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Why the alpha variant (originally found in the U.K.) has been so strong

Posted: 2021, Jul 31, Sat, 4:08 pm
by AHE
They found that lung cells with alpha made drastically less interferon, a protein that switches on a host of immune defenses,” according to The New York Times. “They also found that in the alpha cells, the defensive genes normally switched on by interferon were quieter than in cells infected with other variants.
https://www.deseret.com/coronavirus/202 ... nt-reasons

Evolution of enhanced innate immune evasion by the SARS-CoV-2 B.1.1.7 UK variant

Posted: 2021, Jul 31, Sat, 4:10 pm
by AHE
B.1.1.7 isolates more effectively suppress host innate immune responses in airway epithelial cells. We found that B.1.1.7 isolates have dramatically increased subgenomic RNA and protein levels of Orf9b and Orf6, both known innate immune antagonists. Expression of Orf9b alone suppressed the innate immune response through interaction with TOM70, a mitochondrial protein required for RNA sensing adaptor MAVS activation, and Orf9b binding and activity was regulated via phosphorylation. We conclude that B.1.1.7 has evolved beyond the Spike coding region to more effectively antagonise host innate immune responses through upregulation of specific subgenomic RNA synthesis and increased protein expression of key innate immune antagonists.
https://www.biorxiv.org/content/10.1101 ... 6.446826v1

Evolution of enhanced innate immune evasion by the SARS-CoV-2 B.1.1.7 UK variant

Posted: 2021, Jul 31, Sat, 4:11 pm
by AHE
B.1.1.7 isolates more effectively suppress host innate immune responses in airway epithelial cells. We found that B.1.1.7 isolates have dramatically increased subgenomic RNA and protein levels of Orf9b and Orf6, both known innate immune antagonists. Expression of Orf9b alone suppressed the innate immune response through interaction with TOM70, a mitochondrial protein required for RNA sensing adaptor MAVS activation, and Orf9b binding and activity was regulated via phosphorylation. We conclude that B.1.1.7 has evolved beyond the Spike coding region to more effectively antagonise host innate immune responses through upregulation of specific subgenomic RNA synthesis and increased protein expression of key innate immune antagonists.
https://www.biorxiv.org/content/10.1101 ... 6.446826v1