Mary Wilson
Well-known member
New Results
Posted January 10, 2023.
doi: https://doi.org/10.1101/2022.10.13.512134
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, Armin 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
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 date[SUP]1–7[/SUP]. The Omicron spike (S) protein, with an unusually large number of mutations, is considered the major driver of these phenotypes[SUP]3,8[/SUP]. 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.
https://www.biorxiv.org/content/10.1101/2022.10.13.512134v2.full.pdf
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Previous Preprint Study dated October 14, 2022
https://www.biorxiv.org/content/10.1101/2022.10.13.512134v1.full
Posted January 10, 2023.
doi: https://doi.org/10.1101/2022.10.13.512134
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, Armin 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
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 date[SUP]1–7[/SUP]. The Omicron spike (S) protein, with an unusually large number of mutations, is considered the major driver of these phenotypes[SUP]3,8[/SUP]. 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.
https://www.biorxiv.org/content/10.1101/2022.10.13.512134v2.full.pdf
__________________________________________________ _________________
Previous Preprint Study dated October 14, 2022
https://www.biorxiv.org/content/10.1101/2022.10.13.512134v1.full