OPERATION CORONATION AND OTHER ADVENTURES OF MONICA
🍼🍼🍸🍸Biological, terrorist operation is a world project through a false pandemic corona 👑 to the totalitarian communist collective farm hostel
WORLD HOSPITAL 🏥 (Bank 🏦) has calculated the PROJECT with completion in March 2025 By this time they plan to stab everyone
They plan to mock the world population for at least 5 years.
Project No. PCBASIC0219761.
COVID-19 STRATEGIC PREPAREDNESS AND RESPONSE PROGRAM AND PROPOSED 25 PROJECTS UNDER PHASE 1
The COVID-19 Strategic Training and Response Program has been developed by the International Bank for Reconstruction and Development and the International Development Association. The program involves 25 projects in 1 stage. This project is designed for the whole WORLD. The project completion date is March 31, 2025.
The full version of the project can be found here:
https://t.me/Tribulelouis/5922
At the heart of the pathogenesis of severe COVID-19 are lung immunopathology caused by a cytokine storm.
Similar processes are observed when re-infected after vaccination against RSV, SARS-CoV or influenza.
Vaccination that precedes SARS-CoV-2 infection can significantly increase the disease and increase mortality.
SARS-CoV-2
SARS-CoV-2 has been declared a highly pathogenic strain of a large family of coronaviruses (subfamily Betacoronavirus). Its known pathogenic precursors SARS-CoV and MERS-CoV are SARS and Middle East respiratory syndrome, respectively [1].
According to the literature, the genome of the SARS-CoV-2 strain is a single-stranded RNA, the size of which is about 30,000 nucleotide bases. In the genome of this virus, separate genes encoding 29 proteins with different functions are isolated [2].
SARS-CoV-2 structural proteins have lower values of the effective number of codons compared to bat SARS and other pathogenic strains, which implies a higher efficiency of gene expression of structural proteins SARS-CoV-2 [3].
The penetration of the coronavirus into a living cell is provided by S-proteins that bind to transmembrane receptors. For the MERS-CoV strain, these are DPP4, SARS-CoV - ACE2, SARS-CoV-2 - ACE2 and TMPRSS2 [4].
The 5'-cap structure of mRNA in eukaryotic cells plays an important role for stability, splicing, and mRNA transport, as well as for protein translation. Many viruses have their own excellent mechanisms for creating cap structures that help viral RNAs avoid recognition by the host's innate immune system. Back in the early 1980s, it was found that the RNA genomes of coronaviruses have a 5'-cap structure. For decades, the mechanisms of RNA capping of coronaviruses likely remained unknown. The outbreak of severe acute respiratory syndrome in 2003 stimulated numerous studies in the field of molecular virology. Recently, new functions of viral RNA cap structures in mammalian cells have been demonstrated: they allow avoiding recognition and protect against activation of the host's innate immune response, support viral replication by enhancing viral RNA translation, and help viruses resist interferon-mediated antiviral response [5].
Pathogenesis of COVID-19
COVID-19 is an infectious disease that causes an acute respiratory infection SARS-CoV-2 transmitted by contact or airborne droplets. Thus, COVID-19 is a type of acute respiratory infection, and SARS-CoV-2 is SARS. 80% of those infected carry this disease asymptomatically, 15% - at the level of severe colds, sometimes turning into pneumonia, and only 5% of patients have severe lung damage. It is known that the virus enters the human body through the mucous membranes, mainly the nose and larynx, then enters the lungs, from there to the blood, then to the intestines. Thus, the virus attacks the target organs that express ACE2 (lungs, heart, kidneys, gastrointestinal tract).
Currently, the pathogenesis of SARS-CoV-2 infection in humans is not fully understood. Based on clinical observations of severe patients with COVID-19, the following hypothesis was proposed: at the beginning of the disease, there is a reduction in lymphocytes in the B, which can affect the production of antibodies in patients, while a significant increase in inflammatory factors (mainly IL-6), which also contributes to the exacerbation of the disease. The worse the patient's condition, the more noticeable the reduction of B cells, as well as T cells, while the numbers of inflammatory cytokines and D-dimers continue to increase. As a result, computed tomography (CT) scan of the chest indicates an expansion of lung lesions. On the basis of the presented hypothesis, immunoglobulin and anticoagulant therapy was proposed [6].
Severe pneumonia caused by human pathogenic coronaviruses is often associated with rapid viral replication, inflammatory infiltration, and increased pro-inflammatory cytokine/quemokine reactions leading to acute lung damage and acute respiratory distress syndrome. In general, the picture for severe patients is as follows: immunopathology of the lungs, leading to dangerous clinical manifestations after infection with a pathogenic infection with hCoV, is caused by a violation of the regulation of the immune response [7].
Thus, severe manifestations of coronavirus infection, with high probability, are not pneumonia in the usual sense, but the strongest autoimmune processes.
Nasal immunity or "put on a mask"
The nasal mucosa is an important component of general immunity. The immunogenic particles present in the inhaled air activate the immune system of the nasal mucosa, which leads to its inflammation. In an animal model, it was shown that nasal inoculation of murine coronavirus in the absence of direct lung infection promotes the development of the immune environment in the lungs due to the migration of activated monocytes and killer cells there. Such migration is also observed with direct infection of lung tissue, but in this case, IFN-I signaling is required. Nasally-induced infiltration of inflammatory monocytes into the lungs occurs independently of IFN-I; activated macrophages take up the antigen and migrate to the pulmonary lymph nodes, enhancing both innate and adaptive immunity.
Clinically, nasal inoculation significantly reduced the incidence of fatal pneumonia caused by SARS-CoV or influenza A virus. These data indicate that the nose and upper respiratory tract remotely stimulate lung immunity, thus protecting them from direct viral infections [8] ...
Vaccination problems
The desired effect of vaccination is to induce protective immune responses against pathogenic infection. There are a number of problems in the development and use of vaccines, the most significant of which are: autoimmunity, turning into autoimmune diseases, and a decrease in protective immunity against a homologous infection [9]. Among the disorders of immunological reactivity, immunodeficiencies, allergies and pathological tolerance should also be noted. The association between vaccination and narcolepsy was noted in 2009 during the H1N1 pandemic in recipients of an influenza vaccine with the adjuvant AS03 (used to enhance the immune response) [15].
In addition, the question of immunoinfertility - infertility as a result of vaccination remains open [10].
The development of vaccines against coronavirus infections has been going on since the 1970s. [eleven]. The work [12] of 2012 describes the testing of four such vaccines in animal models. It was shown that each of them, two days after reinfection, induced an immunopathology that occurred in the lungs, while the virus was not detected there. The authors of this work made the following conclusions: vaccines against SARS-CoV induce antibodies and theoretically protect against infection with SARS-CoV. However, re-infection of mice receiving any of these vaccines results in Th2-type immunopathology, suggesting hypersensitivity to the SARS-CoV components.
In addition, the authors of this article expressed their concern and pointed out the dangers of using such vaccines to humans. The researchers cite a failed attempt to vaccinate young children with an inactivated drug against RSV (respiratory syncytial virus). The vaccinated children subsequently contracted the virus and suffered a serious illness requiring hospitalization, two of them died. Most of them showed Th2-type immunopathological reactions.
The conclusion from this experience was clear: RSV lung disease had been exacerbated by prior vaccination. Subsequent studies in animal models showed that an inactivated RSV vaccine induces an increased response of CD4 + T lymphocytes, mainly Th2 cells, and the formation of immune complex deposits in lung tissues. This type of tissue response is associated with an increase in type 2 cytokines (IL-4, IL-5, IL-6, IL-10, IL-13), and the influx of eosinophils into the infected lung. The immunopathological processes caused by vaccination and subsequent re-infection with RSV have significant similarities with the processes induced by SARS-CoV vaccines [12].
More recent studies (2018) have shown that this lethal immunopathology can be induced by the cellular memory of CD8 T cells. Similar processes were observed in animal models after immunization followed by infection with RSV, SARS-CoV, or influenza [13].
One of the main mechanisms for controlling viral infection is cellular cytotoxicity, which can act in an antibody-dependent or independent manner and is mediated by various effector cells. The role of CD8 T cells in controlling infection and influencing the pathological outcome of various types of infection has been demonstrated in numerous animal studies. The CD8 T cell response is an important link between innate immunity and the antibody-mediated immune response. In addition, these cells play a significant role in the development of autoimmune diseases. Simply put, normally, the work of these cells should be reduced to a balance between protective and self-destructive effects. This balance is likely to be upset by vaccination [14].
Relatively little is known about inflammatory mediators and the mechanisms that lead to the progression of influenza infection to a cytokine storm, lung dysfunction, organ failure, and eventually death. Vaccines and antiviral drugs are not able to control the excessive inflammatory response caused by infection. Recently, the rapid release of a powerful inflammatory mediator called Nourin has been demonstrated by local mammalian tissues in response to injury and infection. Nourin is a formylpeptide that acts through the FPR receptor on phagocytic leukocytes. As an initial signal of innate immunity, Nourin stimulates leukocyte chemotaxis, causes acute and chronic inflammation and stimulates the release of a number of cytokine storm mediators from monocytes, neutrophils and endothelial cells. In addition, the content of Nourin in plasma samples of patients with severe influenza was much higher compared to patients who carried the disease in a mild form. Nourin's antagonist, cyclosporine H, an immunosuppressant that is a strong anti-inflammatory compound and acts as a specific competitive FPR receptor antagonist, has been proposed as a therapeutic drug to suppress cytokine storm [16].
A little history: "Spanish Flu" 1918
In the work [17] the flu epidemic of 1918 is called the greatest failure of medical science of the 20th century. The victims of the flu "Spanish flu" were young and healthy people. The cytokine storm caused the destruction of inflamed lung tissue, which manifested itself as a bloody cough, and eventually led to death. The authors of this work note that the high virulence of the 1918 flu is not enough to be the only cause of high mortality recorded in humans during the epidemic, and use the concept of antigenic imprinting to explain an unusual pattern of death. It is known that in 1918 new vaccines were tested, which are the precursors of universal influenza vaccines [17].
It is known that T cells can undergo anthogenic imprinting: during re-infection, these cells, instead of destroying infected cells, exclusively stimulate the production of cytokines, which leads to an increase in vascular permeability, damage to endothelial cells, and, as a result, to aggravation of the disease [18]
Genetic factors
A small overview of genetic factors of resistance and susceptibility to coronavirus infections is presented in [19]. It seems interesting that for almost 20 years such questions have been of interest mainly to scientists from China and Korea.
Summary:
1. Medicine and pharmacology have no right to forget about the victims of vaccination and insufficiently tested drugs.
2. At present, the scientific community does not have sufficient knowledge to foresee the consequences of intrusion into the complex system of interactions of the human body with viruses, bacteria and other biological objects.
3. Any vaccination is able to induce the strongest autoimmune processes immediately or indirectly.
4. Vaccination against coronavirus infections leads to pulmonary immunopathologies with subsequent infection with these infections.
5. Each person, agreeing to vaccination, must understand that any vaccine is experimental, and he participates in this experiment as a test subject.
6. According to the Federal Law of the Russian Federation No. 323-FZ "On the Fundamentals of Health Protection of Citizens in the Russian Federation," no medical intervention can be carried out without the voluntary consent of the patient or the parents of a minor child.
7. According to the 1946 Nuremberg Doctors' Trial, no one can be subjected to medical, scientific or any other experiments without prior voluntary consent.
8. Refusal to vaccinate yourself or your child is not a marginal or thoughtless action, and also does not pose any threat to others.
BIBLIOGRAPHY:
1. Sch; fer A., Baric R.S., Ferris M.T. Systems approaches to Coronavirus pathogenesis. Curr Opin Virol. 2014 Jun; 6: 61–69. [PMID: 24842079]
2.
3. Mahmoud Kandeel, Abdelazim Ibrahim, Mahmoud Fayez, Mohammed Al-Nazawi. From SARS and MERS CoVs to SARS-CoV-2: Moving Toward More Biased Codon Usage in Viral Structural and Nonstructural Genes. J Med Virol. 2020 Mar 11; 10.1002 / jmv.25754. doi: 10.1002 / jmv.25754. [PMID: 32159237]
4. Hou Y., Peng C., Yu M., Li Y., Han Z., Li F., Wang LF, Shi Z. Angiotensin-converting enzyme 2 (ACE2) proteins of different bat species confer variable susceptibility to SARS -CoV entry. Arch Virol. 2010 Oct; 155 (10): 1563-1569. [PMID: 20567988]
5. Yu Chen, Deyin Guo. Molecular Mechanisms of Coronavirus RNA Capping and Methylation. Virol Sin. 2016 Feb; 31 (1): 3-11. doi: 10.1007 / s12250-016-3726-4. [PMID: 26847650]
6. Ling Lin, Lianfeng Lu, Wei Cao, Taisheng Li. Hypothesis for Potential Pathogenesis of SARS-CoV-2 Infection-A Review of Immune Changes in Patients With Viral Pneumonia. Emerg Microbes Infect. 2020 Dec; 9 (1): 727-732. doi: 10.1080 / 22221751.2020.1746199. [PMID: 32196410]
7. Rudragouda Channappanavar, Stanley Perlman. Pathogenic Human Coronavirus Infections: Causes and Semin Immunopathol. 2017 Jul; 39 (5): 529-539. doi: 10.1007 / s00281-017-0629-x. Epub 2017 May 2. Consequences of Cytokine Storm and Immunopathology. [PMID: 28466096]
8. Xiaoyang Hua, Rahul Vijay, Rudragouda Channappanavar, Jeremiah Athmer, David K Meyerholz, Nitin Pagedar, Stephen Tilley, Stanley Perlman. Nasal Priming by a Murine Coronavirus Provides Protective Immunity Against Lethal Heterologous Virus Pneumonia. JCI Insight. 2018 Jun 7; 3 (11): e99025. doi: 10.1172 / jci.insight.99025. [PMID: 29875310]
9. Yo Han Jang, Baik Lin Seong. Cross-protective Immune Responses Elicited by Live Attenuated Influenza Vaccines. Yonsei Med J. 2013 Mar 1; 54 (2): 271-82. doi: 10.3349 / ymj.2013.54.2.271. [PMID: 23364956]
10. Mindy S Christianson, Patricia Wodi, Kawsar Talaat, Neal Halsey. Primary Ovarian Insufficiency and Human Papilloma Virus Vaccines: A Review of the Current Evidence. Am J Obstet Gynecol. 2020 Mar; 222 (3): 239-244. doi: 10.1016 / j.ajog.2019.08.045. Epub 2019 Aug 31. [PMID: 31479634]
11. Coria MF. Protective effect of an inactivated avian coronavirus vaccine administered by aerosol. Arch Gesamte Virusforsch. 1973; 41 (1): 66-70. [PMID: 4716970]
12. Chien-Te Tseng, Elena Sbrana, Naoko Iwata-Yoshikawa, Patrick C Newman, Tania Garron, Robert L Atmar, Clarence J Peters, Robert B Couch. Immunization With SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Challenge With the SARS Virus. PLoS One. 2012; 7 (4): e35421. doi: 10.1371 / journal.pone.0035421. Epub 2012 Apr 20. [PMID: 22536382]
13. Schmidt ME, Knudson CJ, Hartwig SM, Pewe LL, Meyerholz DK, Langlois RA, Harty JT, Varga SM. Memory CD8 T cells mediate severe immunopathology following respiratory syncytial virus infection. PLoS Pathog. 2018 Jan 2; 14 (1): e1006810. [PMID: 29293660]
14. Daniil Korenkov, Irina Isakova-Sivak, Larisa Rudenko. Basics of CD8 T-cell Immune Responses After Influenza Infection and Vaccination With Inactivated or Live Attenuated Influenza Vaccine. Expert Rev Vaccines. 2018 Nov; 17 (11): 977-987. doi: 10.1080 / 14760584.2018.1541407. Epub 2018 Nov 15. [PMID: 30365908]
15. Kathryn Edwards, Paul-Henri Lambert, Steven Black. Narcolepsy and Pandemic Influenza Vaccination: What We Need to Know to Be Ready for the Next Pandemic. Pediatr Infect Dis J. 2019 Aug; 38 (8): 873-876. doi: 10.1097 / INF.0000000000002398. [PMID: 31306400]
16. Salwa A Elgebaly, Tamer Elbayoumi, Donald L Kreutzer. CYCLOSPORIN H: A NOVEL ANTI-INFLAMMATORY THERAPY FOR INFLUENZA FLU PATIENTS. J Egypt Soc Parasitol. 2017 Apr; 47 (1): 25-33. [PMID: 30157330]
17. John S Oxford, Douglas Gill. Unanswered Questions About the 1918 Influenza Pandemic: Origin, Pathology, and the Virus Itself. Lancet Infect Dis. 2018 Nov; 18 (11): e348-e354. doi: 10.1016 / S1473-3099 (18) 30359-1. Epub 2018 Jun 20. [PMID: 29935779]
18. Ramapraba Appanna 1, Tan Lian Huat, Lucy Lum Chai See, Phoay Lay Tan, Jamuna Vadivelu, Shamala Devi. Cross-reactive T-cell Responses to the Nonstructural Regions of Dengue Viruses Among Dengue Fever and Dengue Hemorrhagic Fever Patients in Malaysia. Clin Vaccine Immunol. 2007 Aug; 14 (8): 969-77. doi: 10.1128 / CVI.00069-07. Epub 2007 Jun 13. [PMID: 17567768]
Communists, go ahead. A moment of soulful melodic lyrics in the editorial office in the form of silver age poetry
And when there was a shortage
«... The proposed measures..."
And the vaccine 💉loaded into a backpack 🎒.
Barely audible
quoth
Young Officer :
- Communists, go ahead !.. Communists, go ahead!
Summer morning
A grenade fell into the grass.
On the lawn floor with left wing
All the guards then lay down.
They burned the fence, burned the asphalt.
And then —
barely audible
quoth
commander:
- Communists, go ahead !.. Communists, go ahead!
We ripped off all the doors 🚪 hinges.
The syringe 💉 the wringe of the powers in two hands.
At night, making your way to the houses —
The syringe smells of earth 🌎 the aroma of 🪔.
The day is approaching.
The century continues.
Indeveut vaccines 💉 before our eyes.
everywhere
Where are the syringe tracks crossed,
Or where the boiling of great works,
Through the ages,
for centuries,
Forever
to the end :
"Communists, go ahead! Communists, go ahead!
🤡 Anti-vaccination groups on Facebook change their names to euphemisms such as "dance party" to avoid detection and removal.
These groups are usually secret, not searchable, and can only be accessed by an invitation.
They use code words, for example, "Pizza" means Pfizer and "Moana" means Moderna.
The same thing happens on Instagram. Some influencers use code words.
"Swimmers" means vaccinated, and the act of vaccination is called "joining a swimming club.
In other groups, "danced" or "drank beer" means "grafted".
For example, one of the band members wrote that her husband fell ill after "a trip where we spent 2 nights with the dancers," referring to two people who had just been vaccinated.
"He believes that being near the dancers, the sequins caused him to reactivate shingles."
The sequins, in this case, refer to "vaccine shedding," a false theory among anti-vaccination activists that claims that vaccinated people somehow "spread" their vaccine to the unvaccinated because of what makes them sick.
Death from the vaccine will not be taken into account in the statistics of deaths from COVID-19
Deaths resulting from COVID-19 vaccination will not be included in the overall coronavirus death statistics.
In the new version of the Guidelines for Coding, the Ministry of Health explains how to register the need for immunization and the adverse effects of vaccinations.
The onset of a patient's death as a result of a reaction to a COVID-19 vaccine will not be included in the overall mortality statistics from the novel coronavirus infection.
This follows from the new version of the Guidelines for Coding and Selection of Underlying Condition in the statistics of morbidity and initial cause of death associated with COVID-19.
According to the document, all adverse reactions to vaccination are encoded by a new heading U12.9. The code is used only as an external cause of death.
External causes of death include those that are caused not by diseases, but by various external influences. They can be intentional (murder and suicide) or unintentional (accidents involving traffic or caused by fire; drowning; poisoning; falls), also highlight injuries with uncertain intentions. This is the only class of causes that causes only preventable deaths.
In the case of an abnormal reaction to the introduction of the vaccine, the Ministry of Health recommends the use of double coding and gives an example with vaccine-induced anaphylactic shock (ASH).
As the main disease, ASH is registered under the code T88.6 (Anaphylactic shock caused by a pathological reaction to an adequately prescribed and correctly used drug).
Code U12.9 in mortality statistics is not used and is not subject to use in the coding of the underlying disease, the document says.
It can only be taken into account in morbidity statistics as an additional code in sample statistical studies.
Official statistics of deaths as a result of the introduction of a vaccine against coronavirus in Russia is not publicly available.
Oh, Monica, what else did you think, or say what end did you want at the end of a cute 🥰
get?
Insert diamonds 💎, emeralds and apply thin layers of gold leaf on His Deserved Crown 🤴 asked personally SHE ⬇️
All at your feet Dear, how you love 🥂
https://telegra.ph/AGENTS-OF-THE-NEW-COMMUNIST-CRIMINAL-ORDER-2021-07-27
ℳɼ. ℮ɳᎿɛɼᎿɑⅈɳɛɼ .