{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T01:29:35Z","timestamp":1778549375811,"version":"3.51.4"},"reference-count":52,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2012,5,1]],"date-time":"2012-05-01T00:00:00Z","timestamp":1335830400000},"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":[[2012,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The necessity for pathogen recognition of viral infection by the innate immune system in initiating early innate and adaptive host defenses is well documented. However, little is known about the role these receptors play in the maintenance of adaptive immune responses and their contribution to resolution of persistent viral infections. In this study, we demonstrate a nonredundant functional requirement for both nucleic acid-sensing TLRs and RIG-I\u2013like receptors in the control of a mouse model of chronic viral infection. Whereas the RIG-I\u2013like receptor pathway was important for production of type I IFNs and optimal CD8+ T cell responses, nucleic acid-sensing TLRs were largely dispensable. In contrast, optimal anti-viral Ab responses required intact signaling through nucleic acid-sensing TLRs, and the absence of this pathway correlated with less virus-specific Ab and deficient long-term virus control of a chronic infection. Surprisingly, absence of the TLR pathway had only modest effects on Ab production in an acute infection with a closely related virus strain, suggesting that persistent TLR stimulation may be necessary for optimal Ab responses in a chronic infection. These results indicate that innate virus recognition pathways may play critical roles in the outcome of chronic viral infections through distinct mechanisms.<\/jats:p>","DOI":"10.4049\/jimmunol.1103656","type":"journal-article","created":{"date-parts":[[2012,3,24]],"date-time":"2012-03-24T07:56:04Z","timestamp":1332575764000},"page":"4432-4440","source":"Crossref","is-referenced-by-count":27,"title":["Differential Roles for RIG-I\u2013like Receptors and Nucleic Acid-Sensing TLR Pathways in Controlling a Chronic Viral Infection"],"prefix":"10.1093","volume":"188","author":[{"given":"Jonathan M","family":"Clingan","sequence":"first","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, University of California , San Francisco, San Francisco, CA 94143"},{"name":"Rosalind Russell Medical Research Center for Arthritis, University of California , San Francisco, San Francisco, CA 94143"},{"name":"Graduate Program in Biomedical Sciences, University of California , San Francisco, San Francisco, CA 94143"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kristin","family":"Ostrow","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, University of California , San Francisco, San Francisco, CA 94143"},{"name":"Rosalind Russell Medical Research Center for Arthritis, University of California , San Francisco, San Francisco, CA 94143"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karoline A","family":"Hosiawa","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, University of California , San Francisco, San Francisco, CA 94143"},{"name":"Rosalind Russell Medical Research Center for Arthritis, University of California , San Francisco, San Francisco, CA 94143"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhijian J","family":"Chen","sequence":"additional","affiliation":[{"name":"Howard Hughes Medical Institute, University of Texas Southwestern Medical Center , Dallas, TX 75390"},{"name":"Department of Molecular Biology, University of Texas Southwestern Medical Center , Dallas, TX 75390"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mehrdad","family":"Matloubian","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, University of California , San Francisco, San Francisco, CA 94143"},{"name":"Rosalind Russell Medical Research Center for Arthritis, University of California , San Francisco, San Francisco, CA 94143"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2012,5,1]]},"reference":[{"key":"2025032410041960400_r1","doi-asserted-by":"crossref","first-page":"30","DOI":"10.1016\/j.cell.2009.06.036","article-title":"Redefining chronic viral infection","volume":"138","author":"Virgin","year":"2009","journal-title":"Cell"},{"key":"2025032410041960400_r2","doi-asserted-by":"crossref","first-page":"4911","DOI":"10.1128\/JVI.77.8.4911-4927.2003","article-title":"Viral persistence alters CD8 T-cell immunodominance and tissue distribution and results in distinct stages of functional impairment","volume":"77","author":"Wherry","year":"2003","journal-title":"J. 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