Come dice Mike Yeadon, ex vicepresidente di Pfizer, se la Banca Centrale controllerà i nostri portafogli digitali potrà costringerci a iniettarci qualsiasi prodotto pena il blocco dei soldi. Già ci hanno provato multando e togliendo il lavoro ai non vaccinati, e il grosso della popolazione li ha lasciati fare.
Al prox giro - dopo il clima tornerà una pandemia - non ci sarà scelta.

Robin Monotti mostra #laltrastoria

TRANSLATION: Like Mike Yeadon, ex Pfizer VP says, if the Central Bank gets to control our digital wallets they then can use this to try and force us to inject any product threatening to block our money if we don't. They already tried this with fines and taking work away from the non "vaccinated", and the majority of the population just let them do it.
In the next round - after the climate it will be the pandemic turn again - they won't leave it optional.

Robin Monotti shows the other story.

https://t.me/robinmg/29909

🚧🎬SHUTDOWN LONDON💥✅
We NEED to...
#UniteTheUnions
#UniteTheTribes
#UniteTheClans
#OccupyWEFminster
#OccupyStJamesPark
#DestroyTheWEF
#GeneralStrike

The EU's contract with Pfizer is clear proof this is an experiment, and therefore subject to the Nuremberg Code: 1. The voluntary consent of the human subject is absolutely essential, without coercion.

https://twitter.com/robinmonotti/status/1697140018517508461

Atomic force microscopy analysis of native infectious and inactivated SARS-CoV-2 virions

"Here, single viruses were analyzed by atomic force microscopy (AFM) operating directly in a level 3 biosafety (BSL3) facility, which appeared as a fast and powerful method to assess at the nanoscale level and in 3D infectious virus morphology in its native conformation, or upon inactivation treatments. AFM imaging reveals structurally intact infectious and inactivated SARS-CoV-2 upon low concentration of formaldehyde treatment. This protocol combining AFM and plaque assays allows the preparation of intact inactivated SARS-CoV-2 particles for safe use of samples out of level 3 laboratory to accelerate researches against the COVID-19 pandemic. Overall, we illustrate how adapted BSL3-AFM is a remarkable toolbox for rapid and direct virus analysis based on nanoscale morphology."

https://www.nature.com/articles/s41598-021-91371-4

This showed that PCR for a common cold coronavirus also resulted positive for SARSCoV:

"An Outbreak of Human Coronavirus OC43 Infection and Serological Cross-reactivity with SARS Coronavirus"

"In summer 2003, a respiratory outbreak was investigated in British Columbia, during which nucleic acid tests and serology unexpectedly indicated reactivity for severe acute respiratory syndrome coronavirus (SARS-CoV)."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2095096/

Robin,
Pictures do not tell us that that which is imaged causes any disease or is capable of causing contagion.
Not my words, but I’ve heard the extensive use of images called “the point & declare” school of virology.
It doesn’t advance the cause one way or the other, unfortunately.
I wish it did, as the too & fro on this topic, which wasn’t susceptible to properly evidenced settlement, even before the covid era, isn’t helping our fight against tyranny, which we both agree is descending, and it’s not got any easier now.

I’ve laid out why I’m convinced that the evidence in the current (2020-on) case is a PsyOp:

*No increase in illness or death prior to installation of lethal medical protocols after WHO declared a pandemic*
*Prior evidence against a single successful attempt to transmit respiratory symptoms from a symptomatic person to another person*
*Failure to isolate infectious particles from respiratory symptomatic individuals or from cell / tissue cultures, believed to be infected, when proper control experiments are conducted*
*The systematic failure of flu vaccines to reduce hospitalisation or death is unsupported of annual flu vaccination*

I don’t have an informed opinion beyond respiratory illnesses, but in the respiratory field, I am faced with strong evidence that illness-conveying viruses aren’t a thing.

This is all I have to say on this narrow but important topic & I’d appreciate it being made available for consideration by readers of our channel (with or without my comments in the paper you kindly shared).

Best wishes
Mike

https://t.me/robinmg/29913

This paper proved that SARSCoV2 is contagious. They took it from one person's nose and put it in other people's noses and half of them got ill with Covid:

@RobinMG

https://t.me/robinmg/29814

HCoV-OC43, as well as HCoV-HKU1, MERS-CoV, SARS-CoV and SARS-CoV-2 are all classified within the Betacoronavirus genus.

How does HCoV-OC43 enter cells?
The entry of HCoV-OC43 into human cells is largely achieved through the caveolin-1-dependent pathway of endocytosis; however, virus-containing vesicles at the cell surface can also undergo scission to also penetrate human cells.
Notably, while host factors like interferon-inducible transmembrane proteins (IFITMs) often prevent the entry of coronaviruses like HCoV-229E, -NL63, SARS-CoV and MERS-CoV from entering cells through its various antiviral functions, IFITM2 and IFITM3 promote the entry and subsequent infection of HCoV-OC43 into human cells.

Infection mechanisms
Once HCoV-OC43 enters the cell, infection is primarily due to a stress response by the endoplasmic reticulum (ER). Under normal circumstances, the ER is responsible for performing the synthesis, folding and post-translational modifications of many proteins; however, when the processing capacity of the ER is reached, accumulation of misfolded or unfolded proteins will occur, thereby leading to a stress response by this vital organelle.

Otherwise referred to as an unfolded protein response (UPR), the ER stress response by HCoV specifically activates inositol requiring enzyme 1 (IRE1) and induces X-box protein 1 (XBP1) mRNA splicing.
Furthermore, the S proteins of HCoV-OC43 can introduce two-point mutations of H183R and Y241H into the human cells, both of which further contribute to XBP1 mRNA splicing and an overall greater extent of apoptotic death in the infected cell.
The apoptosis of cells caused by HCoV-OC43 has also been shown to arise due to the mitochondrial translocation of Bcl-2-associated X protein (BAX).
In addition to its direct role in inducing the ER stress response, HCoV-OC43 has also been shown to downregulate over 30 genes that are involved in the innate immune response, some of which include MAP kinases, toll-like receptors, interferons, interleukins, and signal transduction proteins."

The similarity in clinical symptoms of patients with both HCoV-OC43 and HCoV-229E often cause these infections to be indistinguishable from each other; however, sore throat manifestations are more commonly associated with HCoV-OC43 than HCoV-229E, which typically causes a greater extent of nasal inflammation.

Clinical features
Along with HCoV-229E, -NL63 and -HKU1, HCoV-OC43 is responsible for up to 30% of all common colds in adults; however, more severe forms of these viral infections can lead to upper respiratory tract disease.
Like many other respiratory tract infections, HCoV-OC43 typically mild respiratory tract infections that can be spread to other individuals by coughing and sneezing.

THIS IS WHERE IT GETS INTERESTING:
"Although most of the replication of HCoV-OC43 occurs in the epithelial cells of the upper respiratory tract, this virus is unique in its ability to tolerate mutations and even cause infection in the brain.
Rather than utilizing the BAX protein to induce apoptosis within neuronal cells, research has shown that HCoV-OC43 infection within the brain is most likely due to the necroptosis-inducing actions of the RIP1 and MLK1 proteins.
The ability of HCoV-OC43 to enter and infect neurons has been shown to induce acute encephalitis in mice that can be accompanied by various neurological disabilities post-infection, some of which include abnormal limb clasping reflex and decreased motor activity.  
In addition to its most notable effects on the upper respiratory tract and possible neuronal infiltration, a 2001 outbreak of HCoV-OC43 in Normandy, France found that this virus can also cause a wide range of digestive problems to occur."

https://www.news-medical.net/health/What-is-OC43.aspx

And this is why the neurological factors "unique" to HCoV OC43 are interesting.

I have now reason to believe that some (not all) of the "no virus" voices on this channel and in the freedom movement are not benevolent.

Some are genuine (Mike), but others are infiltrators trying to push a narrative on the entire movement. I am not going to name names, but I received highly abusive messages which is consistent with attempts to intimidate me. These are clear narrative counterpsyops.

Part of the fake binary damage limitation. The tactics become clearer in the private messages "no virus" theorists send me.

I now have no doubts that they have infiltrated the freedom movement with "no virus" pushers in order to discredit it from within with this counterpsyop.

I have absolutely no doubt that this is the tactic they chose to destroy the credibility of the freedom movement. Gullibility is present both in the freedom movement and outside of it.

@RobinMG

WE'VE KNOWN SINCE 2006 THAT A COMMON COLD WILL TEST POSITIVE TO SARSCOV! No indication that this "glitch" has been addressed:

https://t.me/robinmg/29915

https://twitter.com/robinmonotti/status/1697209297782833254

ROYAL SOCIETY OF SCIENCE

Royal Medal Winners 2023
https://royalsociety.org/grants-schemes-awards/awards/royal-medal/

"Sir Patrick Vallance KCB FMedSci FRS and Sir Christopher Whitty KCB FRS are jointly awarded the Royal Medal 2023 for their pivotal role in ensuring that the UK’s response to the covid-19 pandemic has benefitted from the very best science and evidence."

https://royalsociety.org/grants-schemes-awards/awards/royal-medal/

https://twitter.com/royalsociety/status/1696849267103539631

Neurotropism of SARS-CoV 2: Mechanisms and manifestations:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7141641/

"Respiratory involvement is the most common in patients confirmed with Covid-19, however there are already reports of neurological manifestations [2,3]. It should be mencioned that the central nervous system (CNS) involvement was also reported in other coronaviruses [4] and studies in humans and experimental models revealed a possible neural pathway given by the olfactory nerve [[5], [6], [7]].

Viruses can reach the CNS through hematogenous or neural propagation [8]. Nerve dissemination is possible by the polarization of neurons, this property gives them the ability to receive and transfer information. This transport can be retrograde or antegrade and is facilitated by proteins called dinein and kinesin, which can be targets of viruses [9]. Once entered the CNS, viruses can generate alterations in neurons, as evidenced by a study carried out by Gu et al., who detected in 8 autopsies of victims of SARS, neuronal histopathological changes in the cortex and hypothalamus [6].

The olfactory pathway begins in bipolar cells located in the olfactory epithelium, from there its axons and dendrites extend to the olfactory bulb, where they make synapses with the cells present in this structure. Subsequently, this cranial pair is divided into two branches and is directed towards the olfactory nucleus present in the pyriform cortex [10] . This nerve route has been used by some coronaviruses in rodent models exposed to nasal inoculation [11,12]. 

Similar results were found in a Canadian study with another coronavirus, HCoV-OC43. In this case, by the fourth day of inoculation, the virus had already spread to the piriformis cortex, brain stem, and spinal cord [12]. 

The interesting thing about this possible propagation mechanism is the presence of the virus in areas of the brain stem [11,12], because this structure contains nuclei that regulate the respiratory rhythm. Breathing has central control given by the regulation of a number of neural groups. Through the nucleus of the solitary fascicle, the CNS receives information from the chemoreceptors that detect changes in the concentrations of CO2 and O2, alterations in these components lead to an increase or decrease in respiratory effort [13]. In this way, stem nuclei have connections with the respiratory system [1,13], and the entry of the coronavirus into this structure could trigger death by alteration of these neuronal groups [1].

In their analysis they found that 36.4% of the patients had neurological symptoms, these being directly related to the severity of the patient (severe cases VS non-severe: 40 [45.5%] vs. 38 [30.2%], P < .05). In patients with central symptoms (24.8%), 16.8% and 13.1% presented dizziness and headache, respectively. Among the peripheral symptoms (8.9%), the most common were hypogeusia and hyposmia with 5.6 and 5.1%.

"Zhou et al., detected the presence of the virus genome in the CSF [CerebroSpinal Fluid] of a 59-year-old patient with COVID-19 pneumonia, diagnosing viral encephalitis, demonstrating the direct damage that the virus produces in the CNS [Central Nervous System] [16]

The aforementioned makes us think that respiratory distress is not only the result of pulmonary inflammatory structural damage, but also due to the damage caused by the virus in the respiratory centers of the brain, making it more difficult to manage these patients."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7141641/

Last day tomorrow:
It's official - Train operators have announced plans to close nearly 1,000 ticket offices. We have until 1st September to take part in the public consultation. Can you take two minutes to respond to your train company’s consultation and object to the closure of ticket offices? The RMT has prepared template letters for each train operator. 🚆 Please have your say 👉https://www.rmt.org.uk/campaigns/rail/save-ticket-offices/

💉 C19 INJECTIONS:

OVER 1 MILLION INJURIES
OVER 21,000 CASUALTIES

And that's with an under-reporting factor of 41X

"Mr. Johnson wrote: "Sadly, we passed two milestones on VAERS. Over 1 million advisers events and over 21,000 deaths, 30 percent of those deaths occurred on day 0, 1, or 2 following vaccination."

https://www.theepochtimes.com/article/sen-johnson-claims-cdc-abused-authority-engaged-in-censorship-campaign-of-covid-19-vaccine-posts-5483931

https://twitter.com/robinmonotti/status/1697237934897033557

COVID-19 VACCINATION IN CHILDREN (AND ADULTS) DECREASES IMMUNE RESPONSE TO OTHER PATHOGENS:

https://www.frontiersin.org/articles/10.3389/fimmu.2023.1242380/full

"Our study showed that, in children, SARS-CoV-2 mRNA vaccination decreases inflammatory cytokine responses (IFN-γ, MCP-1, IL-6, IL-8 and IL-15) to heterologous bacterial, fungal and viral re-stimulation. A pre-print of a study in 16 adult healthcare workers reported heterologous effects of the same mRNA-based vaccine used in our study (26). The study in adults found decreases in IFN-γ and IL-6 production after stimulation with heterologous stimulants of bacterial and viral origin and increases in inflammatory cytokine production after C. albicans stimulation (26), in keeping with our findings.

Our findings suggest SARS-CoV-2 mRNA vaccination could alter the immune response to other pathogens, which cause both vaccine-preventable and non-vaccine-preventable diseases (34, 35). This is particularly relevant in children as they: have extensive exposure to microbes at daycare, school, and social occasions; are often encountering these microbes for the first time; and receive multiple vaccines as part of routine childhood vaccination schedules. There are currently no data on the clinical effects of COVID-19 vaccination-related heterologous effects in children."

These data show that a SARS-CoV-2 mRNA-based vaccine alters heterologous immunity in children and that these effects can persist up to six months after vaccination. Whether SARS-CoV-2 mRNA-based vaccines can induce the epigenetic and metabolic changes associated with trained immunity to provide protection against other infectious diseases remains an open question. That SARS-CoV-2 mRNA vaccination in children could impact immune responses to other pathogens emphasises the need for further research and consideration of heterologous effects in vaccination policies given their broad public health implications."

https://twitter.com/robinmonotti/status/1697244206711160953