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  1. Article ; Online: Azithromycin susceptibility of

    Gernert, Kim M / Seby, Sandra / Schmerer, Matthew W / Thomas, Jesse C / Pham, Cau D / Cyr, Sancta St / Schlanger, Karen / Weinstock, Hillard / Shafer, William M / Raphael, Brian H / Kersh, Ellen N

    The Lancet. Microbe

    2020  Volume 1, Issue 4, Page(s) e154–e164

    Abstract: Background: The number of cases of gonorrhoea in the USA and worldwide caused by : Methods: We did a genomic analysis of : Findings: 410 isolates were sorted into more than 20 unique phylogenetic clades. One predominant persistent clade ( ... ...

    Abstract Background: The number of cases of gonorrhoea in the USA and worldwide caused by
    Methods: We did a genomic analysis of
    Findings: 410 isolates were sorted into more than 20 unique phylogenetic clades. One predominant persistent clade (consisting of 97 isolates) included the most isolates with azithromycin MICs of 2 μg/mL or higher (61 of 97 [63%]
    Interpretation: Reduced azithromycin susceptibility was associated with expanding and persistent clades harbouring two well described resistance mechanisms, mosaic
    Funding: US Centers for Disease Control and Prevention (CDC), CDC Combating Antibiotic Resistant Bacteria initiative, Oak Ridge Institute for Science Education, US Department of Energy/CDC/Emory University, National Institutes of Health, and Biomedical Laboratory Research and Development Service of the US Department of Veterans Affairs.
    MeSH term(s) Anti-Bacterial Agents/pharmacology ; Azithromycin/pharmacology ; Genomics ; Gonorrhea/drug therapy ; Humans ; Neisseria gonorrhoeae/genetics ; Phylogeny ; RNA, Ribosomal, 23S/genetics
    Chemical Substances Anti-Bacterial Agents ; RNA, Ribosomal, 23S ; Azithromycin (83905-01-5)
    Language English
    Publishing date 2020-09-28
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ISSN 2666-5247
    ISSN (online) 2666-5247
    DOI 10.1016/S2666-5247(20)30059-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Signatures of somatic mutations and gene expression from p16INK4A positive head and neck squamous cell carcinomas (HNSCC).

    Saba, Nabil F / Dinasarapu, Ashok R / Magliocca, Kelly R / Dwivedi, Bhakti / Seby, Sandra / Qin, Zhaohui S / Patel, Mihir / Griffith, Christopher C / Wang, Xu / El-Deiry, Mark / Steuer, Conor Ernst / Kowalski, Jeanne / Shin, Dong Moon / Zwick, Michael E / Chen, Zhuo Georgia

    PloS one

    2020  Volume 15, Issue 9, Page(s) e0238497

    Abstract: Human papilloma virus (HPV) causes a subset of head and neck squamous cell carcinomas (HNSCC) of the oropharynx. We combined targeted DNA- and genome-wide RNA-sequencing to identify genetic variants and gene expression signatures respectively from ... ...

    Abstract Human papilloma virus (HPV) causes a subset of head and neck squamous cell carcinomas (HNSCC) of the oropharynx. We combined targeted DNA- and genome-wide RNA-sequencing to identify genetic variants and gene expression signatures respectively from patients with HNSCC including oropharyngeal squamous cell carcinomas (OPSCC). DNA and RNA were purified from 35- formalin fixed and paraffin embedded (FFPE) HNSCC tumor samples. Immuno-histochemical evaluation of tumors was performed to determine the expression levels of p16INK4A and classified tumor samples either p16+ or p16-. Using ClearSeq Comprehensive Cancer panel, we examined the distribution of somatic mutations. Somatic single-nucleotide variants (SNV) were called using GATK-Mutect2 ("tumor-only" mode) approach. Using RNA-seq, we identified a catalog of 1,044 and 8 genes as significantly expressed between p16+ and p16-, respectively at FDR 0.05 (5%) and 0.1 (10%). The clinicopathological characteristics of the patients including anatomical site, smoking and survival were analyzed when comparing p16+ and p16- tumors. The majority of tumors (65%) were p16+. Population sequence variant databases, including gnomAD, ExAC, COSMIC and dbSNP, were used to identify the mutational landscape of somatic sequence variants within sequenced genes. Hierarchical clustering of The Cancer Genome Atlas (TCGA) samples based on HPV-status was observed using differentially expressed genes. Using RNA-seq in parallel with targeted DNA-seq, we identified mutational and gene expression signatures characteristic of p16+ and p16- HNSCC. Our gene signatures are consistent with previously published data including TCGA and support the need to further explore the biologic relevance of these alterations in HNSCC.
    MeSH term(s) Adult ; Aged ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; DNA, Viral/genetics ; Data Management ; Databases, Nucleic Acid ; Diagnostic Tests, Routine ; Female ; Gene Expression ; Gene Expression Profiling ; Head and Neck Neoplasms/genetics ; Head and Neck Neoplasms/metabolism ; Head and Neck Neoplasms/virology ; Humans ; Male ; Middle Aged ; Mutation ; Oropharyngeal Neoplasms/genetics ; Oropharyngeal Neoplasms/metabolism ; Oropharyngeal Neoplasms/virology ; Papillomaviridae/genetics ; Papillomavirus Infections/genetics ; Papillomavirus Infections/metabolism ; Papillomavirus Infections/virology ; Squamous Cell Carcinoma of Head and Neck/genetics ; Squamous Cell Carcinoma of Head and Neck/metabolism ; Squamous Cell Carcinoma of Head and Neck/virology ; Transcriptome
    Chemical Substances CDKN2A protein, human ; Cyclin-Dependent Kinase Inhibitor p16 ; DNA, Viral
    Language English
    Publishing date 2020-09-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0238497
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Genomic Characterization of Neisseria gonorrhoeae Strains from 2016 U.S. Sentinel Surveillance Displaying Reduced Susceptibility to Azithromycin.

    Schmerer, Matthew W / Abrams, A Jeanine / Seby, Sandra / Thomas, Jesse C / Cartee, John / Lucking, Sean / Vidyaprakash, Eshaw / Pham, Cau D / Sharpe, Samera / Pettus, Kevin / St Cyr, Sancta B / Torrone, Elizabeth A / Kersh, Ellen N / Gernert, Kim M

    Antimicrobial agents and chemotherapy

    2020  Volume 64, Issue 5

    Abstract: In 2016, the proportion ... ...

    Abstract In 2016, the proportion of
    MeSH term(s) Alleles ; Anti-Bacterial Agents/pharmacology ; Azithromycin/pharmacology ; Drug Resistance, Bacterial/genetics ; Genetic Loci/genetics ; Gonorrhea/epidemiology ; Gonorrhea/microbiology ; Humans ; Microbial Sensitivity Tests ; Molecular Epidemiology ; Neisseria gonorrhoeae/drug effects ; Neisseria gonorrhoeae/genetics ; RNA, Ribosomal, 23S/genetics ; Sentinel Surveillance ; United States/epidemiology
    Chemical Substances Anti-Bacterial Agents ; RNA, Ribosomal, 23S ; Azithromycin (83905-01-5)
    Language English
    Publishing date 2020-04-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 217602-6
    ISSN 1098-6596 ; 0066-4804
    ISSN (online) 1098-6596
    ISSN 0066-4804
    DOI 10.1128/AAC.02420-19
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Epigenetically heterogeneous tumor cells direct collective invasion through filopodia-driven fibronectin micropatterning.

    Summerbell, Emily R / Mouw, Janna K / Bell, Joshua S K / Knippler, Christina M / Pedro, Brian / Arnst, Jamie L / Khatib, Tala O / Commander, Rachel / Barwick, Benjamin G / Konen, Jessica / Dwivedi, Bhakti / Seby, Sandra / Kowalski, Jeanne / Vertino, Paula M / Marcus, Adam I

    Science advances

    2020  Volume 6, Issue 30, Page(s) eaaz6197

    Abstract: Tumor heterogeneity drives disease progression, treatment resistance, and patient relapse, yet remains largely underexplored in invasion and metastasis. Here, we investigated heterogeneity within collective cancer invasion by integrating DNA methylation ... ...

    Abstract Tumor heterogeneity drives disease progression, treatment resistance, and patient relapse, yet remains largely underexplored in invasion and metastasis. Here, we investigated heterogeneity within collective cancer invasion by integrating DNA methylation and gene expression analysis in rare purified lung cancer leader and follower cells. Our results showed global DNA methylation rewiring in leader cells and revealed the filopodial motor
    Language English
    Publishing date 2020-07-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.aaz6197
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: CDK5 Inhibition Resolves PKA/cAMP-Independent Activation of CREB1 Signaling in Glioma Stem Cells.

    Mukherjee, Subhas / Tucker-Burden, Carol / Kaissi, Emily / Newsam, Austin / Duggireddy, Hithardhi / Chau, Monica / Zhang, Changming / Diwedi, Bhakti / Rupji, Manali / Seby, Sandra / Kowalski, Jeanne / Kong, Jun / Read, Renee / Brat, Daniel J

    Cell reports

    2018  Volume 23, Issue 6, Page(s) 1651–1664

    Abstract: Cancer stem cells promote neoplastic growth, in part by deregulating asymmetric cell division and enhancing self-renewal. To uncover mechanisms and potential therapeutic targets in glioma stem cell (GSC) self-renewal, we performed a genetic suppressor ... ...

    Abstract Cancer stem cells promote neoplastic growth, in part by deregulating asymmetric cell division and enhancing self-renewal. To uncover mechanisms and potential therapeutic targets in glioma stem cell (GSC) self-renewal, we performed a genetic suppressor screen for kinases to reverse the tumor phenotype of our Drosophila brain tumor model and identified dCdk5 as a critical regulator. CDK5, the human ortholog of dCdk5 (79% identity), is aberrantly activated in GBMs and tightly aligned with both chromosome 7 gains and stem cell markers affecting tumor-propagation. Our investigation revealed that pharmaceutical inhibition of CDK5 prevents GSC self-renewal in vitro and in xenografted tumors, at least partially by suppressing CREB1 activation independently of PKA/cAMP. Finally, our TCGA GBM data analysis revealed that CDK5, stem cell, and asymmetric cell division markers segregate within non-mesenchymal patient clusters, which may indicate preferential dependence on CDK5 signaling and sensitivity to its inhibition in this group.
    MeSH term(s) Animals ; Asymmetric Cell Division/drug effects ; Biomarkers, Tumor/metabolism ; Brain Neoplasms/genetics ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Cell Proliferation/drug effects ; Cell Self Renewal/drug effects ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cyclin-Dependent Kinase 5/antagonists & inhibitors ; Cyclin-Dependent Kinase 5/genetics ; Cyclin-Dependent Kinase 5/metabolism ; Drosophila Proteins/antagonists & inhibitors ; Drosophila Proteins/metabolism ; Drosophila melanogaster/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Glioma/genetics ; Glioma/metabolism ; Glioma/pathology ; Mesoderm/drug effects ; Mesoderm/pathology ; Mice ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Phosphorylation/drug effects ; Protein Binding/drug effects ; Protein Kinase Inhibitors/pharmacology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Signal Transduction ; Xenograft Model Antitumor Assays
    Chemical Substances Biomarkers, Tumor ; Cyclic AMP Response Element-Binding Protein ; Drosophila Proteins ; Protein Kinase Inhibitors ; RNA, Messenger ; Cyclin-Dependent Kinase 5 (EC 2.7.11.1) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; CDK5 protein, human (EC 2.7.11.22) ; Cdk5 protein, Drosophila (EC 2.7.11.22)
    Language English
    Publishing date 2018-05-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2018.04.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Distinct Gene Expression Profiles Define Anaplastic Grade in Retinoblastoma.

    Hudson, Lauren E / Mendoza, Pia / Hudson, William H / Ziesel, Alison / Hubbard, G Baker / Wells, Jill / Dwivedi, Bhakti / Kowalski, Jeanne / Seby, Sandra / Patel, Viren / Geisert, Eldon / Specht, Charles / Grossniklaus, Hans E

    The American journal of pathology

    2018  Volume 188, Issue 10, Page(s) 2328–2338

    Abstract: Morbidity and mortality associated with retinoblastoma have decreased drastically in recent decades, in large part owing to better prediction of high-risk disease and appropriate treatment stratification. High-risk histopathologic features and severe ... ...

    Abstract Morbidity and mortality associated with retinoblastoma have decreased drastically in recent decades, in large part owing to better prediction of high-risk disease and appropriate treatment stratification. High-risk histopathologic features and severe anaplasia both predict the need for more aggressive treatment; however, not all centers are able to assess tumor samples easily for the degree of anaplasia. Instead, identification of genetic signatures that are able to distinguish among anaplastic grades and thus predict high- versus low-risk retinoblastoma would facilitate appropriate risk stratification in a wider patient population. A better understanding of genes dysregulated in anaplasia also would yield valuable insights into pathways underlying the development of more severe retinoblastoma. Here, we present the histopathologic and gene expression analysis of 28 retinoblastoma cases using microarray analysis. Tumors of differing anaplastic grade show clear differential gene expression, with significant dysregulation of unique genes and pathways in severe anaplasia. Photoreceptor and nucleoporin expression in particular are identified as highly dysregulated in severe anaplasia and suggest particular cellular processes contributing to the development of increased retinoblastoma severity. A limited set of highly differentially expressed genes also are able to predict severe anaplasia accurately in our data set. Together, these data contribute to the understanding of the development of anaplasia and facilitate the identification of genetic markers of high-risk retinoblastoma.
    MeSH term(s) Anaplasia/genetics ; Anaplasia/pathology ; Child, Preschool ; Female ; Gene Expression/genetics ; Gene Expression Profiling ; Genes, Retinoblastoma/genetics ; Genetic Markers/genetics ; Humans ; Infant ; Male ; Neoplasm Grading ; Retinal Neoplasms/genetics ; Retinal Neoplasms/pathology ; Retinoblastoma/genetics ; Retinoblastoma/pathology ; Risk Factors
    Chemical Substances Genetic Markers
    Language English
    Publishing date 2018-07-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2018.06.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Evidence of Recent Genomic Evolution in Gonococcal Strains With Decreased Susceptibility to Cephalosporins or Azithromycin in the United States, 2014-2016.

    Thomas, Jesse C / Seby, Sandra / Abrams, A Jeanine / Cartee, Jack / Lucking, Sean / Vidyaprakash, Eshaw / Schmerer, Matthew / Pham, Cau D / Hong, Jaeyoung / Torrone, Elizabeth / Cyr, Sancta St / Shafer, William M / Bernstein, Kyle / Kersh, Ellen N / Gernert, Kim M

    The Journal of infectious diseases

    2019  Volume 220, Issue 2, Page(s) 294–305

    Abstract: Background: Given the lack of new antimicrobials or a vaccine, understanding the evolutionary dynamics of Neisseria gonorrhoeae is a significant public and global health priority. We investigated the emergence and spread of gonococcal strains with ... ...

    Abstract Background: Given the lack of new antimicrobials or a vaccine, understanding the evolutionary dynamics of Neisseria gonorrhoeae is a significant public and global health priority. We investigated the emergence and spread of gonococcal strains with decreased susceptibility to cephalosporins and azithromycin using detailed genomic analyses of gonococcal isolates collected in the United States, 2014-2016.
    Methods: We sequenced genomes of 649 isolates collected through the Gonococcal Isolate Surveillance Project. We examined the genetic relatedness of isolates and assessed associations between clades and various genotypic and phenotypic combinations.
    Results: We identified a large and clonal lineage of strains (MLST ST9363) associated with elevated azithromycin minimum inhibitory concentration (AZIem), characterized by a mosaic mtr locus (C substitution in the mtrR promoter, mosaic mtrR and mtrD). Mutations in 23S rRNA were sporadically distributed among AZIem strains. Another clonal group (MLST ST1901) possessed 7 unique PBP2 patterns, and it shared common mutations in other genes associated with cephalosporin resistance.
    Conclusions: Whole-genome sequencing methods can enhance monitoring of antimicrobial resistant gonococcal strains by identifying gonococcal populations containing mutations of concern. These methods could inform the development of point-of-care diagnostic tests designed to determine the specific antibiotic susceptibility profile of a gonococcal infection in a patient.
    MeSH term(s) Anti-Bacterial Agents/therapeutic use ; Azithromycin/therapeutic use ; Bacterial Proteins/genetics ; Cephalosporins/therapeutic use ; Drug Resistance, Bacterial/drug effects ; Evolution, Molecular ; Genomics ; Genotype ; Gonorrhea/drug therapy ; Gonorrhea/microbiology ; Humans ; Male ; Microbial Sensitivity Tests/methods ; Mutation/drug effects ; Mutation/genetics ; Neisseria gonorrhoeae/drug effects ; Neisseria gonorrhoeae/genetics ; Phenotype ; Promoter Regions, Genetic/drug effects ; Promoter Regions, Genetic/genetics ; RNA, Ribosomal, 23S/genetics ; United States ; Whole Genome Sequencing/methods
    Chemical Substances Anti-Bacterial Agents ; Bacterial Proteins ; Cephalosporins ; RNA, Ribosomal, 23S ; Azithromycin (83905-01-5)
    Language English
    Publishing date 2019-01-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 3019-3
    ISSN 1537-6613 ; 0022-1899
    ISSN (online) 1537-6613
    ISSN 0022-1899
    DOI 10.1093/infdis/jiz079
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Cellular and Molecular Identity of Tumor-Associated Macrophages in Glioblastoma.

    Chen, Zhihong / Feng, Xi / Herting, Cameron J / Garcia, Virginia Alvarez / Nie, Kai / Pong, Winnie W / Rasmussen, Rikke / Dwivedi, Bhakti / Seby, Sandra / Wolf, Susanne A / Gutmann, David H / Hambardzumyan, Dolores

    Cancer research

    2017  Volume 77, Issue 9, Page(s) 2266–2278

    Abstract: In glioblastoma (GBM), tumor-associated macrophages (TAM) represent up to one half of the cells of the tumor mass, including both infiltrating macrophages and resident brain microglia. In an effort to delineate the temporal and spatial dynamics of TAM ... ...

    Abstract In glioblastoma (GBM), tumor-associated macrophages (TAM) represent up to one half of the cells of the tumor mass, including both infiltrating macrophages and resident brain microglia. In an effort to delineate the temporal and spatial dynamics of TAM composition during gliomagenesis, we used genetically engineered and GL261-induced mouse models in combination with CX3CR1
    MeSH term(s) Animals ; CX3C Chemokine Receptor 1 ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic ; Glioblastoma/genetics ; Glioblastoma/pathology ; High-Throughput Nucleotide Sequencing ; Humans ; Macrophages/pathology ; Mice ; Mice, Transgenic ; Microglia/pathology ; Monocytes/pathology ; Receptors, CCR2/biosynthesis ; Receptors, CCR2/genetics ; Receptors, Chemokine/biosynthesis ; Receptors, Chemokine/genetics
    Chemical Substances CX3C Chemokine Receptor 1 ; Ccr2 protein, mouse ; Cx3cr1 protein, mouse ; Receptors, CCR2 ; Receptors, Chemokine
    Language English
    Publishing date 2017-05-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-16-2310
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Genomic Surveillance for SARS-CoV-2 Variants: Predominance of the Delta (B.1.617.2) and Omicron (B.1.1.529) Variants - United States, June 2021-January 2022.

    Lambrou, Anastasia S / Shirk, Philip / Steele, Molly K / Paul, Prabasaj / Paden, Clinton R / Cadwell, Betsy / Reese, Heather E / Aoki, Yutaka / Hassell, Norman / Zheng, Xiao-Yu / Talarico, Sarah / Chen, Jessica C / Oberste, M Steven / Batra, Dhwani / McMullan, Laura K / Halpin, Alison Laufer / Galloway, Summer E / MacCannell, Duncan R / Kondor, Rebecca /
    Barnes, John / MacNeil, Adam / Silk, Benjamin J / Dugan, Vivien G / Scobie, Heather M / Wentworth, David E / Caravas, Jason / Kovacs, Nicholas A / Gerhart, Jonathan G / Jia Ng, Han / Beck, Andrew / Chau, Reina / Cintron, Roxana / Cook, Peter W / Gulvik, Christopher A / Howard, Dakota / Jang, Yunho / Knipe, Kristen / Lacek, Kristine A / Moser, Kara A / Paskey, Adrian C / Rambo-Martin, Benjamin L / Nagilla, Roopa R / Retchless, Adam C / Schmerer, Matthew W / Seby, Sandra / Shepard, Samuel S / Stanton, Richard A / Stark, Thomas J / Uehara, Anna / Unoarumhi, Yvette / Bentz, Meghan L / Burgin, Alex / Burroughs, Mark / Davis, Morgan L / Keller, Matthew W / Keong, Lisa M / Le, Shoshona S / Lee, Justin S / Madden Jr, Joseph C / Nobles, Sarah / Owuor, D. Collins / Padilla, Jasmine / Sheth, Mili / Wilson, Malania M

    MMWR. Morbidity and mortality weekly report

    2022  Volume 71, Issue 6, Page(s) 206–211

    Abstract: Genomic surveillance is a critical tool for tracking emerging variants of SARS-CoV-2 (the virus that causes COVID-19), which can exhibit characteristics that potentially affect public health and clinical interventions, including increased ... ...

    Abstract Genomic surveillance is a critical tool for tracking emerging variants of SARS-CoV-2 (the virus that causes COVID-19), which can exhibit characteristics that potentially affect public health and clinical interventions, including increased transmissibility, illness severity, and capacity for immune escape. During June 2021-January 2022, CDC expanded genomic surveillance data sources to incorporate sequence data from public repositories to produce weighted estimates of variant proportions at the jurisdiction level and refined analytic methods to enhance the timeliness and accuracy of national and regional variant proportion estimates. These changes also allowed for more comprehensive variant proportion estimation at the jurisdictional level (i.e., U.S. state, district, territory, and freely associated state). The data in this report are a summary of findings of recent proportions of circulating variants that are updated weekly on CDC's COVID Data Tracker website to enable timely public health action.
    MeSH term(s) COVID-19/epidemiology ; COVID-19/virology ; Centers for Disease Control and Prevention, U.S. ; Genomics ; Humans ; Prevalence ; Public Health Surveillance/methods ; SARS-CoV-2/genetics ; United States/epidemiology
    Language English
    Publishing date 2022-02-11
    Publishing country United States
    Document type Technical Report
    ZDB-ID 412775-4
    ISSN 1545-861X ; 0149-2195
    ISSN (online) 1545-861X
    ISSN 0149-2195
    DOI 10.15585/mmwr.mm7106a4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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