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469 results on '"Rieder, Mark J."'

1. Cryptic transmission of SARS-CoV-2 in Washington state

Author

Bedford, Trevor, Greninger, Alexander L, Roychoudhury, Pavitra, Starita, Lea M, Famulare, Michael, Huang, Meei-Li, Nalla, Arun, Pepper, Gregory, Reinhardt, Adam, Xie, Hong, Shrestha, Lasata, Nguyen, Truong N, Adler, Amanda, Brandstetter, Elisabeth, Cho, Shari, Giroux, Danielle, Han, Peter D, Fay, Kairsten, Frazar, Chris D, Ilcisin, Misja, Lacombe, Kirsten, Lee, Jover, Kiavand, Anahita, Richardson, Matthew, Sibley, Thomas R, Truong, Melissa, Wolf, Caitlin R, Nickerson, Deborah A, Rieder, Mark J, Englund, Janet A, Hadfield, James, Hodcroft, Emma B, Huddleston, John, Moncla, Louise H, Müller, Nicola F, Neher, Richard A, Deng, Xianding, Gu, Wei, Federman, Scot, Chiu, Charles, Duchin, Jeffrey S, Gautom, Romesh, Melly, Geoff, Hiatt, Brian, Dykema, Philip, Lindquist, Scott, Queen, Krista, Tao, Ying, Uehara, Anna, Tong, Suxiang, MacCannell, Duncan, Armstrong, Gregory L, Baird, Geoffrey S, Chu, Helen Y, Shendure, Jay, Jerome, Keith R, Boeckh, Michael, Lutz, Barry R, Thompson, Matthew, Huang, Shichu, Jackson, Michael L, Kimball, Louise E, Logue, Jennifer, Lyon, Victoria, Newman, Kira L, and Suchsland, Monica L Zigman

Subjects
Infectious Diseases, Pneumonia & Influenza, Lung, Prevention, Emerging Infectious Diseases, Biodefense, Vaccine Related, Pneumonia, Infection, Good Health and Well Being, Bayes Theorem, Betacoronavirus, COVID-19, Coronavirus Infections, Genome, Viral, Humans, Likelihood Functions, Pandemics, Phylogeny, Pneumonia, Viral, SARS-CoV-2, Washington, Seattle Flu Study Investigators, General Science & Technology
Abstract

After its emergence in Wuhan, China, in late November or early December 2019, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus rapidly spread globally. Genome sequencing of SARS-CoV-2 allows the reconstruction of its transmission history, although this is contingent on sampling. We analyzed 453 SARS-CoV-2 genomes collected between 20 February and 15 March 2020 from infected patients in Washington state in the United States. We find that most SARS-CoV-2 infections sampled during this time derive from a single introduction in late January or early February 2020, which subsequently spread locally before active community surveillance was implemented.

Published
2020

2. SwabExpress: An end-to-end protocol for extraction-free COVID-19 testing

Author

Srivatsan, Sanjay, Heidl, Sarah, Pfau, Brian, Martin, Beth K, Han, Peter D, Zhong, Weizhi, van Raay, Katrina, McDermot, Evan, Opsahl, Jordan, Gamboa, Luis, Smith, Nahum, Truong, Melissa, Cho, Shari, Barrow, Kaitlyn A, Rich, Lucille M, Stone, Jeremy, Wolf, Caitlin R, McCulloch, Denise J, Kim, Ashley E, Brandstetter, Elisabeth, Sohlberg, Sarah L, Ilcisin, Misja, Geyer, Rachel E, Chen, Wei, Gehring, Jase, Investigators, Seattle Flu Study, Kosuri, Sriram, Bedford, Trevor, Rieder, Mark J, Nickerson, Deborah A, Chu, Helen Y, Konnick, Eric Q, Debley, Jason S, Shendure, Jay, Lockwood, Christina M, and Starita, Lea M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Lung, HIV/AIDS, Clinical Research, Good Health and Well Being, Seattle Flu Study Investigators
Abstract

The urgent need for massively scaled clinical or surveillance testing for SARS-CoV-2 has necessitated a reconsideration of the methods by which respiratory samples are collected, transported, processed and tested. Conventional testing for SARS-CoV-2 involves collection of a clinical specimen with a nasopharyngeal swab, storage of the swab during transport in universal transport medium (UTM), extraction of RNA, and quantitative reverse transcription PCR (RT-qPCR). As testing has scaled across the world, supply chain challenges have emerged across this entire workflow. Here we sought to evaluate how eliminating the UTM storage and RNA extraction steps would impact the results of molecular testing. Using paired mid-turbinate swabs self-collected by 11 individuals with previously established SARS-CoV-2 positivity, we performed a comparison of conventional (swab → UTM → RNA extraction → RT-qPCR) vs. simplified (direct elution from dry swab → RT-qPCR) protocols. Our results suggest that dry swabs eluted directly into a simple buffered solution (TE) can support molecular detection of SARS-CoV-2 via endpoint RT-qPCR without substantially compromising sensitivity. Although further confirmation with a larger sample size and variation of other parameters is necessary, these results are encouraging for the possibility of a simplified workflow that could support massively scaled testing for COVID-19 control.

Published
2020

3. Preliminary support for a "dry swab, extraction free" protocol for SARS-CoV-2 testing via RT-qPCR.

Author

Srivatsan, Sanjay, Han, Peter D, van Raay, Katrina, Wolf, Caitlin R, McCulloch, Denise J, Kim, Ashley E, Brandstetter, Elisabeth, Martin, Beth, Gehring, Jase, Chen, Wei, Seattle Flu Study Investigators, Kosuri, Sriram, Konnick, Eric Q, Lockwood, Christina M, Rieder, Mark J, Nickerson, Deborah A, Chu, Helen Y, Shendure, Jay, and Starita, Lea M

Subjects
Seattle Flu Study Investigators
Abstract

The urgent need for massively scaled clinical or surveillance testing for SARS-CoV-2 has necessitated a reconsideration of the methods by which respiratory samples are collected, transported, processed and tested. Conventional testing for SARS-CoV-2 involves collection of a clinical specimen with a nasopharyngeal swab, storage of the swab during transport in universal transport medium (UTM), extraction of RNA, and quantitative reverse transcription PCR (RT-qPCR). As testing has scaled across the world, supply chain challenges have emerged across this entire workflow. Here we sought to evaluate how eliminating the UTM storage and RNA extraction steps would impact the results of molecular testing. Using paired mid-turbinate swabs self-collected by 11 individuals with previously established SARS-CoV-2 positivity, we performed a comparison of conventional (swab → UTM → RNA extraction → RT-qPCR) vs. simplified (direct elution from dry swab → RT-qPCR) protocols. Our results suggest that dry swabs eluted directly into a simple buffered solution (TE) can support molecular detection of SARS-CoV-2 via endpoint RT-qPCR without substantially compromising sensitivity. Although further confirmation with a larger sample size and variation of other parameters is necessary, these results are encouraging for the possibility of a simplified workflow that could support massively scaled testing for COVID-19 control.

Published
2020

4. Evidence for Limited Early Spread of COVID-19 Within the United States, January–February 2020

Author

CDC COVID-19 Response Team, Jorden, Michelle A., Rudman, Sarah L., Villarino, Elsa, Hoferka, Stacey, Patel, Megan T., Bemis, Kelley, Simmons, Cristal R., Jespersen, Megan, Johnson, Jenna Iberg, Mytty, Elizabeth, Arends, Katherine D., Henderson, Justin J., Mathes, Robert W., Weng, Charlene X., Duchin, Jeffrey, Lenahan, Jennifer, Close, Natasha, Bedford, Trevor, Boeckh, Michael, Chu, Helen Y., Englund, Janet A., Famulare, Michael, Nickerson, Deborah A., Rieder, Mark J., Shendure, Jay, and Starita, Lea M.

Published
2020

5. Whole-Exome Sequencing Identifies Rare and Low-Frequency Coding Variants Associated with LDL Cholesterol

Author

Lange, Leslie A, Hu, Youna, Zhang, He, Xue, Chenyi, Schmidt, Ellen M, Tang, Zheng-Zheng, Bizon, Chris, Lange, Ethan M, Smith, Joshua D, Turner, Emily H, Jun, Goo, Kang, Hyun Min, Peloso, Gina, Auer, Paul, Li, Kuo-ping, Flannick, Jason, Zhang, Ji, Fuchsberger, Christian, Gaulton, Kyle, Lindgren, Cecilia, Locke, Adam, Manning, Alisa, Sim, Xueling, Rivas, Manuel A, Holmen, Oddgeir L, Gottesman, Omri, Lu, Yingchang, Ruderfer, Douglas, Stahl, Eli A, Duan, Qing, Li, Yun, Durda, Peter, Jiao, Shuo, Isaacs, Aaron, Hofman, Albert, Bis, Joshua C, Correa, Adolfo, Griswold, Michael E, Jakobsdottir, Johanna, Smith, Albert V, Schreiner, Pamela J, Feitosa, Mary F, Zhang, Qunyuan, Huffman, Jennifer E, Crosby, Jacy, Wassel, Christina L, Do, Ron, Franceschini, Nora, Martin, Lisa W, Robinson, Jennifer G, Assimes, Themistocles L, Crosslin, David R, Rosenthal, Elisabeth A, Tsai, Michael, Rieder, Mark J, Farlow, Deborah N, Folsom, Aaron R, Lumley, Thomas, Fox, Ervin R, Carlson, Christopher S, Peters, Ulrike, Jackson, Rebecca D, van Duijn, Cornelia M, Uitterlinden, André G, Levy, Daniel, Rotter, Jerome I, Taylor, Herman A, Gudnason, Vilmundur, Siscovick, David S, Fornage, Myriam, Borecki, Ingrid B, Hayward, Caroline, Rudan, Igor, Chen, Y Eugene, Bottinger, Erwin P, Loos, Ruth JF, Sætrom, Pål, Hveem, Kristian, Boehnke, Michael, Groop, Leif, McCarthy, Mark, Meitinger, Thomas, Ballantyne, Christie M, Gabriel, Stacey B, O’Donnell, Christopher J, Post, Wendy S, North, Kari E, Reiner, Alexander P, Boerwinkle, Eric, Psaty, Bruce M, Altshuler, David, Kathiresan, Sekar, Lin, Dan-Yu, Jarvik, Gail P, Cupples, L Adrienne, Kooperberg, Charles, Wilson, James G, Nickerson, Deborah A, Abecasis, Goncalo R, and Rich, Stephen S

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Human Genome, Prevention, Clinical Research, Heart Disease, Cardiovascular, Atherosclerosis, Aetiology, 2.1 Biological and endogenous factors, Adult, Aged, Apolipoproteins E, Cholesterol, LDL, Cohort Studies, Dyslipidemias, Exome, Female, Follow-Up Studies, Gene Frequency, Genetic Code, Genome-Wide Association Study, Genotype, Humans, Lipase, Male, Middle Aged, Phenotype, Polymorphism, Single Nucleotide, Proprotein Convertase 9, Proprotein Convertases, Receptors, LDL, Sequence Analysis, DNA, Serine Endopeptidases, NHLBI Grand Opportunity Exome Sequencing Project, Medical and Health Sciences, Genetics & Heredity, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Elevated low-density lipoprotein cholesterol (LDL-C) is a treatable, heritable risk factor for cardiovascular disease. Genome-wide association studies (GWASs) have identified 157 variants associated with lipid levels but are not well suited to assess the impact of rare and low-frequency variants. To determine whether rare or low-frequency coding variants are associated with LDL-C, we exome sequenced 2,005 individuals, including 554 individuals selected for extreme LDL-C (>98(th) or

Published
2014

6. A statin-dependent QTL for GATM expression is associated with statin-induced myopathy

Author

Mangravite, Lara M, Engelhardt, Barbara E, Medina, Marisa W, Smith, Joshua D, Brown, Christopher D, Chasman, Daniel I, Mecham, Brigham H, Howie, Bryan, Shim, Heejung, Naidoo, Devesh, Feng, QiPing, Rieder, Mark J, Chen, Yii-Der I, Rotter, Jerome I, Ridker, Paul M, Hopewell, Jemma C, Parish, Sarah, Armitage, Jane, Collins, Rory, Wilke, Russell A, Nickerson, Deborah A, Stephens, Matthew, and Krauss, Ronald M

Subjects
Genetics, 2.1 Biological and endogenous factors, Aetiology, Amidinotransferases, Cell Line, Cholesterol, Gene Expression Regulation, Gene Knockdown Techniques, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Lymphocytes, Muscular Diseases, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Simvastatin, Sterol Regulatory Element Binding Proteins, Transcription, Genetic, General Science & Technology
Abstract

Statins are prescribed widely to lower plasma low-density lipoprotein (LDL) concentrations and cardiovascular disease risk and have been shown to have beneficial effects in a broad range of patients. However, statins are associated with an increased risk, albeit small, of clinical myopathy and type 2 diabetes. Despite evidence for substantial genetic influence on LDL concentrations, pharmacogenomic trials have failed to identify genetic variations with large effects on either statin efficacy or toxicity, and have produced little information regarding mechanisms that modulate statin response. Here we identify a downstream target of statin treatment by screening for the effects of in vitro statin exposure on genetic associations with gene expression levels in lymphoblastoid cell lines derived from 480 participants of a clinical trial of simvastatin treatment. This analysis identified six expression quantitative trait loci (eQTLs) that interacted with simvastatin exposure, including rs9806699, a cis-eQTL for the gene glycine amidinotransferase (GATM) that encodes the rate-limiting enzyme in creatine synthesis. We found this locus to be associated with incidence of statin-induced myotoxicity in two separate populations (meta-analysis odds ratio = 0.60). Furthermore, we found that GATM knockdown in hepatocyte-derived cell lines attenuated transcriptional response to sterol depletion, demonstrating that GATM may act as a functional link between statin-mediated lowering of cholesterol and susceptibility to statin-induced myopathy.

Published
2013

7. Genome-wide association of lipid-lowering response to statins in combined study populations.

Author

Barber, Mathew J, Mangravite, Lara M, Hyde, Craig L, Chasman, Daniel I, Smith, Joshua D, McCarty, Catherine A, Li, Xiaohui, Wilke, Russell A, Rieder, Mark J, Williams, Paul T, Ridker, Paul M, Chatterjee, Aurobindo, Rotter, Jerome I, Nickerson, Deborah A, Stephens, Matthew, and Krauss, Ronald M

Subjects
Humans, Inflammation, Pyrroles, Simvastatin, Pravastatin, Cholesterol, Lipids, Heptanoic Acids, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Bayes Theorem, Genotype, Phenotype, Polymorphism, Single Nucleotide, Adult, Aged, Middle Aged, Female, Male, Genome-Wide Association Study, Atorvastatin, Polymorphism, Single Nucleotide, Atorvastatin Calcium, General Science & Technology
Abstract

BackgroundStatins effectively lower total and plasma LDL-cholesterol, but the magnitude of decrease varies among individuals. To identify single nucleotide polymorphisms (SNPs) contributing to this variation, we performed a combined analysis of genome-wide association (GWA) results from three trials of statin efficacy.Methods and principal findingsBayesian and standard frequentist association analyses were performed on untreated and statin-mediated changes in LDL-cholesterol, total cholesterol, HDL-cholesterol, and triglyceride on a total of 3932 subjects using data from three studies: Cholesterol and Pharmacogenetics (40 mg/day simvastatin, 6 weeks), Pravastatin/Inflammation CRP Evaluation (40 mg/day pravastatin, 24 weeks), and Treating to New Targets (10 mg/day atorvastatin, 8 weeks). Genotype imputation was used to maximize genomic coverage and to combine information across studies. Phenotypes were normalized within each study to account for systematic differences among studies, and fixed-effects combined analysis of the combined sample were performed to detect consistent effects across studies. Two SNP associations were assessed as having posterior probability greater than 50%, indicating that they were more likely than not to be genuinely associated with statin-mediated lipid response. SNP rs8014194, located within the CLMN gene on chromosome 14, was strongly associated with statin-mediated change in total cholesterol with an 84% probability by Bayesian analysis, and a p-value exceeding conventional levels of genome-wide significance by frequentist analysis (P = 1.8 x 10(-8)). This SNP was less significantly associated with change in LDL-cholesterol (posterior probability = 0.16, P = 4.0 x 10(-6)). Bayesian analysis also assigned a 51% probability that rs4420638, located in APOC1 and near APOE, was associated with change in LDL-cholesterol.Conclusions and significanceUsing combined GWA analysis from three clinical trials involving nearly 4,000 individuals treated with simvastatin, pravastatin, or atorvastatin, we have identified SNPs that may be associated with variation in the magnitude of statin-mediated reduction in total and LDL-cholesterol, including one in the CLMN gene for which statistical evidence for association exceeds conventional levels of genome-wide significance.Trial registrationPRINCE and TNT are not registered. CAP is registered at Clinicaltrials.gov NCT00451828.

Published
2010

8. Remote surveillance and detection of SARS-CoV-2 transmission among household members in King County, Washington.

Author

Emanuels, Anne, Casto, Amanda M., Heimonen, Jessica, O'Hanlon, Jessica, Chow, Eric J., Ogokeh, Constance, Rolfes, Melissa A., Han, Peter D., Hughes, James P., Uyeki, Timothy M., Frazar, Christian, Chung, Erin, Starita, Lea M., Englund, Janet A., Chu, Helen Y., Boeckh, Michael, Famulare, Michael, Lutz, Barry R., Nickerson, Deborah A., and Rieder, Mark J.

Subjects
WHOLE genome sequencing, COVID-19 pandemic, SARS-CoV-2, HOUSEHOLDS, CONTACT tracing, BIOLOGICAL weed control
Abstract

Background: Early during the COVID-19 pandemic, it was important to better understand transmission dynamics of SARS-CoV-2, the virus that causes COVID-19. Household contacts of infected individuals are particularly at risk for infection, but delays in contact tracing, delays in testing contacts, and isolation and quarantine posed challenges to accurately capturing secondary household cases. Methods: In this study, 346 households in the Seattle region were provided with respiratory specimen collection kits and remotely monitored using web-based surveys for respiratory illness symptoms weekly between October 1, 2020, and June 20, 2021. Symptomatic participants collected respiratory specimens at symptom onset and mailed specimens to the central laboratory in Seattle. Specimens were tested for SARS-CoV-2 using RT-PCR with whole genome sequencing attempted when positive. SARS-CoV-2-infected individuals were notified, and their household contacts submitted specimens every 2 days for 14 days. Results: In total, 1371 participants collected 2029 specimens that were tested; 16 individuals (1.2%) within 6 households tested positive for SARS-CoV-2 during the study period. Full genome sequences were generated from 11 individuals within 4 households. Very little genetic variation was found among SARS-CoV-2 viruses sequenced from different individuals in the same household, supporting transmission within the household. Conclusions: This study indicates web-based surveillance of respiratory symptoms, combined with rapid and longitudinal specimen collection and remote contact tracing, provides a viable strategy to monitor households and detect household transmission of SARS-CoV-2. Trial registration identifier: NCT04141930, Date of registration 28/10/2019. [ABSTRACT FROM AUTHOR]

Published
2024
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9. Allele Frequency Matching Between SNPs Reveals an Excess of Linkage Disequilibrium in Genic Regions of the Human Genome

Author

Eberle, Michael A, Rieder, Mark J, Kruglyak, Leonid, and Nickerson, Deborah A

Subjects
Clinical Research, Genetics, Human Genome, Animals, DNA, Intergenic, Gene Frequency, Genes, Genetic Markers, Genome, Human, Humans, Linkage Disequilibrium, Models, Genetic, Pan troglodytes, Polymorphism, Single Nucleotide, Recombination, Genetic, Selection, Genetic, Sequence Alignment, Developmental Biology
Abstract

Significant interest has emerged in mapping genetic susceptibility for complex traits through whole-genome association studies. These studies rely on the extent of association, i.e., linkage disequilibrium (LD), between single nucleotide polymorphisms (SNPs) across the human genome. LD describes the nonrandom association between SNP pairs and can be used as a metric when designing maximally informative panels of SNPs for association studies in human populations. Using data from the 1.58 million SNPs genotyped by Perlegen, we explored the allele frequency dependence of the LD statistic r(2) both empirically and theoretically. We show that average r(2) values between SNPs unmatched for allele frequency are always limited to much less than 1 (theoretical approximately 0.46 to 0.57 for this dataset). Frequency matching of SNP pairs provides a more sensitive measure for assessing the average decay of LD and generates average r(2) values across nearly the entire informative range (from 0 to 0.89 through 0.95). Additionally, we analyzed the extent of perfect LD (r(2) = 1.0) using frequency-matched SNPs and found significant differences in the extent of LD in genic regions versus intergenic regions. The SNP pairs exhibiting perfect LD showed a significant bias for derived, nonancestral alleles, providing evidence for positive natural selection in the human genome.

Published
2006

10. Population History and Natural Selection Shape Patterns of Genetic Variation in 132 Genes

Author

Akey, Joshua M, Eberle, Michael A, Rieder, Mark J, Carlson, Christopher S, Shriver, Mark D, Nickerson, Deborah A, and Kruglyak, Leonid

Subjects
Genetics, Human Genome, Blacks, Chromosomes, Human, Pair 7, Computational Biology, Evolution, Molecular, Genetic Variation, Genetics, Population, Genome, Human, Humans, Models, Genetic, Models, Statistical, Polymorphism, Genetic, Polymorphism, Single Nucleotide, Population Groups, Selection, Genetic, Sequence Analysis, DNA, Whites, White People, Black People, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Identifying regions of the human genome that have been targets of natural selection will provide important insights into human evolutionary history and may facilitate the identification of complex disease genes. Although the signature that natural selection imparts on DNA sequence variation is difficult to disentangle from the effects of neutral processes such as population demographic history, selective and demographic forces can be distinguished by analyzing multiple loci dispersed throughout the genome. We studied the molecular evolution of 132 genes by comprehensively resequencing them in 24 African-Americans and 23 European-Americans. We developed a rigorous computational approach for taking into account multiple hypothesis tests and demographic history and found that while many apparent selective events can instead be explained by demography, there is also strong evidence for positive or balancing selection at eight genes in the European-American population, but none in the African-American population. Our results suggest that the migration of modern humans out of Africa into new environments was accompanied by genetic adaptations to emergent selective forces. In addition, a region containing four contiguous genes on Chromosome 7 showed striking evidence of a recent selective sweep in European-Americans. More generally, our results have important implications for mapping genes underlying complex human diseases.

Published
2004

11. Whole-Exome Sequencing Identifies Rare and Low-Frequency Coding Variants Associated with LDL Cholesterol

Author

Gabriel, Stacey B., Altshuler, David M., Abecasis, Gonçalo R., Allayee, Hooman, Cresci, Sharon, Daly, Mark J., de Bakker, Paul I.W., DePristo, Mark A., Do, Ron, Donnelly, Peter, Farlow, Deborah N., Fennell, Tim, Garimella, Kiran, Hazen, Stanley L., Hu, Youna, Jordan, Daniel M., Jun, Goo, Kathiresan, Sekar, Kang, Hyun Min, Kiezun, Adam, Lettre, Guillaume, Li, Bingshan, Li, Mingyao, Newton-Cheh, Christopher H., Padmanabhan, Sandosh, Peloso, Gina, Pulit, Sara, Rader, Daniel J., Reich, David, Reilly, Muredach P., Rivas, Manuel A., Schwartz, Steve, Scott, Laura, Siscovick, David S., Spertus, John A., Stitziel, Nathaniel O., Stoletzki, Nina, Sunyaev, Shamil R., Voight, Benjamin F., Willer, Cristen J., Rich, Stephen S., Akylbekova, Ermeg, Atwood, Larry D., Ballantyne, Christie M., Barbalic, Maja, Barr, R. Graham, Benjamin, Emelia J., Bis, Joshua, Boerwinkle, Eric, Bowden, Donald W., Brody, Jennifer, Budoff, Matthew, Burke, Greg, Buxbaum, Sarah, Carr, Jeff, Chen, Donna T., Chen, Ida Y., Chen, Wei-Min, Concannon, Pat, Crosby, Jacy, Cupples, L. Adrienne, D’Agostino, Ralph, DeStefano, Anita L., Dreisbach, Albert, Dupuis, Josée, Durda, J. Peter, Ellis, Jaclyn, Folsom, Aaron R., Fornage, Myriam, Fox, Caroline S., Fox, Ervin, Funari, Vincent, Ganesh, Santhi K., Gardin, Julius, Goff, David, Gordon, Ora, Grody, Wayne, Gross, Myron, Guo, Xiuqing, Hall, Ira M., Heard-Costa, Nancy L., Heckbert, Susan R., Heintz, Nicholas, Herrington, David M., Hickson, DeMarc, Huang, Jie, Hwang, Shih-Jen, Jacobs, David R., Jenny, Nancy S., Johnson, Andrew D., Johnson, Craig W., Kawut, Steven, Kronmal, Richard, Kurz, Raluca, Lange, Ethan M., Lange, Leslie A., Larson, Martin G., Lawson, Mark, Lewis, Cora E., Levy, Daniel, Li, Dalin, Lin, Honghuang, Liu, Chunyu, Liu, Jiankang, Liu, Kiang, Liu, Xiaoming, Liu, Yongmei, Longstreth, William T., Loria, Cay, Lumley, Thomas, Lunetta, Kathryn, Mackey, Aaron J., Mackey, Rachel, Manichaikul, Ani, Maxwell, Taylor, McKnight, Barbara, Meigs, James B., Morrison, Alanna C., Musani, Solomon K., Mychaleckyj, Josyf C., Nettleton, Jennifer A., North, Kari, O’Donnell, Christopher J., O’Leary, Daniel, Ong, Frank, Palmas, Walter, Pankow, James S., Pankratz, Nathan D., Paul, Shom, Perez, Marco, Person, Sharina D., Polak, Joseph, Post, Wendy S., Psaty, Bruce M., Quinlan, Aaron R., Raffel, Leslie J., Ramachandran, Vasan S., Reiner, Alexander P., Rice, Kenneth, Rotter, Jerome I., Sanders, Jill P., Schreiner, Pamela, Seshadri, Sudha, Shea, Steve, Sidney, Stephen, Silverstein, Kevin, Smith, Nicholas L., Sotoodehnia, Nona, Srinivasan, Asoke, Taylor, Herman A., Taylor, Kent, Thomas, Fridtjof, Tracy, Russell P., Tsai, Michael Y., Volcik, Kelly A., Wassel, Chrstina L., Watson, Karol, Wei, Gina, White, Wendy, Wiggins, Kerri L., Wilk, Jemma B., Williams, O. Dale, Wilson, Gregory, Wilson, James G., Wolf, Phillip, Zakai, Neil A., Hardy, John, Meschia, James F., Nalls, Michael, Singleton, Andrew, Worrall, Brad, Bamshad, Michael J., Barnes, Kathleen C., Abdulhamid, Ibrahim, Accurso, Frank, Anbar, Ran, Beaty, Terri, Bigham, Abigail, Black, Phillip, Bleecker, Eugene, Buckingham, Kati, Cairns, Anne Marie, Caplan, Daniel, Chatfield, Barbara, Chidekel, Aaron, Cho, Michael, Christiani, David C., Crapo, James D., Crouch, Julia, Daley, Denise, Dang, Anthony, Dang, Hong, De Paula, Alicia, DeCelie-Germana, Joan, Drumm, Allen DozorMitch, Dyson, Maynard, Emerson, Julia, Emond, Mary J., Ferkol, Thomas, Fink, Robert, Foster, Cassandra, Froh, Deborah, Gao, Li, Gershan, William, Gibson, Ronald L., Godwin, Elizabeth, Gondor, Magdalen, Gutierrez, Hector, Hansel, Nadia N., Hassoun, Paul M., Hiatt, Peter, Hokanson, John E., Howenstine, Michelle, Hummer, Laura K., Kanga, Jamshed, Kim, Yoonhee, Knowles, Michael R., Konstan, Michael, Lahiri, Thomas, Laird, Nan, Lange, Christoph, Lin, Lin, Lin, Xihong, Louie, Tin L., Lynch, David, Make, Barry, Martin, Thomas R., Mathai, Steve C., Mathias, Rasika A., McNamara, John, McNamara, Sharon, Meyers, Deborah, Millard, Susan, Mogayzel, Peter, Moss, Richard, Murray, Tanda, Nielson, Dennis, Noyes, Blakeslee, O’Neal, Wanda, Orenstein, David, O’Sullivan, Brian, Pace, Rhonda, Pare, Peter, Parker, H. Worth, Passero, Mary Ann, Perkett, Elizabeth, Prestridge, Adrienne, Rafaels, Nicholas M., Ramsey, Bonnie, Regan, Elizabeth, Ren, Clement, Retsch-Bogart, George, Rock, Michael, Rosen, Antony, Rosenfeld, Margaret, Ruczinski, Ingo, Sanford, Andrew, Schaeffer, David, Sell, Cindy, Sheehan, Daniel, Silverman, Edwin K., Sin, Don, Spencer, Terry, Stonebraker, Jackie, Tabor, Holly K., Varlotta, Laurie, Vergara, Candelaria I., Weiss, Robert, Wigley, Fred, Wise, Robert A., Wright, Fred A., Wurfel, Mark M., Zanni, Robert, Zou, Fei, Nickerson, Deborah A., Rieder, Mark J., Green, Phil, Shendure, Jay, Akey, Joshua M., Bustamante, Carlos D., Crosslin, David R., Eichler, Evan E., Fox, P. Keolu, Fu, Wenqing, Gordon, Adam, Gravel, Simon, Jarvik, Gail P., Johnsen, Jill M., Kan, Mengyuan, Kenny, Eimear E., Kidd, Jeffrey M., Lara-Garduno, Fremiet, Leal, Suzanne M., Liu, Dajiang J., McGee, Sean, O’Connor, Timothy D., Paeper, Bryan, Robertson, Peggy D., Smith, Joshua D., Staples, Jeffrey C., Tennessen, Jacob A., Turner, Emily H., Wang, Gao, Yi, Qian, Jackson, Rebecca, Peters, Ulrike, Carlson, Christopher S., Anderson, Garnet, Anton-Culver, Hoda, Assimes, Themistocles L., Auer, Paul L., Beresford, Shirley, Bizon, Chris, Black, Henry, Brunner, Robert, Brzyski, Robert, Burwen, Dale, Caan, Bette, Carty, Cara L., Chlebowski, Rowan, Cummings, Steven, Curb, J. David, Eaton, Charles B., Ford, Leslie, Franceschini, Nora, Fullerton, Stephanie M., Gass, Margery, Geller, Nancy, Heiss, Gerardo, Howard, Barbara V., Hsu, Li, Hutter, Carolyn M., Ioannidis, John, Jiao, Shuo, Johnson, Karen C., Kooperberg, Charles, Kuller, Lewis, LaCroix, Andrea, Lakshminarayan, Kamakshi, Lane, Dorothy, Lasser, Norman, LeBlanc, Erin, Li, Kuo-Ping, Limacher, Marian, Lin, Dan-Yu, Logsdon, Benjamin A., Ludlam, Shari, Manson, JoAnn E., Margolis, Karen, Martin, Lisa, McGowan, Joan, Monda, Keri L., Kotchen, Jane Morley, Nathan, Lauren, Ockene, Judith, O’Sullivan, Mary Jo, Phillips, Lawrence S., Prentice, Ross L., Robbins, John, Robinson, Jennifer G., Rossouw, Jacques E., Sangi-Haghpeykar, Haleh, Sarto, Gloria E., Shumaker, Sally, Simon, Michael S., Stefanick, Marcia L., Stein, Evan, Tang, Hua, Taylor, Kira C., Thomson, Cynthia A., Thornton, Timothy A., Van Horn, Linda, Vitolins, Mara, Wactawski-Wende, Jean, Wallace, Robert, Wassertheil-Smoller, Sylvia, Zeng, Donglin, Applebaum-Bowden, Deborah, Feolo, Michael, Gan, Weiniu, Paltoo, Dina N., Sholinsky, Phyliss, Sturcke, Anne, Zhang, He, Xue, Chenyi, Schmidt, Ellen M., Tang, Zheng-Zheng, Auer, Paul, Li, Kuo-ping, Flannick, Jason, Zhang, Ji, Fuchsberger, Christian, Gaulton, Kyle, Lindgren, Cecilia, Locke, Adam, Manning, Alisa, Sim, Xueling, Holmen, Oddgeir L., Gottesman, Omri, Lu, Yingchang, Ruderfer, Douglas, Stahl, Eli A., Duan, Qing, Li, Yun, Durda, Peter, Isaacs, Aaron, Hofman, Albert, Bis, Joshua C., Correa, Adolfo, Griswold, Michael E., Jakobsdottir, Johanna, Smith, Albert V., Schreiner, Pamela J., Feitosa, Mary F., Zhang, Qunyuan, Huffman, Jennifer E., Wassel, Christina L., Martin, Lisa W., Rosenthal, Elisabeth A., Tsai, Michael, Fox, Ervin R., Jackson, Rebecca D., van Duijn, Cornelia M., Uitterlinden, André G., Gudnason, Vilmundur, Jr., Borecki, Ingrid B., Hayward, Caroline, Rudan, Igor, Chen, Y. Eugene, Bottinger, Erwin P., Loos, Ruth J.F., Sætrom, Pål, Hveem, Kristian, Boehnke, Michael, Groop, Leif, McCarthy, Mark, Meitinger, Thomas, North, Kari E., Altshuler, David, and Abecasis, Goncalo R.

Published
2014
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12. Genetic variants associated with warfarin dose in African-American individuals: a genome-wide association study

Author

Perera, Minoli A, Cavallari, Larisa H, Limdi, Nita A, Gamazon, Eric R, Konkashbaev, Anuar, Daneshjou, Roxana, Pluzhnikov, Anna, Crawford, Dana C, Wang, Jelai, Liu, Nianjun, Tatonetti, Nicholas, Bourgeois, Stephane, Takahashi, Harumi, Bradford, Yukiko, Burkley, Benjamin M, Desnick, Robert J, Halperin, Jonathan L, Khalifa, Sherief I, Langaee, Taimour Y, Lubitz, Steven A, Nutescu, Edith A, Oetjens, Matthew, Shahin, Mohamed H, Patel, Shitalben R, Sagreiya, Hersh, Tector, Matthew, Weck, Karen E, Rieder, Mark J, Scott, Stuart A, Wu, Alan HB, Burmester, James K, Wadelius, Mia, Deloukas, Panos, Wagner, Michael J, Mushiroda, Taisei, Kubo, Michiaki, Roden, Dan M, Cox, Nancy J, Altman, Russ B, Klein, Teri E, Nakamura, Yusuke, and Johnson, Julie A

Published
2013
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14. Evolution and Functional Impact of Rare Coding Variation from Deep Sequencing of Human Exomes

Author

Tennessen, Jacob A., Bigham, Abigail W., O'Connor, Timothy D., Fu, Wenqing, Kenny, Eimear E., Gravel, Simon, McGee, Sean, Do, Ron, Liu, Xiaoming, Jun, Goo, Kang, Hyun Min, Jordan, Daniel, Leal, Suzanne M., Gabriel, Stacey, Rieder, Mark J., Abecasis, Goncalo, Altshuler, David, Nickerson, Deborah A., Boerwinkle, Eric, Sunyaev, Shamil, Bustamante, Carlos D., Bamshad, Michael J., and Akey, Joshua M.

Published
2012
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20. Evidence for Limited Early Spread of COVID-19 Within the United States, January-February 2020

Author

Jorden, Michelle A., Rudman, Sarah L., Villarino, Elsa, Hoferka, Stacey, Patel, Megan T., Bemis, Kelley, Simmons, Cristal R., Jespersen, Megan, Johnson, Jenna Iberg, Mytty, Elizabeth, Arends, Katherine D., Henderson, Justin J., Mathes, Robert W., Weng, Charlene X., Duchin, Jeffrey, Lenahan, Jennifer, Close, Natasha, Bedford, Trevor, Boeckh, Michael, Chu, Helen Y., Englund, Janet A., Famulare, Michael, Nickerson, Deborah A., Rieder, Mark J., Shendure, Jay, and Starita, Lea M.

Subjects
Coronaviruses -- Analysis, Health
Abstract

On May 29, 2019, this report was posted as an MMWR Early Release on the MMWR website (https://www.cdc.gov/mmwr). From January 21 through February 23, 2020, public health agencies detected 14 [...]

Published
2020

21. Comparison of Symptoms and RNA Levels in Children and Adults With SARS-CoV-2 Infection in the Community Setting

Author

Chung, Erin, primary, Chow, Eric J., additional, Wilcox, Naomi C., additional, Burstein, Roy, additional, Brandstetter, Elisabeth, additional, Han, Peter D., additional, Fay, Kairsten, additional, Pfau, Brian, additional, Adler, Amanda, additional, Lacombe, Kirsten, additional, Lockwood, Christina M., additional, Uyeki, Timothy M., additional, Shendure, Jay, additional, Duchin, Jeffrey S., additional, Rieder, Mark J., additional, Nickerson, Deborah A., additional, Boeckh, Michael, additional, Famulare, Michael, additional, Hughes, James P., additional, Starita, Lea M., additional, Bedford, Trevor, additional, Englund, Janet A., additional, and Chu, Helen Y., additional

Published
2021
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23. Genome-wide association study of plasma lipoprotein(a) levels identifies multiple genes on chromosome 6q

Author

Ober, Carole, Nord, Alex S., Thompson, Emma E., Pan, Lin, Tan, Zheng, Cusanovich, Darren, Sun, Ying, Nicolae, Raluca, Edelstein, Celina, Schneider, Daniel H., Billstrand, Christine, Pfaffinger, Ditta, Phillips, Natasha, Anderson, Rebecca L., Philips, Binu, Rajagopalan, Ramakrishnan, Hatsukami, Thomas S., Rieder, Mark J., Heagerty, Patrick J., Nickerson, Deborah A., Abney, Mark, Marcovina, Santica, Jarvik, Gail P., Scanu, Angelo M., and Nicolae, Dan L.

Published
2009
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24. Additional file 1 of Effects of weather-related social distancing on city-scale transmission of respiratory viruses: a retrospective cohort study

Author

Jackson, Michael L., Hart, Gregory R., McCulloch, Denise J., Adler, Amanda, Brandstetter, Elisabeth, Kairsten Fay, Han, Peter, Lacombe, Kirsten, Jover Lee, Sibley, Thomas R., Nickerson, Deborah A., Rieder, Mark J., Starita, Lea, Englund, Janet A., Bedford, Trevor, Chu, Helen, and Famulare, Michael

Subjects
Data_FILES
Abstract

Additional file 1.

Published
2021
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25. Sporadic autism exomes reveal a highly interconnected protein network of de novo mutations

Author

O'Roak, Brian J., Vives, Laura, Girirajan, Santhosh, Karakoc, Emre, Krumm, Niklas, Coe, Bradley P., Levy, Roie, Ko, Arthur, Lee, Choli, Smith, Joshua D., Turner, Emily H., Stanaway, Ian B., Vernot, Benjamin, Malig, Maika, Baker, Carl, Reilly, Beau, Akey, Joshua M., Borenstein, Elhanan, Rieder, Mark J., Nickerson, Deborah A., Bernier, Raphael, Shendure, Jay, and Eichler, Evan E.

Subjects
Gene mutations -- Health aspects, Pervasive developmental disorders -- Risk factors -- Genetic aspects -- Care and treatment -- Research, Genetic variation -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

It is well established that autism spectrum disorders (ASD) have a strong genetic component; however, for at least 70% of cases, the underlying genetic cause is unknown (1). Under the hypothesis that de novo mutations underlie a substantial fraction of the risk for developing ASD in families with no previous history of ASD or related phenotypes--so-called sporadic or simplex families (2,3)--we sequenced all coding regions of the genome (the exome) for parent-child trios exhibiting sporadic ASD, including 189 new trios and 20 that were previously reported (4). Additionally, we also sequenced the exomes of 50 unaffected siblings corresponding to these new (n = 31) and previously reported trios (n = 19) (4), for a total of 677 individual exomes from 209 families. Here we show that de novo point mutations are overwhelmingly paternal in origin (4:1 bias) and positively correlated with paternal age, consistent with the modest increased risk for children of older fathers to develop ASD (5). Moreover, 39% (49 of 126) of the most severe or disruptive de novo mutations map to a highly interconnected β-catenin/chromatin remodelling protein network ranked significantly for autism candidate genes. In proband exomes, recurrent protein-altering mutations were observed in two genes: CHD8 and NTNG1. Mutation screening of six candidate genes in 1,703 ASD probands identified additional de novo, protein-altering mutations in GRIN2B, LAMC3 and SCN1A. Combined with copy number variant (CNV) data, these results indicate extreme locus heterogeneity but also provide a target for future discovery, diagnostics and therapeutics., We selected 189 autism trios from the Simons Simplex Collection (SSC) (6), which included males significantly impaired with autism and intellectual disability (n = 47), a female sample set (n [...]

Published
2012
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28. Quantifying rare, deleterious variation in 12 human cytochrome P450 drug-metabolism genes in a large-scale exome dataset

Author

Gordon, Adam S., Tabor, Holly K., Johnson, Andrew D., Snively, Beverly M., Assimes, Themistocles L., Auer, Paul L., Ioannidis, John P.A., Peters, Ulrike, Robinson, Jennifer G., Sucheston, Lara E., Wang, Danxin, Sotoodehnia, Nona, Rotter, Jerome I., Psaty, Bruce M., Jackson, Rebecca D., Herrington, David M., OʼDonnell, Christopher J., Reiner, Alexander P., Rich, Stephen S., Rieder, Mark J., Bamshad, Michael J., and Nickerson, Deborah A.

Published
2014
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29. Viral genomes reveal patterns of the SARS-CoV-2 outbreak in Washington State

Author

Müller, Nicola F., primary, Wagner, Cassia, additional, Frazar, Chris D., additional, Roychoudhury, Pavitra, additional, Lee, Jover, additional, Moncla, Louise H., additional, Pelle, Benjamin, additional, Richardson, Matthew, additional, Ryke, Erica, additional, Xie, Hong, additional, Shrestha, Lasata, additional, Addetia, Amin, additional, Rachleff, Victoria M., additional, Lieberman, Nicole A. P., additional, Huang, Meei-Li, additional, Gautom, Romesh, additional, Melly, Geoff, additional, Hiatt, Brian, additional, Dykema, Philip, additional, Adler, Amanda, additional, Brandstetter, Elisabeth, additional, Han, Peter D., additional, Fay, Kairsten, additional, Ilcisin, Misja, additional, Lacombe, Kirsten, additional, Sibley, Thomas R., additional, Truong, Melissa, additional, Wolf, Caitlin R., additional, Boeckh, Michael, additional, Englund, Janet A., additional, Famulare, Michael, additional, Lutz, Barry R., additional, Rieder, Mark J., additional, Thompson, Matthew, additional, Duchin, Jeffrey S., additional, Starita, Lea M., additional, Chu, Helen Y., additional, Shendure, Jay, additional, Jerome, Keith R., additional, Lindquist, Scott, additional, Greninger, Alexander L., additional, Nickerson, Deborah A., additional, and Bedford, Trevor, additional

Published
2021
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30. Evaluating Specimen Quality and Results from a Community-Wide, Home-Based Respiratory Surveillance Study

Author

Kim, Ashley E., primary, Brandstetter, Elisabeth, additional, Wilcox, Naomi, additional, Heimonen, Jessica, additional, Graham, Chelsey, additional, Han, Peter D., additional, Starita, Lea M., additional, McCulloch, Denise J., additional, Casto, Amanda M., additional, Nickerson, Deborah A., additional, Van de Loo, Margaret M., additional, Mooney, Jennifer, additional, Ilcisin, Misja, additional, Fay, Kairsten A., additional, Lee, Jover, additional, Sibley, Thomas R., additional, Lyon, Victoria, additional, Geyer, Rachel E., additional, Thompson, Matthew, additional, Lutz, Barry R., additional, Rieder, Mark J., additional, Bedford, Trevor, additional, Boeckh, Michael, additional, Englund, Janet A., additional, and Chu, Helen Y., additional

Published
2021
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31. Comparable Specimen Collection from Both Ends of At-Home Midturbinate Swabs

Author

Truong, Melissa, primary, Pfau, Brian, additional, McDermot, Evan, additional, Han, Peter D., additional, Brandstetter, Elisabeth, additional, Richardson, Matthew, additional, Kim, Ashley E., additional, Rieder, Mark J., additional, Chu, Helen Y., additional, Englund, Janet A., additional, Nickerson, Deborah A., additional, Shendure, Jay, additional, Lockwood, Christina M., additional, Konnick, Eric Q., additional, and Starita, Lea M., additional

Published
2021
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32. Polymorphisms of the HNF1A gene encoding hepatocyte nuclear factor-1[alpha] are associated with C-reactive protein

Author

Reiner, Alexander P., Barber, Mathew J., Yongtao Guan, Ridker, Paul M., Lange, Leslie A., Chasman, Daniel I., Walston, Jeremy D., Cooper, Gregory M., Jenny, Nancy S., Rieder, Mark J., Durda, Peter, Smith, Joshua D., Novembre, John, Tracy, Russell P., Rotter, Jerome I., Stephens, Matthew, Nickerson, Deborah A., and Krauss, Ronald M.

Subjects
C-reactive protein -- Research, Genetic polymorphisms -- Analysis, Liver cells -- Genetic aspects, Human genetics -- Research, Biological sciences
Abstract

Several studies are conducted to study the association between the common polymorphisms of the HNF1A gene encoding hepatocyte nuclear factor-1[alpha] and plasma C-reactive protein (CRP) concentration. The two discussed phenomenon are shown to be completely related and dependent on each other.

Published
2008

37. An overview of the environmental genome project

Author

Nickerson, Deborah A., Rieder, Mark J., Crawford, Dana C. Carlson, Christopher S., and Livingston, Robert J.

Abstract

Providing a Resource to Explore Phenotype-Genotype-Environment Interactions Understanding the causes of common diseases such as cancer, asthma, diabetes, hypertension, and atherosclerosis, which have high population prevalence, is a significant priority [...]

Published
2005

38. Effect of VKORC1 haplotypes on transcriptional regulation and warfarin dose

Author

Rieder, Mark J., Reiner, Alexander P., Gage, Brian F., Nickerson, Deborah A., Eby, Charles S., Rettie, Allan E., Thummel, Kenneth E., McLeod, Howard L., and Blough, David K.

Subjects
Genetic disorders -- Drug therapy, Haplotypes -- Research, Warfarin -- Dosage and administration
Abstract

A retrospective study of European-American patients was conducted to determine the effect of vitamin K epoxide reductase complex 1 (VKORC1) haplotypes on the warfarin dose. The result showed that VKORC1 haplotypes can be used to stratify patients into low-, intermediate and high dose warfarin groups and may explain differences in dose requirements among the patients of different ancestries.

Published
2005

39. Sequence-based linkage analysis

Author

Furman, Itay, Rieder, Mark J., da Ponte, Suzanne, Carrington, Dana P., Nickerson, Deborah A., Kruglyak, Leonid, and Markianos, Kyriacos

Subjects
Linkage (Genetics) -- Research, Biological sciences
Published
2004

45. Sporadic autism exomes reveal a highly interconnected protein network of de novo mutations

Author

OʼRoak, Brian J., Vives, Laura, Girirajan, Santhosh, Karakoc, Emre, Krumm, Niklas, Coe, Bradley P., Levy, Roie, Ko, Arthur, Lee, Choli, Smith, Joshua D., Turner, Emily H., Stanaway, Ian B., Vernot, Benjamin, Malig, Maika, Baker, Carl, Reilly, Beau, Akey, Joshua M., Borenstein, Elhanan, Rieder, Mark J., Nickerson, Deborah A., Bernier, Raphael, Shendure, Jay, and Eichler, Evan E.

Published
2012
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46. Evidence for involvement of GNB1L in autism

Author

Chen, Ying-Zhang, Matsushita, Mark, Girirajan, Santhosh, Lisowski, Mark, Sun, Elizabeth, Sul, Youngmee, Bernier, Raphael, Estes, Annette, Dawson, Geraldine, Minshew, Nancy, Shellenberg, Gerard D., Eichler, Evan E., Rieder, Mark J., Nickerson, Deborah A., Tsuang, Debby W., Tsuang, Ming T., Wijsman, Ellen M., Raskind, Wendy H., and Brkanac, Zoran

Published
2012
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48. Comparable specimen collection from both ends of at-home mid-turbinate swabs

Author

Truong, Melissa, primary, Pfau, Brian, additional, McDermot, Evan, additional, Han, Peter D., additional, Brandstetter, Elisabeth, additional, Richardson, Matthew, additional, Kim, Ashley E., additional, Rieder, Mark J., additional, Chu, Helen Y., additional, Englund, Janet A., additional, Nickerson, Deborah A., additional, Shendure, Jay, additional, Lockwood, Christina M., additional, Konnick, Eric Q., additional, and Starita, Lea M., additional

Published
2020
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49. Evaluating Specimen Quality and Results from a Community-Wide, Home-Based Respiratory Surveillance Study

Author

Kim, Ashley E., primary, Brandstetter, Elisabeth, additional, Wilcox, Naomi, additional, Heimonen, Jessica, additional, Graham, Chelsey, additional, Han, Peter D., additional, Starita, Lea M., additional, McCulloch, Denise J., additional, Casto, Amanda M., additional, Nickerson, Deborah A., additional, Van de Loo, Margaret M., additional, Mooney, Jennifer, additional, Ilcisin, Misja, additional, Fay, Kairsten A., additional, Lee, Jover, additional, Sibley, Thomas R., additional, Lyon, Victoria, additional, Geyer, Rachel E., additional, Thompson, Matthew, additional, Lutz, Barry R., additional, Rieder, Mark J., additional, Bedford, Trevor, additional, Boeckh, Michael, additional, Englund, Janet A., additional, and Chu, Helen Y., additional

Published
2020
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50. Viral genome sequencing places White House COVID-19 outbreak into phylogenetic context

Author

Bedford, Trevor, primary, Logue, Jennifer K., additional, Han, Peter D., additional, Wolf, Caitlin R., additional, Frazar, Chris D., additional, Pelle, Benjamin, additional, Ryke, Erica, additional, Hadfield, James, additional, Lee, Jover, additional, Rieder, Mark J., additional, Nickerson, Deborah A., additional, Lockwood, Christina M., additional, Starita, Lea M., additional, Chu, Helen Y., additional, and Shendure, Jay, additional

Published
2020
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