it has primed the host’s immune system).
In vaccinees with poor experience in fighting productive infection (and hence, poor training of their innate immune defense according to pathway 1a-1b-1c) prior to C-19 vaccination, infection-enhancing Abs[6] that are responsible for preventing severe disease by binding to DC-tethered virus (according to 3a-3b-3c-3d pathway) can synergize with strongly activated cytotoxic CD8+ Tc-mediated killing (3c’) to even prevent C-19 disease all together and hence, render vaccinees asymptomatic despite their high susceptibility to re-infection (B + C ? D). As prevention of disease is not due to prevention of productive infection but to accelerated abrogation of infection, these vaccinees will continue to shed and transmit SC-2 upon re-infection. Whereas innate immune effector cells are MHC-unrestricted and polyspecific (i.e., NK cells) and, therefore, don’t drive immune escape, the infection-enhancing-Abs are Ag-specific (i.e., S-specific) and – if produced at high enough titers and with high enough affinity by a large part of the population – will promote natural selection of immune escape variants that can resist the virulence-inhibiting capacity of these Abs. This is because vaccinees cannot prevent productive viral infection; consequently, the immune pressure they exert on viral virulence is suboptimal in that it cannot prevent the expansion in prevalence of immune escape SC-2 variants that have the capacity to overcome this immune pressure. Resistance of viral variants to the virulence-inhibiting activity of infection-enhancing Abs will inevitably cause Ab-dependent enhancement of severe disease (ADESD).
1. Education of NK cells that lack self-MHC-I inhibitory receptors but are endowed with germline-encoded NK cell activation receptors dictates their functional capability to recognize self- or pathogen-derived self-mimicking ligands and mediate innate effector functions; https://www.frontiersin.org/articles/10.3389/fimmu.2018.01869/full
2. Besides their neutralizing activity, natural/innate Abs can, indeed, serve as immune potentiators (‘natural
adjuvants’) to upregulate the presentation of antigens on cell surface-expressed MHC class I molecules
https://pubmed.ncbi.nlm.nih.gov/14502281/)
3. https://onlinelibrary.wiley.com/doi/full/10.1038/icb.2008.48;
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966069/
4. Enveloped glycosylated viruses are critical to educate the child’s innate immune system in ways that allow
recognition and elimination of somatic cells expressing PSMPs (as a result of viral infection or other pathologic
alteration) which may otherwise induce tolerance (e.g., cancer cells) or provoke autoreactive or immune
inflammatory responses (i.e., causing autoimmune or hyperinflammatory disease, respectively).
5. i.e., ‘spike protein-specific’ in case of SC-2
6. As previously explained, the non-neutralizing, infection-enhancing Abs are currently hampering trans infection at the level of distant organs such as the lower respiratory tract; this is what’s currently exerting population-level immune pressure on viral virulence: https://www.voiceforscienceandsolidarity.org/scientific-blog/predictions-gvb-on-evolution-c-19-pandemic).
NorthShore University HealthSystem in Chicago was sued by a nonprofit religious organization called Liberty Counsel. The group claims that NorthShore violated workers’ religious autonomy by dismissing religious exemptions and forcing all workers to receive the COVID-19 vaccine. NorthShore was in the wrong and decided to settle for $10,337,500.
Over 500 current and past employees will receive a payout, and the group will notify others of the lawsuits and give them the option to submit a claim. “NorthShore will also change its unlawful ‘no religious accommodations’ policy to make it consistent with the law, and to provide religious accommodations in every position across its numerous facilities,” Liberty Counsel stated.
Other groups will follow suit. They may have granted the pharmaceutical companies immunity, but there was a grey area for employers. Countless people lost their jobs due to the vaccine mandate, which likely was a violation of the Constitution.
Lawsuits may begin with large corporations, but if the Republicans regain control, health agencies and government officials may be investigated as well. This lawsuit is a major win for medical autonomy as companies will be less likely to comply with government mandates as they now know they could risk legal retaliation.
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