Due to the urgency of the rapidly spreading coronavirus pandemic, Sequencing.com is making this report free for a limited time.
|Report Section||Information Provided|
|Risk of Infection||Your genetic risk of becoming infected by the coronavirus; backed by preliminary genetic research studies|
|Severity||Your genetic risk of a severe, potentially life-threatening, infection (if you are infected); backed by preliminary genetic research studies|
Your genetic risk of experiencing a harmful reaction to a common medication (oseltamivir phosphate) used to prevent and treat influenza (the flu).
While this medication is not a COVID-19 prevention or treatment, this medication may be used more often during the pandemic because of the similarity of some symptoms between the flu and COVID-19.
|Non-Genetic Factors||Your non-genetic risk of becoming infected and experiencing a more severe infection|
|Insights||Straightforward information about ways to limit exposure and stay healthy|
|Latest News||stay up-to-date on the latest insights and health guidance|
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The blog post Your DNA and COVID-19, written by Dr. Brandon Colby MD, Sequencing.com's Founder, provides an overview of the Coronavirus DNA Health Report including why and how we created the DNA analysis for this report.
The Coronavirus DNA Health Report is backed by science based on the following references.
The Severe Covid-19 GWAS Group. Genomewide Association Study of Severe Covid-19 with Respiratory Failure. N Engl J Med 2020; 383:1522-1534. doi: 10.1056/NEJMoa2020283
Renieri A. et al. ACE2 variants underlie interindividual variability and susceptibility to COVID-19 in Italian population. medRxiv 2020.04.03. doi: 10.1101/2020.04.03.20047977.
Zhou F. et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet March 11, 2020. doi: 10.1016/S0140-6736(20)30566-3.
Wu A. et al. Genome Composition and Divergence of the Novel Coronavirus (2019-nCoV) Originating in China. Cell Host Microbe. pii: S1931-3128(20) 30072-X (2020). doi: 10.1016/j.chom.2020.02.001.
Cai, G. Bulk and Single-Cell Transcriptomics Identify Tobacco-Use Disparity in Lung Gene Expression of ACE2, the Receptor of 2019-nCov. Preprints (2020) 2020020051. doi: 10.20944/preprints202002.0051.v3.
Dong E., et al. An interactive web-based dashboard to track COVID-19 in real time. Lancet Infect Dis (2020). pii: S1473-3099(20)30120-1. doi: 10.1016/S1473-3099(20)30120-1.
Lu, R. et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet (2020). doi: 10.1016/S0140-6736(20)30251-8.
Cao Y., et al. Comparative genetic analysis of the novel coronavirus (2019-nCoV/SARS-CoV-2) receptor ACE2 in different populations. Cell Discov 6, 11 (2020). doi: 10.1038/s41421-020-0147-1.
Zhao Y. et al. Single-cell RNA expression profiling of ACE2, the putative receptor of Wuhan 2019-nCoV. bioRxiv (2020). doi: 10.1101/2020.01.26.919985.
Rothe C. et al. Transmission of 2019-nCoV infection from an asymptomatic contact in Germany. N. Engl. J. Med (2020). doi: 10.1056/NEJMc2001468.
Morimoto, K. et al. Analysis of a child who developed abnormal neuropsychiatric symptoms after administration of oseltamivir: a case report. BMC Neurol. 15:130 (2015). doi: 10.1186/s12883-015-0393-2.
Suzuki Y. Identification of oseltamivir resistance among pandemic and seasonal influenza A (H1N1) viruses by an His275Tyr genotyping assay using the cycling probe method. J Clin Microbiol. 49(1): 125–30 (2011). doi:10.1128/JCM.01401-10.
Zhu X. et al. Genetic variation of the human alpha-2-Heremans-Schmid glycoprotein (AHSG) gene associated with the risk of SARS-CoV infection. PLoS ONE 6:e23730 (2011). doi: 10.1371/journal.pone.0023730.
L’Huillier A. G. et al. ABCB1 polymorphisms and neuropsychiatric adverse events in oseltamivir-treated children during influenza H1N1/09 pandemia. Pharmacogenomics 12(10): 1493-501 (2011). 10.2217/pgs.11.91.
Ching J. C. et al. Significance of the Myxovirus Resistance A (MxA) Gene — 123C>A Single-Nucleotide Polymorphism in Suppressed Interferon β Induction of Severe Acute Respiratory Syndrome Coronavirus Infection. The Journal of Infectious Diseases 201(12): 1899–908 (2010). doi: 10.1086/652799.
Li H. et al. Polymorphisms in the C-type lectin genes cluster in chromosome 19 and predisposition to severe acute respiratory syndrome coronavirus (SARS-CoV) infection. Journal of Medical Genetics 45: 752-8 (2008). doi: 10.1136/jmg.2008.058966.
Tang F. et al. LIL-12 RB1 Genetic Variants Contribute to Human Susceptibility to Severe Acute Respiratory Syndrome Infection among Chinese. PLoS ONE 3(5): e2183 (2008). doi: 10.1371/journal.pone.0002183.
Li C. et al. A nonsynonymous SNP in human cytosolic sialidase in a small Asian population results in reduced enzyme activity: potential link with severe adverse reactions to oseltamivir. Cell Res. 17: 357–62 (2007). doi: 10.1038/cr.2007.27.
Ng M. W., et al. The association of RANTES polymorphism with severe acute respiratory syndrome in Hong Kong and Beijing Chinese. BMC Infect Dis. 7:50 (2007). doi: 10.1186/1471-2334-7-50.
Li W. et al. The S proteins of human coronavirus NL63 and severe acute respiratory syndrome coronavirus bind overlapping regions of ACE2. Virology 367: 367–74 (2007). doi: 10.1016/j.virol.2007.04.035.
Long, M. Side effects of Tamiflu: clues from an Asian single nucleotide polymorphism. Cell Res. 17: 309–10 (2007). 10.1038/cr.2007.30.
Kelvin Y. K. et al. Association of ICAM3 Genetic Variant with Severe Acute Respiratory Syndrome, The Journal of Infectious Diseases 196(2): 271–80 (2007). doi: 10.1086/518892.
Chan K. Y. K. et al. Reply to 'Lack of support for an association between CLEC4M homozygosity and protection against SARS coronavirus infection'. (Letter) Nature Genet. 39: 694-696 (2007). doi: 10.1038/ng0607-694.
Zhi L. et al. Lack of support for an association between CLEC4M homozygosity and protection against SARS coronavirus infection. Nat Genet. 39: 692–3 (2007). doi: 10.1038/ng0607-692.
Tang N. et al. Lack of support for an association between CLEC4M homozygosity and protection against SARS coronavirus infection. Nat Genet 39: 691–2 (2007). doi: 10.1038/ng0607-691.
Chan V. S. et al. Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection. Nat Genet. 38: 38-46 (2006). doi: 10.1038/ng1698.
He J. et al. Association of SARS susceptibility with single nucleic acid polymorphisms of OAS1 and MxA genes: a case-control study. BMC Infect Dis 6:106 (2006). doi: 10.1186/1471-2334-6-106.
Wei-Ju C. et al. Nasopharyngeal Shedding of Severe Acute Respiratory Syndrome—Associated Coronavirus Is Associated with Genetic Polymorphisms, Clinical Infectious Diseases. 42(11): 1561-9 (2006). doi: 10.1086/503843.
Imai Y. et al. Angiotensin-converting enzyme 2 protects from severe acute lung failure. Nature 436: 112–6 (2005). doi: 10.1038/nature03712.
Li W. et al. Receptor and viral determinants of SARS-coronavirus adaptation to human ACE2. EMBO J. 24: 1634–43 (2005). doi: 10.1038/sj.emboj.7600640.
W. K. Eddie Ip. et al. Mannose-Binding Lectin in Severe Acute Respiratory Syndrome Coronavirus Infection. The Journal of Infectious Diseases 191(10): 1697–704 (2005). doi: 10.1086/429631.
Hongxing Z. et al. Association between Mannose-Binding Lectin Gene Polymorphisms and Susceptibility to Severe Acute Respiratory Syndrome Coronavirus Infection. The Journal of Infectious Diseases 192(8): 1355–61 (2005). doi: 10.1086/491479.
Wang H. W. et al. [A case-control study on the mxA polymorphisms and susceptibility to severe acute respiratory syndromes.] Zhonghua Liu Xing Bing Xue Za Zhi. 26(8): 574-7 (2005). pubmed: 16390004.
Hamano E. et al. Polymorphisms of interferon-inducible genes OAS-1 and MxA associated with SARS in the Vietnamese population. Biochem Biophys Res Commun. 329: 1234-9 (2005). doi: 10.1016/j.bbrc.2005.02.101.
Huang K. J. An interferon-gamma-related cytokine storm in SARS patients. J Med Virol. 75(2): 185-94 (2005). doi: 10.1002/jmv.20255.
Gabriella A. et al. Fatal Severe Acute Respiratory Syndrome Is Associated with Multiorgan Involvement by Coronavirus. J Infect Dis. 191(2):193-7 (2005). doi: 10.1086/426870.
Hofmann H. et al. Susceptibility to SARS coronavirus S protein-driven infection correlates with expression of angiotensin converting enzyme 2 and infection can be blocked by soluble receptor. Biochem. Biophys. Res. Commun. 319: 1216–21 (2004). doi: 10.1016/j.bbrc.2004.05.114.
Chan M. H. et al. Serum LD1 isoenzyme and blood lymphocyte subsets as prognostic indicators for severe acute respiratory syndrome. J Intern Med. 255: 512-8 (2004). doi: 10.1111/j.1365-2796.2004.01323.x.
Leung G. M. et al. SARS-CoV antibody prevalence in all Hong Kong patient contacts. Emerg Infect Dis. 10: 1653-6 (2004). doi: 10.3201/eid1009.040155.
Jones B. M. et al. Prolonged disturbances of in vitro cytokine production in patients with severe acute respiratory syndrome (SARS) treated with ribavirin and steroids. Clin Exp Immunol. 135: 467-73 (2004). doi: 10.1111/j.1365-2249.2003.02391.x.
Margaret H. L. et al. Association of Human-Leukocyte-Antigen Class I (B*0703) and Class II (DRB1*0301) Genotypes with Susceptibility and Resistance to the Development of Severe Acute Respiratory Syndrome. The Journal of Infectious Diseases 190(3): 515-8 (2004). doi: 10.1086/421523.
Pavlovic-Lazetic G. M. et al. Bioinformatics analysis of SARS coronavirus genome polymorphism. BMC Bioinformatics 5(65): (2004). doi: 10.1186/1471-2105-5-65.
Stroher U. et al. Severe acute respiratory syndrome-related coronavirus is inhibited by interferon-alpha. J Infect Dis. 189: 1164-7 (2004). doi: 10.1086/382597.
Jeffers S. A. et al. CD209L (L-SIGN) is a receptor for severe acute respiratory syndrome coronavirus. Proc Natl Acad Sci U S A. 101(44): 15748-53 (2004). doi: 10.1073/pnas.0403812101.
Keyaerts E. et al. Inhibition of SARS-coronavirus infection in vitro by S-nitroso-N-acetylpenicillamine, a nitric oxide donor compound. Int J Infect Dis. 8(4): 223-6 (2004). doi: 10.1016/j.ijid.2004.04.012.
Chu C. M. et al. Initial viral load and the outcomes of SARS. CMAJ. 171(11): 1349–52 (2004). doi: 10.1503/cmaj.1040398.
Rainer T. H. et al. The spectrum of severe acute respiratory syndrome-associated coronavirus infection. Ann Intern Med. 140(8): 614-9 (2004). doi: 10.7326/0003-4819-140-8-200404200-00008.
Cheung O.Y. et al. The spectrum of pathological changes in severe acute respiratory syndrome (SARS). Histopathology 45(2): 119-24 (2004). doi: 10.1111/j.1365-2559.2004.01926.x.
Wong C. K. Plasma inflammatory cytokines and chemokines in severe acute respiratory syndrome. Clin Exp Immunol. 136(1): 95–103 (2004). doi: 10.1111/j.1365-2249.2004.02415.x.
Cinatl J. et al. Treatment of SARS with human interferons. Lancet 362: 293-4 (2003). doi: 10.1016/S0140-6736(03)13973-6.
Lin M. et al. Association of HLA class I with severe acute respiratory syndrome coronavirus infection. BMC Med Genet. 4: 9 (2003). doi:10.1186/1471-2350-4-9.
Tsui, P. T. et al. Severe Acute Respiratory Syndrome: Clinical Outcome and Prognostic Correlates. Emerg Infect Dis. 9(9): 1064-9 (2003). doi: 10.3201/eid0909.030362.
Li W. et al. Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus. Nature 426: 450–4 (2003). doi: 10.1038/nature02145.
Cui W. et al. Expression of lymphocytes and lymphocyte subsets in patients with severe acute respiratory syndrome. Clin Infect Dis. 37: 857-9 (2003). doi: 10.1086/378587.
Xu J. et al. Genome organization of the SARS-CoV. Genomics Proteomics Bioinformatics 1(3): 226–35 (2003). doi: 10.1016/s1672-0229(03)01028-3.
Booth C. M. et al. Clinical Features and Short-term Outcomes of 144 Patients With SARS in the Greater Toronto Area. JAMA 289(21): 2801–9 (2003). doi: 10.1001/jama.289.21.JOC30885.
Peiris J. S. et al. Clinical progression and viral load in a community outbreak of coronavirus-associated SARS pneumonia: a prospective study. Lancet 361(9371): 1767-72 (2003). doi: 10.1016/s0140-6736(03)13412-5.
Tsui P. T. et al. Severe acute respiratory syndrome: clinical outcome and prognostic correlates. Emerg Infect Dis. 9(9): 1064–9 (2003). doi: 10.3201/eid0909.030362.
Morris J. G. Jr. et al. Emergence of new pathogens as a function of changes in host susceptibility. Emerg Infect Dis. 3: 433-41 (1997). doi: 10.3201/eid0304.970404.
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|Analysis of your DNA using almost any DNA test||Everything included in the Free version||Everything in the Plus version|
|Personalized report on how your genes may impact your health risk from the coronavirus||Additional insights about your genetic risk from coronavirus||Full genetic analysis for all genes known to impact coronavirus risk|
|Insights about personalized prevention||Includes analysis of changes in genes that are not tested by 23andMe, AncestryDNA, MyHeritage, FamilyTreeDNA or any similar test|
|Updated on a regular basis whenever there's new research pertaining to coronavirus risk|
|Real-Time Monitoring of the outbreak|
|Up-to-Date News about coronavirus-related health insights and prevention tips|
|Test Compatibility||Format Compatibility||Variant Compatibility||Reference Genome Compatibility|
|Whole Genome Sequencing||FASTQ and FQ||SNP / SNV
(Single Nucleotide Variants)
|hg38 / GRCh38|
|Exome Sequencing||FASTA and FA||INDEL
(Insertion Deletion Variants)
|hg19 / GRCh37|
|Ultimate DNA Test||BAM||hg18 / GRCh36|
|23andMe||SAM||hg17 / GRCh35|
|Dante Labs||Genome VCF (gVCF and GVCF)|
|Genes for Good||CSV|
|HomeDNA||gz and zip compressed files|
|FTDNA||almost all other genetic data formats|
|New Amsterdam Genomics|
|almost all other genetic tests|
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The genetic analysis and statements that appear in this app, assessment and report have not been evaluated by the United States Food and Drug Administration. The Sequencing.com website and all software applications (Apps) that use Sequencing.com's website, as well as Sequencing.com's open Application Programming Interface (API), are not intended to diagnose, monitor, treat, cure, prevent nor alleviate any disease.
The Coronavirus DNA Health Assessment does not provide any information relating to the diagnosis, prevention or treatment of Coronavirus CoV-2 infection or COVID-19.