Item talk:Q249887
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{
"USGS Publications Warehouse": { "@context": "https://schema.org", "@type": "Article", "additionalType": "Journal Article", "name": "Mathematical analysis demonstrates that interferons-\u03b2 and -\u03b3 Interact in a multiplicative manner to disrupt herpes simplex virus replication", "identifier": [ { "@type": "PropertyValue", "propertyID": "USGS Publications Warehouse IndexID", "value": "70031494", "url": "https://pubs.usgs.gov/publication/70031494" }, { "@type": "PropertyValue", "propertyID": "USGS Publications Warehouse Internal ID", "value": 70031494 }, { "@type": "PropertyValue", "propertyID": "DOI", "value": "10.1016/j.jtbi.2004.12.007", "url": "https://doi.org/10.1016/j.jtbi.2004.12.007" }, { "@type": "PropertyValue", "propertyID": "ISSN", "value": "00225193" } ], "journal": { "@type": "Periodical", "name": "Journal of Theoretical Biology", "volumeNumber": "234", "issueNumber": "3" }, "inLanguage": "en", "isPartOf": [ { "@type": "CreativeWorkSeries", "name": "Journal of Theoretical Biology" } ], "datePublished": "2005", "dateModified": "2015-05-04", "abstract": "Several studies suggest that the innate interferons (IFNs), IFN-\u03b1\u00a0and IFN-\u03b2, can act in concert with IFN-\u03b3to synergistically inhibit the replication of cytomegalovirus and herpes simplex virus type 1 (HSV-1). The significance of this observation is not yet agreed upon in large part because the nature and magnitude of the interaction between IFN-\u03b1/\u03b2\u00a0and IFN-\u03b3\u00a0is not well defined. In the current study, we resolve this issue by demonstrating three points. First, the hyperbolic tangent function, tanh (x \u00a0), can be used to describe the individual effects of IFN-\u03b2\u00a0or IFN-\u03b3\u00a0on HSV-1 replication over a 320,000-fold range of IFN concentration. Second, pharmacological methods prove that IFN-\u03b2\u00a0and IFN-\u03b3\u00a0interact in a greater-than-additive manner to inhibit HSV-1 replication. Finally, the potency with which combinations of IFN-\u03b2\u00a0and IFN-\u03b3\u00a0inhibit HSV-1 replication is accurately predicted by multiplying the individual inhibitory effects of each cytokine. Thus, IFN-\u03b2\u00a0and IFN-\u03b3\u00a0interact in a multiplicative manner. We infer that a primary antiviral function of IFN-\u03b3\u00a0lies in its capacity to multiply the potency with which IFN-\u03b1/\u03b2\u00a0restricts HSV-1 replication in vivo. 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