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Gene Expression Profiles Link Respiratory Viral Infection, Platelet Response to Aspirin, and Acute Myocardial Infarction.

dc.contributor.author Cyr, Derek
dc.contributor.author Ginsburg, Geoffrey Steven
dc.contributor.author Kraus, William Erle
dc.contributor.author Lucas, Joseph E
dc.contributor.author Newby, Laura Kristin
dc.contributor.author Rose, Jason J
dc.contributor.author Voora, Deepak
dc.contributor.author Woods, Christopher Wildrick
dc.contributor.author Zaas, Aimee Kirsch
dc.coverage.spatial United States
dc.date.accessioned 2016-08-01T13:16:14Z
dc.date.issued 2015
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/26193668
dc.identifier PONE-D-14-57051
dc.identifier.uri http://hdl.handle.net/10161/12503
dc.description.abstract BACKGROUND: Influenza infection is associated with myocardial infarction (MI), suggesting that respiratory viral infection may induce biologic pathways that contribute to MI. We tested the hypotheses that 1) a validated blood gene expression signature of respiratory viral infection (viral GES) was associated with MI and 2) respiratory viral exposure changes levels of a validated platelet gene expression signature (platelet GES) of platelet function in response to aspirin that is associated with MI. METHODS: A previously defined viral GES was projected into blood RNA data from 594 patients undergoing elective cardiac catheterization and used to classify patients as having evidence of viral infection or not and tested for association with acute MI using logistic regression. A previously defined platelet GES was projected into blood RNA data from 81 healthy subjects before and after exposure to four respiratory viruses: Respiratory Syncytial Virus (RSV) (n=20), Human Rhinovirus (HRV) (n=20), Influenza A virus subtype H1N1 (H1N1) (n=24), Influenza A Virus subtype H3N2 (H3N2) (n=17). We tested for the change in platelet GES with viral exposure using linear mixed-effects regression and by symptom status. RESULTS: In the catheterization cohort, 32 patients had evidence of viral infection based upon the viral GES, of which 25% (8/32) had MI versus 12.2% (69/567) among those without evidence of viral infection (OR 2.3; CI [1.03-5.5], p=0.04). In the infection cohorts, only H1N1 exposure increased platelet GES over time (time course p-value = 1e-04). CONCLUSIONS: A viral GES of non-specific, respiratory viral infection was associated with acute MI; 18% of the top 49 genes in the viral GES are involved with hemostasis and/or platelet aggregation. Separately, H1N1 exposure, but not exposure to other respiratory viruses, increased a platelet GES previously shown to be associated with MI. Together, these results highlight specific genes and pathways that link viral infection, platelet activation, and MI especially in the case of H1N1 influenza infection.
dc.language eng
dc.relation.ispartof PLoS One
dc.relation.isversionof 10.1371/journal.pone.0132259
dc.subject Aged
dc.subject Aspirin
dc.subject Blood Platelets
dc.subject Cardiac Catheterization
dc.subject Female
dc.subject Humans
dc.subject Influenza A Virus, H1N1 Subtype
dc.subject Influenza A Virus, H3N2 Subtype
dc.subject Influenza, Human
dc.subject Male
dc.subject Middle Aged
dc.subject Myocardial Infarction
dc.subject Pharmacogenetics
dc.subject Picornaviridae Infections
dc.subject Respiratory Syncytial Virus Infections
dc.subject Respiratory Syncytial Viruses
dc.subject Rhinovirus
dc.subject Transcriptome
dc.title Gene Expression Profiles Link Respiratory Viral Infection, Platelet Response to Aspirin, and Acute Myocardial Infarction.
dc.type Journal article
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/26193668
pubs.begin-page e0132259
pubs.issue 7
pubs.organisational-group Basic Science Departments
pubs.organisational-group Biomedical Engineering
pubs.organisational-group Biostatistics & Bioinformatics
pubs.organisational-group Clinical Science Departments
pubs.organisational-group Duke
pubs.organisational-group Duke Cancer Institute
pubs.organisational-group Duke Clinical Research Institute
pubs.organisational-group Duke Molecular Physiology Institute
pubs.organisational-group Global Health Institute
pubs.organisational-group Institutes and Centers
pubs.organisational-group Institutes and Provost's Academic Units
pubs.organisational-group Medicine
pubs.organisational-group Medicine, Cardiology
pubs.organisational-group Medicine, Infectious Diseases
pubs.organisational-group Molecular Genetics and Microbiology
pubs.organisational-group Pathology
pubs.organisational-group Pratt School of Engineering
pubs.organisational-group School of Medicine
pubs.organisational-group School of Nursing
pubs.organisational-group School of Nursing - Secondary Group
pubs.organisational-group Social Science Research Institute
pubs.organisational-group University Institutes and Centers
pubs.publication-status Published online
pubs.volume 10
dc.identifier.eissn 1932-6203


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