Boston gain of function virus

Please share this video, this research must STOP. Gain of function research in the USA today using enhanced potential pandemic pathogen (ePPP) research Professor Shmuel Shapira, lead scientist, Israeli Government This should be totally forbidden, it’s playing with fire Dr Richard Ebright, Rutgers University, New Brunswick The research is a clear example of gain of function research. If we are to avoid a next lab-generated pandemic, it is imperative that oversight of enhanced potential pandemic pathogen research be strengthened. it is imperative that officials at US-government agencies, who repeatedly have placed the public at risk by repeatedly violating the existing policies be held accountable Prof David Livermore, microbiology, University of East Anglia given the strong likelihood that the Covid pandemic originated from the escape of a lab-manipulated coronavirus in Wuhan, these experiments seem profoundly unwise Boston University’s National Emerging Infectious Diseases Laboratories is one of 13 biosafety level 4 labs in the US Role of spike in the pathogenic and antigenic behavior of SARS-CoV-2 BA.1 Omicron 14th October 2022 Boston University School of Medicine Predominant SARS-CoV-2 Omicron variant (BA.1) is highly transmissible, even in fully vaccinated individuals, and causes attenuated disease compared with other major viral variants recognized to date The Omicron spike (S) protein, unusually large number of mutations, is considered the major driver of these phenotypes We generated chimeric recombinant SARS-CoV-2 A chimera or chimeric virus One virus containing genetic material derived from two or more distinct viruses US Center for Veterinary Biologics A new hybrid microorganism, created by joining nucleic acid fragments from two or more different microorganisms, in which each of at least two of the fragments, contain essential genes necessary for replication We generated chimeric recombinant SARS-CoV-2 Encoding the S gene of Omicron in the backbone of an ancestral SARS-CoV-2 isolate, and compared this virus with the naturally circulating Omicron variant. The Omicron S-bearing virus robustly escapes vaccine-induced humoral immunity, mainly due to mutations in the receptor-binding motif, yet unlike naturally occurring Omicron, efficiently replicates in cell lines and primary-like distal lung cells. In K18-hACE2 mice K18-hACE2 transgenic mice express human ACE2, including airway epithelia where infections typically begin. Because K18-hACE2 are susceptible to SARS-CoV-2 and SARS-CoV viruses, they are useful for studying antiviral therapies to COVID-19 and SARS. In K18-hACE2 mice Omicron causes mild, non-fatal infection, the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80%. This indicates that while the vaccine escape of Omicron is defined by mutations in S, major determinants of viral pathogenicity reside outside of S. Frankenstein, Mary Shelley, 1818 Frightful must it be; for supremely frightful would be the effect of any human endeavour to mock the stupendous mechanism of the Creator of the world (1831 edition)