The Boston Virus

In all cases, emphasis added.

Please see this.

The paper.

Authors:

Da-Yuan Chen, Devin Kenney, Chue Vin Chin, Alexander H. Tavares, Nazimuddin Khan, Hasahn L. Conway, GuanQun Liu, Manish C. Choudhary, Hans P. Gertje, Aoife K. O’Connell, Darrell N. Kotton, Alexandra Herrmann,  View ORCID ProfileArmin Ensser, John H. Connor, Markus Bosmann, Jonathan Z. Li, Michaela U. Gack, Susan C. Baker, Robert N. Kirchdoerfer, Yachana Kataria, Nicholas A. Crossland, Florian Douam, Mohsan Saeed

First author.

Corresponding author.

Abstract:

The recently identified, globally 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 date1–7. The Omicron spike (S) protein, with an unusually large number of mutations, is considered the major driver of these phenotypes3,8. 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 (RBM), yet unlike naturally occurring Omicron, efficiently replicates in cell lines and primary-like distal lung cells. In K18-hACE2 mice, while 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.

Funding:

ACKNOWLEDGEMENT

We thank Dr. Yoshiharu Matsuura from Osaka University, Japan, for providing the pCSII-SARS-CoV-F8 plasmid; the Department of Public Health, Massachusetts, for providing the clinical specimen containing Omicron virus; and the ICCB-Longwood Screening Facility of Harvard Medical School forassistance with IF image acquisition and analysis. This work was supported by Boston University startupfunds (to MS and FD), National Institutes of Health, NIAID grants R01 AI159945 (to SB and MS) andR37 AI087846 (to MUG), NIH SIG grants S10-OD026983 and SS10-OD030269 (to NAC), Peter PaulCareer Development Award (to FD), and BMBF SenseCoV2 01KI20172A (AE) and DFG Fokus COVID19, EN 423/7-1 (AE). We thank the Clinical & Translational Science Institute (CTSI; 1UL1TR001430) andEvans Center for Interdisciplinary Biomedical Research at Boston University School of Medicine for their support of the Affinity Research Collaborative on ‘Respiratory Viruses: A Focus on COVID-19’. 

See this.

However, neither NIH nor NIAID have ever approved any grant that would have supported “gain-of-function” research on coronaviruses that would have increased their transmissibility or lethality for humans.

That’s not true anymore, is it?

Do you really want these people creating and handling deadly viruses? I suggest that American readers contact their Senators and Congressmen (Representatives) and demand that they investigate this fiasco and put an end to it.  Readers in other nations should contact their appropriate national leadership contacts and demand that they contact American equivalents and demand answers.

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