Jennifer M. Zurney

Works (4)

Updated: July 5th, 2023 15:54

2011 journal article

A Single-Amino-Acid Polymorphism in Reovirus Protein mu 2 Determines Repression of Interferon Signaling and Modulates Myocarditis

JOURNAL OF VIROLOGY, 86(4), 2302–2311.

By: S. Irvin n, J. Zurney n, L. Ooms*, J. Chappell *, T. Dermody * & B. Sherry n

MeSH headings : Animals; Cell Line; Cells, Cultured; Down-Regulation; Humans; Interferon-alpha / genetics; Interferon-alpha / metabolism; Interferon-beta / genetics; Interferon-beta / metabolism; Mammalian orthoreovirus 3 / genetics; Mammalian orthoreovirus 3 / metabolism; Mice; Myocarditis / genetics; Myocarditis / metabolism; Myocarditis / virology; Myocytes, Cardiac / metabolism; Myocytes, Cardiac / virology; Orthoreovirus, Mammalian / genetics; Orthoreovirus, Mammalian / metabolism; Polymorphism, Single Nucleotide; Reoviridae Infections / genetics; Reoviridae Infections / metabolism; Reoviridae Infections / virology; Signal Transduction; Viral Proteins / genetics
TL;DR: It is demonstrated that a single amino acid difference between viruses can dictate virus strain-specific differences in suppression of the host IFN-β response and, consequently, damage to the heart. (via Semantic Scholar)
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Added: August 6, 2018

2008 journal article

Reovirus mu 2 Protein Inhibits Interferon Signaling through a Novel Mechanism Involving Nuclear Accumulation of Interferon Regulatory Factor 9

JOURNAL OF VIROLOGY, 83(5), 2178–2187.

By: J. Zurney n, T. Kobayashi *, G. Holm *, T. Dermody * & B. Sherry n

MeSH headings : Animals; Cell Nucleus / metabolism; Cells, Cultured; Gene Expression Regulation; Humans; Interferon-Stimulated Gene Factor 3 / metabolism; Interferon-Stimulated Gene Factor 3, gamma Subunit / metabolism; Interferon-alpha / pharmacology; Interferon-beta / pharmacology; Mammalian orthoreovirus 3 / genetics; Mammalian orthoreovirus 3 / metabolism; Mammalian orthoreovirus 3 / pathogenicity; Mice; Myocarditis / virology; Orthoreovirus, Mammalian / genetics; Orthoreovirus, Mammalian / metabolism; Orthoreovirus, Mammalian / pathogenicity; Reassortant Viruses / genetics; Reassortant Viruses / metabolism; Reassortant Viruses / pathogenicity; STAT1 Transcription Factor / metabolism; STAT2 Transcription Factor / metabolism; Transcriptional Activation; Viral Proteins / genetics; Viral Proteins / metabolism
TL;DR: The first report of an increase in IRF9 nuclear accumulation associated with viral subversion of the IFN response and couple virus strain-specific differences in IFN antagonism to the pathogenesis of viral myocarditis are reported. (via Semantic Scholar)
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2007 journal article

Basal expression levels of IFNAR and Jak-STAT components are determinants of cell-type-specific differences in cardiac antiviral responses

JOURNAL OF VIROLOGY, 81(24), 13668–13680.

By: J. Zurney*, K. Howard n & B. Sherry n

MeSH headings : Animals; Cells, Cultured; Fibroblasts / immunology; Fibroblasts / virology; Gene Expression Regulation; Humans; Interferon-alpha / genetics; Interferon-alpha / metabolism; Interferon-beta / genetics; Interferon-beta / metabolism; Janus Kinases / genetics; Janus Kinases / metabolism; L Cells; Mammalian orthoreovirus 3 / pathogenicity; Mice; Mice, Knockout; Myocarditis / immunology; Myocarditis / virology; Myocytes, Cardiac / immunology; Myocytes, Cardiac / virology; Orthoreovirus, Mammalian / pathogenicity; Receptor, Interferon alpha-beta / genetics; Receptor, Interferon alpha-beta / metabolism; Reoviridae Infections / immunology; Reoviridae Infections / virology; STAT Transcription Factors / genetics; STAT Transcription Factors / metabolism
TL;DR: It is found that greater basal expression of IFN-β in cardiac myocytes results in greater basal activated nuclear STAT1 and STAT2 and greater basal ISG mRNA expression and provides greater basal antiviral protection relative to cardiac fibroblasts, the first indication of an integrated network of cell-type-specific innate immune components for organ protection. (via Semantic Scholar)
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2007 journal article

Retinoic acid-inducible gene-I and interferon-beta promoter stimulator-1 augment proapoptotic responses following mammalian reovirus infection via interferon regulatory factor-3

JOURNAL OF BIOLOGICAL CHEMISTRY, 282(30), 21953–21961.

By: G. Holm *, J. Zurney n, V. Tumilasci*, S. Leveille*, P. Danthi *, J. Hiscott *, B. Sherry n, T. Dermody *

MeSH headings : Animals; Apoptosis / physiology; Cell Line; DEAD Box Protein 58; DEAD-box RNA Helicases / genetics; Fibroblasts / physiology; Genes, Reporter; HeLa Cells; Humans; Interferon Regulatory Factor-3 / physiology; Interferon-beta / genetics; Kidney; Mice; Promoter Regions, Genetic; Receptors, Immunologic; Reoviridae Infections / physiopathology; Transfection
TL;DR: It is shown that reovirus activates IRF-3 with kinetics that parallel the activation of NF-κB, a known mediator of reov virus-induced apoptosis, suggesting a common mechanism of antiviral cytokine induction and activation of the cell death response. (via Semantic Scholar)
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Source: Web Of Science
Added: August 6, 2018

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