{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T22:51:06Z","timestamp":1792018266712,"version":"4.4.0"},"reference-count":47,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2001,1,1]],"date-time":"2001-01-01T00:00:00Z","timestamp":978307200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,1,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>LPS is the major active agent in the pathogenesis of Gram-negative septic shock. In this report we have studied the influence of concurrent viral infection on the outcome of LPS-induced shock. We find that infection with vesicular stomatitis virus sensitizes mice to LPS at an early time point following infection. Treatment of mice with the chemical IFN inducer, polyinosinic:polycytidylic acid, has a similar effect. This hypersensitivity to LPS correlated with hyperproduction of TNF-\u03b1 in vivo. The cellular and molecular mechanisms underlying this phenomenon were investigated using Ab-depleted and gene-targeted mice. Our results revealed that while NK cell depletion and elimination of IFN-\u03b3 partially protected against the sensitizing effects of vesicular stomatitis virus and polyinosinic:polycytidylic acid, the most striking effect was observed in IFN-\u03b1\u03b2R-deficient mice. Thus hyperproduction of TNF-\u03b1 was completely abrogated in IFN-\u03b1\u03b2R-deficient mice, indicating that the principal mechanism underlying rapid virus-induced sensitization to LPS is an IFN-\u03b1\u03b2-mediated priming of mice for an augmented production of TNF-\u03b1 in response to LPS. This conclusion was further supported by the finding that pretreatment of mice with rIFN-\u03b1\u03b2 mimicked the effect of viral infection. In conclusion, our results reveal a previously unrecognized proinflammatory effect of IFN-\u03b1\u03b2 and point to a new pathway through which viral infection may influence the outcome of concurrent bacterial infection.<\/jats:p>","DOI":"10.4049\/jimmunol.166.2.982","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T22:56:47Z","timestamp":1398034607000},"page":"982-988","source":"Crossref","is-referenced-by-count":51,"title":["Viral Infection Causes Rapid Sensitization to Lipopolysaccharide: Central Role of IFN-\u03b1\u03b2"],"prefix":"10.1093","volume":"166","author":[{"given":"Anneline","family":"Nansen","sequence":"first","affiliation":[{"name":"Institute of Medical Microbiology and Immunology, University of Copenhagen , Copenhagen ,","place":["Denmark"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allan","family":"Randrup Thomsen","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology and Immunology, University of Copenhagen , Copenhagen ,","place":["Denmark"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2001,1,15]]},"reference":[{"key":"2026020208061274600_R1","first-page":"732","volume-title":"Lancet","year":"1991"},{"key":"2026020208061274600_R2","first-page":"2920","volume-title":"J. 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