In order to prove a new pathogenic “virus” exists, Koch’s Postulates must be satisfied first. They are four logic-based rules established by Robert Koch in 1890 and are considered the bare minimum requirements needed to be fulfilled in order to prove a microbe causes disease. Postulates 3 and 4, in particular, deal with the use of animal models in order to prove purified particles cause the same disease in animals as found in a human host:
- the pathogen from the pure culture must cause the same disease when inoculated into a healthy, susceptible laboratory animal
- the pathogen must be reisolated from the new host and shown to be the same as the originally inoculated pathogen
Sadly, even the early “SARS-COV-2” researchers admitted to not fulfilling these basic postulates, specifically in regards to proving pathogenicity in an animal model:
From two of the original studies:
“Although our study does not fulfill Koch’s postulates, our analyses provide evidence implicating 2019-nCoV in the Wuhan outbreak. Additional evidence to confirm the etiologic significance of 2019-nCoV in the Wuhan outbreak include identification of a 2019-nCoV antigen in the lung tissue of patients by immunohistochemical analysis, detection of IgM and IgG antiviral antibodies in the serum samples from a patient at two time points to demonstrate seroconversion, and animal (monkey) experiments to provide evidence of pathogenicity.”
https://www.nejm.org/doi/full/10.1056/NEJMoa2001017
“However, there are still many urgent questions that remain to be answered. The association between 2019-nCoV and the disease has not been verified by animal experiments to fulfil the Koch’s postulates to establish a causative relationship between a microorganism and a disease. We do not yet know the transmission routine of this virus among hosts.”
https://www.nature.com/articles/s41586-020-2012-7
In other words, they assumed that the unpurified cell culture soup they created in a lab (which contains everything from monkey kidney cells, antibiotics, fetal bovine serum, etc. along with the host specimen) was a “virus” without ever proving they actually had a pathogenic “virus.” They not only ignored Koch’s 2nd Postulate stating the particles must be PURE, they entirely skipped over the final two crucial steps of showing that what they created in a lab caused the same disease in animals that it does in humans.
Don’t just take my word for it.
From an interview with Xu Jianguo on January 10, 2020, head of an evaluation committee advising the Chinese government:
“Q: Are researchers trying to replicate the disease in lab animals to prove that it is really the cause of the outbreak?
A: People have recommended that [investigators] do tests to see if the virus can cause the infection in animals, but they need time.”
Need time, huh?
This is from a review published at the end of June 2020, a good 6 months after the Xu interview requesting more time:
“There is an urgent need for an ideal animal model that can reflect clinical symptoms and underlying etiopathogenesis similar to COVID-19 patients which can be further used for evaluation of underlying mechanisms, potential vaccines, and therapeutic strategies.”
“This emphasizes the surge for a suitable animal model to explore the pathogenesis and evaluation of countermeasures for the disease.”
“The novel coronavirus (COVID-19) pathology is linked to viral respiratory infection, hyper-immune response, and coagulopathy (Lin et al.2020; Connors and Levy 2020), therefore, to understand the mechanism or to evaluate therapeutic countermeasures, the animal models should involve all these interplays in a single model.”
“Further, validation of the animal model is crucial. The error in the animal experimental study narrows the chances of the potential drugs or repurposing or repositioning drugs or vaccines to translate successfully to clinics and moreover, it is a wastage of resources. Thus, it is the need of the hour to validate the animal model using different criteria, for instance, face, construct, and predictive validity (Denayer et al.2014).”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7324485/
From September 2020 (9 months after Xu):
“Animal models that faithfully reproduce human COVID-19 (i.e., incorporating the most important disease mechanisms, clinical signs, and response to treatment) are of utmost importance in order to achieve this. As commented by others (Callaway, 2020; Cleary et al., 2020; Cohen, 2020) animal species ranging from mice to non-human primates are actively being investigated in the quest for reproducible and faithful models of COVID-19.”
“Thus, currently, no animal model of severe COVID-19 that reproduces the salient clinical and pathological features of the disease has been described. Mild symptoms are achievable in permissive species, but no model reproducing severe COVID-19, characterized by both upper and lower respiratory tract infection, pro-inflammatory cytokine activation, and prolonged disease is available, although such models obviously are of particular interest for investigation of intervention modalities and for biomarker research.”
https://www.frontiersin.org/articles/10.3389/fmicb.2020.573756/full
This is from a review published in October 2020 (10 months post Xu interview):
“Most of the animal models of COVID-19 recapitulated mild pattern of human COVID-19 with full recovery phenotype. No severe illness associated with mortality was observed, suggesting a wide gap between COVID-19 in humans and animal models.”
“However, none of the animal models replicated the severe or critical patterns associated with mortality as observed in humans with COVID-19 [3].
The results of this systematic review are consistent with studies of animal models of SARS-CoV and MERS-CoV, which failed to replicate the full spectrum of humans’ illness.”
“This systematic review revealed that none of these newly established animal models replicated the common complications of human COVID-19 such as ARDS and coagulopathy.”
“None of the animal models replicated the respiratory failure, thromboembolic manifestations, and their pathological expression, hence, indicating that a wide gap separates the animal models from the full spectrum of COVID-19 in humans.”
“Since the emergence of SARS-CoV infection in 2003 [76], followed by the MERS-CoV in 2012 [77], and now with COVID-19, researchers have not been able to develop a model of coronavirus infection that reproduces the severity and lethality seen in humans.”
https://ccforum.biomedcentral.com/articles/10.1186/s13054-020-03304-8
From a study in November 2020 (11 months after the Xu interview):
“To interpret the process of infection and understand the systematic pathology of the disease caused by SARS-CoV-2 in humans, an effective SARS-CoV-2 infection animal model is urgently needed.”
https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1008949
And finally, from a review published April 2021 (a good 16 months after Xu said more time was needed):
“The emergence of the novel SARS-CoV-2 pathogen has resulted in the need for the development of an appropriate animal model to aid in the understanding of disease causation, transmission, and pathogenesis, as well as to elucidate the details of the host
immune response. Perhaps the most perplexing aspect of SARS-CoV-2 infection is the wide range of disease severity in humans, which can vary from asymptomatic or mild presentation to severe and fatal disease. Developing animal models that can reflect such diverse clinical manifestations is remarkably important, albeit arduous. While many SARS-CoV-2 infection models have been developed and investigated thus far, including mice, hamsters, ferrets, and NHPs, a large variation in results has been obtained both between and within species.”
“Although numerous animal models are available, however, currently, no single existing animal model can really recapitulate the totality of human SARS-CoV-2 infection. Several possible reasons may explain why experimental animal models only reflect moderate lung pathology and disease manifestation. These include, route and method of virus inoculation, absence nor not been rigorously explored effects of co-morbidities and other risk factors associated with high-case fatality such as advancement in the age of the animal, obesity, diabetes, cardiovascular disease and immunocompromised state.”
https://pubmed.ncbi.nlm.nih.gov/33996168/
16 + months in and there are still no valid “SARS-COV-2” animal models. Remember, this isn’t something that can just be pushed off to the side for someone to create at a later date. Being able to recreate the same disease in animals is an essential step in proving a “virus” exists and is actually pathogenic. The original “SARS-COV-2” researchers admitted they never fulfilled this basic requirement. Many other researchers have tried and failed. Without proof of pathogenicity, how was it ever allowed to be claimed that a new “virus” exists and is causing disease?
Clearly, we have been put under lockdown, quarantined, social distanced, masked, and vaccinated with a rushed, experimental mRNA gene therapy for a “virus” that has never been proven to exist in a pure form nor proven pathogenic in any animal models, thus failing Koch’s Postulates.
We’ve been lied to from the very start and virology continues to kick the can down the road in order to avoid providing the neccessary evidence of pathogenicity. They say that they will have it someday…they just “need more time.”
Time has run out.
ViroLIEgy 
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