{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T01:53:48Z","timestamp":1791251628665,"version":"4.1.0"},"reference-count":67,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2009,6,1]],"date-time":"2009-06-01T00:00:00Z","timestamp":1243814400000},"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":[[2009,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Type 1 IFNs, innate cytokines with important effector and immunomodulatory properties, are rapidly induced in the acute phase of many virus infections; however, this is generally a transient response that is not sustained during virus persistence. To gain insight into mechanisms that can contribute to down-regulation of type 1 IFN production during virus persistence, we analyzed type 1 IFN production during acute and chronic lymphocytic choriomeningitis virus (LCMV) infection. High-level type 1 IFN production was transiently up-regulated in cells including plasmacytoid and conventional dendritic cells (DCs) following LCMV infection of mice, but LCMV persistence was associated with only low-level type 1 IFN production. Nonetheless, chronically infected mice were able to up-regulate type 1 IFN production in response to TLR3, 7, and 9 ligands, albeit less efficiently than uninfected mice. Splenic DC numbers in mice chronically infected with LCMV were decreased, and the remaining cells exhibited a reduced response to TLR stimulation. LCMV-infected cell lines efficiently up-regulated type 1 IFN production following TLR ligation and infection with a DNA virus, but exhibited a defect in type 1 IFN induction following infection with Sendai, an RNA virus. This block in type 1 IFN production by infected cells, together with abnormalities in DC numbers and functions, likely contribute to the low-level type 1 IFN production in mice chronically infected with LCMV. Impairment of type 1 IFN production may both promote virus persistence and impact on host immunocompetence. Understanding the mechanisms involved may assist in development of strategies for control of virus persistence and superinfection.<\/jats:p>","DOI":"10.4049\/jimmunol.0802526","type":"journal-article","created":{"date-parts":[[2009,5,19]],"date-time":"2009-05-19T17:00:29Z","timestamp":1242752429000},"page":"7178-7189","source":"Crossref","is-referenced-by-count":61,"title":["Multiple Mechanisms Contribute to Impairment of Type 1 Interferon Production during Chronic Lymphocytic Choriomeningitis Virus Infection of Mice"],"prefix":"10.1093","volume":"182","author":[{"given":"Lian Ni","family":"Lee","sequence":"first","affiliation":[{"name":"The Edward Jenner Institute for Vaccine Research , Compton, Berkshire,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shannon","family":"Burke","sequence":"additional","affiliation":[{"name":"The Edward Jenner Institute for Vaccine Research , Compton, Berkshire,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Montoya","sequence":"additional","affiliation":[{"name":"The Edward Jenner Institute for Vaccine Research , Compton, Berkshire,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Persephone","family":"Borrow","sequence":"additional","affiliation":[{"name":"The Edward Jenner Institute for Vaccine Research , Compton, Berkshire,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,6,1]]},"reference":[{"key":"2025032715464964200_R1","first-page":"321","article-title":"Interferons and Other Cytokines. 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