{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T11:34:50Z","timestamp":1761824090813,"version":"3.41.2"},"reference-count":43,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2019,5,1]],"date-time":"2019-05-01T00:00:00Z","timestamp":1556668800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI127370"],"award-info":[{"award-number":["AI127370"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000072","name":"HHS | NIH | National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","award":["DE021985"],"award-info":[{"award-number":["DE021985"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000048","name":"American Cancer Society","doi-asserted-by":"publisher","award":["RSG-15-049-01-MPC"],"award-info":[{"award-number":["RSG-15-049-01-MPC"]}],"id":[{"id":"10.13039\/100000048","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2019,5]]},"abstract":"<jats:p>\n            Innate immune signaling is a critical defense against viral infection and represents a central host-virus interaction that frequently determines the outcomes of infections. NF-\u03baB signaling is an essential component of innate immunity that is extensively modulated by HCMV, a significant cause of morbidity in neonates and immunosuppressed individuals. However, the roles that various facets of NF-\u03baB signaling play during HCMV infection have remained elusive. We find that the two major regulatory kinases in this pathway, IKK\u03b1 and IKK\u03b2, limit the initiation of infection, viral replication, and cell-to-cell spread. In addition, our results indicate that these kinases contribute differently to the host cell response to infection in the absence of a virally encoded NF-\u03baB inhibitor, U\n            <jats:sub>L<\/jats:sub>\n            26. Given the importance of NF-\u03baB in viral infection, elucidating the contributions of various NF-\u03baB constituents to infection is an essential first step toward the possibility of targeting this pathway therapeutically.\n          <\/jats:p>","DOI":"10.1128\/jvi.02030-18","type":"journal-article","created":{"date-parts":[[2019,2,13]],"date-time":"2019-02-13T14:21:42Z","timestamp":1550067702000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":6,"title":["The I\u03baB Kinases Restrict Human Cytomegalovirus Infection"],"prefix":"10.1128","volume":"93","author":[{"given":"Christopher M.","family":"Goodwin","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joshua","family":"Munger","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","volume-title":"Cytomegaloviruses","author":"Mocarski ES","year":"2006","unstructured":"Mocarski ES, Shenk T, Pass RF, Knipe DM. 2006. 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