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Boston University Creates Lab Made Frankenstein COVID Virus

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Are we attempting to prove the lab-leak hypothesis by carrying it out in the United States? Were the lessons learned from the COVID-19 outbreak not severe enough? Boston University has created a lab made Frankenstein COVID virus.

Boston University Creates Lab Made Frankenstein COVID Virus

A public outcry has been caused by the development of a new recombinant COVID-19 virus at Boston University, which many people have dubbed a “Frankenstein virus.” This is not just a dangerous gain-of-function experiment on “enhanced potential pandemic pathogens (ePPPs)”, but also the development of an enhanced pandemic pathogen. NO “potential” is present.

What is the justification for this assertion? What exactly is the chimeric virus we are discussing here?

On October 14, 2022, a group of scientists from Boston University’s National Emerging Infectious Diseases Laboratories published a paper (read below) on BioRxiv, a preprint server for biology, announcing that they had developed a COVID-19 chimeric virus in the lab using reverse genetics.

To be more precise, they have switched the S gene of the spike protein in the original SARS-CoV-2 Wuhan strain with the equivalent S gene from the Omicron strain. Ergo, all the genes in the laboratory-created Chimeric virus (Wuhan-Omi-S chimeric virus), which is significantly more pathogenic than the Omicron strain, are from the Wuhan strain, with the exception of the S gene, which is from the highly transmissible but only marginally pathogenic Omicron strain.

Boston University Creates Lab Made Frankenstein COVID Virus 2

The Omicron spike-bearing virus is able to successfully and robustly evade vaccine-induced humoral immunity, according to the preprint publication. Additionally, the Wuhan-Omi-S chimeric virus successfully replicates in cell lines and distal lung cells that resemble primary lung cells, unlike the naturally occurring Omicron strain.

Additionally, it killed at least 80% of infected K18-hACE2 mice (a subtype of transgenic mice harboring human ACE2 receptors), whilst the Omicron strain caused 0% mortality in control studies within the same transgenic mice and the Wuhan strain caused 100% death in two weeks. The Wuhan-Omi-S chimeric virus caused an 80 percent mortality rate in mice over a two-week period. The study did not offer any additional findings on whether the mice who survived died sooner or later than the control mice group who were infected with Omicron variants.

The proponents of this dangerous study claimed that the chimeric virus product demonstrated reduced pathogenicity (100 versus 80% mortality) when contrasted to Wuhan strains, indicating that it is not a gain-of-function research. This, however, is an overly idealistic statement. The study did not include a complete or comprehensive pathological examination of several organs in transgenic mice infected with the Wuhan-Omi-S virus. Do we know, for instance, whether this chimeric virus shares the same neuropathogenesis as the Omicron or Wuhan viruses? This study did not offer any information on the subject.

Furthermore, while this research was reported as a swap of the S gene on the backbone of the Wuhan strain, it may also be interpreted as a swap of other viral genes on the backbone of the Omicron strain, given the overall high genome homology among different SARS-CoV-2 virus variants. Rather than studying specific gene motifs that could have influenced the pathogenicity of the Omicron strain, researchers at Boston University transferred all pathogenicity-related viral gene motifs/sites from the Wuhan strain into the Omicron strain.

Then, this research is a genuine verified gain-of-function study: it allows the Omicron virus to acquire more virulent components, increasing its infectivity and pathogenicity in in vitro and in vivo trials. Furthermore, no study was disclosed in this report to test the transmissibility of the chimeric lab-made virus in animal models. Is the Wuhan-Omi-S virus more or less communicable in animal models? Can any of the scientists in this research confirm that this novel chimeric virus is not more transmissible in different animal models, such as golden hamsters, ferrets, and primates?

“While the vaccine escape of Omicron is defined by 53 mutations in S, major determinants of viral pathogenicity reside outside of S,” was the study’s main finding. It is established that several genes other than S are crucial to viral pathogenicity in various tissues, organs, and animal hosts, and that other genes other than S are engaged in viral-host interactions at various stages of the viral life cycle. The researchers would therefore anticipate to produce a virus that is both extremely lethal and very contagious by fusing the pathogenicity-related elements of the original Wuhan strain with Omicron’s spike protein. There is no assurance that the degree of the hazards or threats cannot be precisely managed or assessed, even if it is fortunate that the final chimeric virus strains are less lethal and/or less contagious than the Wuhan and/or Omicron strains. With full awareness of the risks, Boston University researchers are purposefully experimenting with fire.

In other words, scientists at Boston University engineered a lab-made Omicron variant with increased pathogenicity. This study has produced an improved pandemic pathogen since Omicron is a clear pandemic pathogen that replaces Delta and other COVID-19 viral strains. Not an “enhanced pandemic potential pathogen.”

The ability of this laboratory-created chimeric virus to outcompete naturally occurring omicron strains when co-circulating in human civilization is something that is unknown. Additionally, proponents of this gain-of-function study pointed out that a related recombinant variant called Deltacron, which combines an Omicron S gene with a Delta variant backbone, was available earlier this year. They claimed that because the Omicron variants swiftly replaced the Deltacron and did not cause a pandemic wave, the Boston University experiment did not pose an elevated risk. So, are these advocates saying that humanity was just too fortunate and that we must take on more risks?

This study should be categorically prohibited since it is playing with fire. It is incredible that Boston University approved of this study being conducted. The Boston University bioethics committee, which assesses proposals involving biological research, has ultimately failed.

Additionally, the National Institute of Allergy and Infectious Diseases (NIAID) of the National Institutes of Health, which has denied knowing about these trials, is funding a portion of this gain-of-function research effort. It is impossible to verify whether NIAID was aware of these studies throughout the entire process because the relevant award paperwork and the correspondence between Boston University and NIAID are not currently available to the public. However, it indicates that the oversight process for reviewing funding relating to “enhanced potential pandemic pathogens (ePPPs)” established by NIAID following the suspension of all gain-of-function studies in 2014 did not function at all in this instance.

The NIH relaxed the funding moratorium in December 2017 and solicited fresh gain-of-function (GOF) applications. And, by 2019, Dr. Yoshihiro Kawaoka of the University of Wisconsin in Madison and Dr. Ron Fouchier of the Netherlands have received NIAID money to pursue their dangerous research with influenza viruses. Dr. Fouchier’s suggested studies included finding chemical alterations that make flu viruses more dangerous, as well as mutations that occur when H5N1 is passed through ferrets. As a result, it appears that the NIAID is now alright with producing a more virulent H5N1 virus strain.

Even if NIAID had established a relevant oversight framework to evaluate grant applications pertaining to ePPPs, it would seem that the system would be entirely ineffective since grant reviewers or health agencies have a predisposition to endorse gain-of-function research in the moniker of pursuing a better understanding of viral-host interactions or pandemic controls. If authorization is granted to generate more hazardous highly pathogenic H5N1 influenza viruses, it is only a matter of time before permission is issued to develop more virulent pandemic-ready SARS-CoV-2 omicron strains.

So, can the public have faith in government bodies like the NIAID to undertake a more effective regulatory role in such risky gain-of-function research projects? The NIAID and Boston University should take this issue seriously and immediately shut down all linked laboratories. Since the researchers have perfected reverse genetics technology, they may theoretically easily undertake more gain-of-function experiments, including the generation of new virus strains. The NIAID and Boston University can not hide behind risk-aversion policies. Public monitoring and transparency are required to prevent putting ourselves in grave danger on a regular basis.

In the absence of competing viral strains, such as after the natural COVID-19 pandemic, this lab-made Wuhan-Omi-S chimeric virus will cause a fresh wave of pandemic if it escapes. The globe was worried in the last two to three years that the COVID-19 pandemic was caused by a tragic gain-of-function lab-leaked catastrophe at the Wuhan Institute of Virology. Are we attempting to prove the lab-leak hypothesis by carrying it out in the United States? Were the lessons learned from the COVID-19 outbreak not severe enough?

Read the full study below:

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