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Basic Characteristics of Mutations
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Mutation Site
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G496K |
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Mutation Site Sentence
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To experimentally verify the hypothesis, we made several constructs expressing WA1 spike bearing the following combinations of mutations: N501Y-Q493K, N501Y-Q493R, G496K-Q493K, N501Y-S494R, N501Y-G496K, N501F-G496K, and N501K-Q493K. |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
|
S |
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Standardized Encoding Gene
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S
|
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Genotype/Subtype
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Omicron |
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Viral Reference
|
-
|
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Functional Impact and Mechanisms
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Disease
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COVID-19
|
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Immune
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- |
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Target Gene
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-
|
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Clinical and Epidemiological Correlations
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Clinical Information
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- |
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Treatment
|
- |
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Location
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- |
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Literature Information
|
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PMID
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36075211
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Title
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Spike protein-independent attenuation of SARS-CoV-2 Omicron variant in laboratory mice
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Author
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Liu S,Selvaraj P,Sangare K,Luan B,Wang TT
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Journal
|
Cell reports
|
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Journal Info
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2022 Sep 13;40(11):111359
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Abstract
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Despite being more transmissible, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant only causes milder diseases in laboratory animals, often accompanied by a lower viral load compared with previous variants of concern. In this study, we report the structural basis for a robust interaction between the receptor-binding domain of the Omicron spike protein and mouse ACE2. We show that pseudovirus bearing the Omicron spike protein efficiently utilizes mouse ACE2 for entry. By comparing viral load and disease severity among laboratory mice infected by a natural Omicron variant or recombinant ancestral viruses bearing either the entire Omicron spike or only the N501Y/Q493R mutations in its spike, we find that mutations outside the spike protein in the Omicron variant may be responsible for the observed lower viral load. Together, our results imply that a post-entry block to the Omicron variant exists in laboratory mice.
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Sequence Data
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-
|