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  1. Article ; Online: Antibody escape and cryptic cross-domain stabilization in the SARS-CoV-2 Omicron spike protein.

    Javanmardi, Kamyab / Segall-Shapiro, Thomas H / Chou, Chia-Wei / Boutz, Daniel R / Olsen, Randall J / Xie, Xuping / Xia, Hongjie / Shi, Pei-Yong / Johnson, Charlie D / Annapareddy, Ankur / Weaver, Scott / Musser, James M / Ellington, Andrew D / Finkelstein, Ilya J / Gollihar, Jimmy D

    Cell host & microbe

    2022  Volume 30, Issue 9, Page(s) 1242–1254.e6

    Abstract: The worldwide spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to the repeated emergence of variants of concern. For the Omicron variant, sub-lineages BA.1 and BA.2, respectively, contain 33 and 29 nonsynonymous and indel ... ...

    Abstract The worldwide spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to the repeated emergence of variants of concern. For the Omicron variant, sub-lineages BA.1 and BA.2, respectively, contain 33 and 29 nonsynonymous and indel spike protein mutations. These amino acid substitutions and indels are implicated in increased transmissibility and enhanced immune evasion. By reverting individual spike mutations of BA.1 or BA.2, we characterize the molecular effects of the Omicron spike mutations on expression, ACE2 receptor affinity, and neutralizing antibody recognition. We identified key mutations enabling escape from neutralizing antibodies at a variety of epitopes. Stabilizing mutations in the N-terminal and S2 domains of the spike protein can compensate for destabilizing mutations in the receptor binding domain, enabling the record number of mutations in Omicron. Our results provide a comprehensive account of the mutational effects in the Omicron spike protein and illustrate previously uncharacterized mechanisms of host evasion.
    MeSH term(s) Angiotensin-Converting Enzyme 2/genetics ; Antibodies, Neutralizing/genetics ; Antibodies, Viral ; COVID-19 ; Epitopes ; Humans ; Membrane Glycoproteins ; Mutation ; SARS-CoV-2/genetics ; Spike Glycoprotein, Coronavirus/genetics ; Viral Envelope Proteins
    Chemical Substances Antibodies, Neutralizing ; Antibodies, Viral ; Epitopes ; Membrane Glycoproteins ; Spike Glycoprotein, Coronavirus ; Viral Envelope Proteins ; spike protein, SARS-CoV-2 ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Language English
    Publishing date 2022-08-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2278004-X
    ISSN 1934-6069 ; 1931-3128
    ISSN (online) 1934-6069
    ISSN 1931-3128
    DOI 10.1016/j.chom.2022.07.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Antibody escape and cryptic cross-domain stabilization in the SARS CoV-2 Omicron spike protein

    Javanmardi, Kamyab / Segall-Shapiro, Thomas H / Chou, Chia-Wei / Boutz, Daniel R / Olsen, Randall J / Xie, Xuping / Xia, Hongjie / Shi, Pei-Yong / Johnson, Charlie D / Annapareddy, Ankur / Weaver, Scott / Musser, James M / Ellington, Andrew D / Finkelstein, Ilya J / Gollihar, Jimmy D

    bioRxiv

    Abstract: The worldwide spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to the repeated emergence of variants of concern. The Omicron variant has two dominant sub-lineages, BA.1 and BA.2, each with unprecedented numbers of ... ...

    Abstract The worldwide spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to the repeated emergence of variants of concern. The Omicron variant has two dominant sub-lineages, BA.1 and BA.2, each with unprecedented numbers of nonsynonymous and indel spike protein mutations: 33 and 29, respectively. Some of these mutations individually increase transmissibility and enhance immune evasion, but their interactions within the Omicron mutational background is unknown. We characterize the molecular effects of all Omicron spike mutations on expression, human ACE2 receptor affinity, and neutralizing antibody recognition. We show that key mutations enable escape from neutralizing antibodies at a variety of epitopes. Stabilizing mutations in the N-terminal and S2 domains of the spike protein compensate for destabilizing mutations in the receptor binding domain, thereby enabling the record number of mutations in Omicron sub-lineages. Taken together, our results provide a comprehensive account of the mutational effects in the Omicron spike protein and illuminate previously unknown mechanisms of how the N-terminal domain can compensate for destabilizing mutations within the more evolutionarily constrained RBD.
    Keywords covid19
    Language English
    Publishing date 2022-04-18
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2022.04.18.488614
    Database COVID19

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  3. Article ; Online: Whole-genome sequencing and genetic variant analysis of a Quarter Horse mare.

    Doan, Ryan / Cohen, Noah D / Sawyer, Jason / Ghaffari, Noushin / Johnson, Charlie D / Dindot, Scott V

    BMC genomics

    2012  Volume 13, Page(s) 78

    Abstract: Background: The catalog of genetic variants in the horse genome originates from a few select animals, the majority originating from the Thoroughbred mare used for the equine genome sequencing project. The purpose of this study was to identify genetic ... ...

    Abstract Background: The catalog of genetic variants in the horse genome originates from a few select animals, the majority originating from the Thoroughbred mare used for the equine genome sequencing project. The purpose of this study was to identify genetic variants, including single nucleotide polymorphisms (SNPs), insertion/deletion polymorphisms (INDELs), and copy number variants (CNVs) in the genome of an individual Quarter Horse mare sequenced by next-generation sequencing.
    Results: Using massively parallel paired-end sequencing, we generated 59.6 Gb of DNA sequence from a Quarter Horse mare resulting in an average of 24.7X sequence coverage. Reads were mapped to approximately 97% of the reference Thoroughbred genome. Unmapped reads were de novo assembled resulting in 19.1 Mb of new genomic sequence in the horse. Using a stringent filtering method, we identified 3.1 million SNPs, 193 thousand INDELs, and 282 CNVs. Genetic variants were annotated to determine their impact on gene structure and function. Additionally, we genotyped this Quarter Horse for mutations of known diseases and for variants associated with particular traits. Functional clustering analysis of genetic variants revealed that most of the genetic variation in the horse's genome was enriched in sensory perception, signal transduction, and immunity and defense pathways.
    Conclusions: This is the first sequencing of a horse genome by next-generation sequencing and the first genomic sequence of an individual Quarter Horse mare. We have increased the catalog of genetic variants for use in equine genomics by the addition of novel SNPs, INDELs, and CNVs. The genetic variants described here will be a useful resource for future studies of genetic variation regulating performance traits and diseases in equids.
    MeSH term(s) Animals ; DNA Copy Number Variations ; Female ; Genome ; Genomics/methods ; Genotype ; Horse Diseases/genetics ; Horses/genetics ; Molecular Sequence Annotation ; Mutation ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci ; Sequence Analysis, DNA ; Signal Transduction
    Language English
    Publishing date 2012-02-17
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1471-2164
    ISSN (online) 1471-2164
    DOI 10.1186/1471-2164-13-78
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Whole-Genome sequencing and genetic variant analysis of a quarter Horse mare

    Doan Ryan / Cohen Noah D / Sawyer Jason / Ghaffari Noushin / Johnson Charlie D / Dindot Scott V

    BMC Genomics, Vol 13, Iss 1, p

    2012  Volume 78

    Abstract: Abstract Background The catalog of genetic variants in the horse genome originates from a few select animals, the majority originating from the Thoroughbred mare used for the equine genome sequencing project. The purpose of this study was to identify ... ...

    Abstract Abstract Background The catalog of genetic variants in the horse genome originates from a few select animals, the majority originating from the Thoroughbred mare used for the equine genome sequencing project. The purpose of this study was to identify genetic variants, including single nucleotide polymorphisms (SNPs), insertion/deletion polymorphisms (INDELs), and copy number variants (CNVs) in the genome of an individual Quarter Horse mare sequenced by next-generation sequencing. Results Using massively parallel paired-end sequencing, we generated 59.6 Gb of DNA sequence from a Quarter Horse mare resulting in an average of 24.7X sequence coverage. Reads were mapped to approximately 97% of the reference Thoroughbred genome. Unmapped reads were de novo assembled resulting in 19.1 Mb of new genomic sequence in the horse. Using a stringent filtering method, we identified 3.1 million SNPs, 193 thousand INDELs, and 282 CNVs. Genetic variants were annotated to determine their impact on gene structure and function. Additionally, we genotyped this Quarter Horse for mutations of known diseases and for variants associated with particular traits. Functional clustering analysis of genetic variants revealed that most of the genetic variation in the horse's genome was enriched in sensory perception, signal transduction, and immunity and defense pathways. Conclusions This is the first sequencing of a horse genome by next-generation sequencing and the first genomic sequence of an individual Quarter Horse mare. We have increased the catalog of genetic variants for use in equine genomics by the addition of novel SNPs, INDELs, and CNVs. The genetic variants described here will be a useful resource for future studies of genetic variation regulating performance traits and diseases in equids.
    Keywords Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Genetics ; DOAJ:Biology ; DOAJ:Biology and Life Sciences ; Biotechnology ; TP248.13-248.65
    Subject code 630
    Language English
    Publishing date 2012-02-01T00:00:00Z
    Publisher BioMed Central
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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