{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T16:26:48Z","timestamp":1780590408728,"version":"3.54.1"},"update-to":[{"DOI":"10.1371\/journal.ppat.1012058","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2024,5,31]],"date-time":"2024-05-31T00:00:00Z","timestamp":1717113600000}}],"reference-count":70,"publisher":"Public Library of Science (PLoS)","issue":"5","license":[{"start":{"date-parts":[[2024,5,20]],"date-time":"2024-05-20T00:00:00Z","timestamp":1716163200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National Institute of Health","award":["AI150698 and AI181865"],"award-info":[{"award-number":["AI150698 and AI181865"]}]},{"name":"National Institute of Health","award":["AI1049815 and GM068411"],"award-info":[{"award-number":["AI1049815 and GM068411"]}]},{"DOI":"10.13039\/100008091","name":"University of Rochester","doi-asserted-by":"crossref","award":["Elon Huntington Hooker Fellowship"],"award-info":[{"award-number":["Elon Huntington Hooker Fellowship"]}],"id":[{"id":"10.13039\/100008091","id-type":"DOI","asserted-by":"crossref"}]},{"name":"The University of Rochester","award":["start up funds"],"award-info":[{"award-number":["start up funds"]}]}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p>Viral disruption of innate immune signaling is a critical determinant of productive infection. The Human Cytomegalovirus (HCMV) UL26 protein prevents anti-viral gene expression during infection, yet the mechanisms involved are unclear. We used TurboID-driven proximity proteomics to identify putative UL26 interacting proteins during infection to address this issue. We find that UL26 forms a complex with several immuno-regulatory proteins, including several STAT family members and various PIAS proteins, a family of E3 SUMO ligases. Our results indicate that UL26 prevents STAT phosphorylation during infection and antagonizes transcriptional activation induced by either interferon \u03b1 (IFNA) or tumor necrosis factor \u03b1 (TNF\u03b1). Additionally, we find that the inactivation of PIAS1 sensitizes cells to inflammatory stimulation, resulting in an anti-viral transcriptional environment similar to \u0394UL26 infection. Further, PIAS1 is important for HCMV cell-to-cell spread, which depends on the presence of UL26, suggesting that the UL26-PIAS1 interaction is vital for modulating intrinsic anti-viral defense.<\/jats:p>","DOI":"10.1371\/journal.ppat.1012058","type":"journal-article","created":{"date-parts":[[2024,5,20]],"date-time":"2024-05-20T13:48:34Z","timestamp":1716212914000},"page":"e1012058","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":12,"title":["A UL26-PIAS1 complex antagonizes anti-viral gene expression during Human Cytomegalovirus infection"],"prefix":"10.1371","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5305-5783","authenticated-orcid":true,"given":"Jessica","family":"Ciesla","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai-Lieh","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric J.","family":"Wagner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5379-9440","authenticated-orcid":true,"given":"Joshua","family":"Munger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"340","published-online":{"date-parts":[[2024,5,20]]},"reference":[{"issue":"4","key":"ppat.1012058.ref001","doi-asserted-by":"crossref","first-page":"253","DOI":"10.1002\/rmv.535","article-title":"Review and meta-analysis of the epidemiology of congenital cytomegalovirus (CMV) infection.","volume":"17","author":"A Kenneson","year":"2007","journal-title":"Rev Med Virol."},{"issue":"5","key":"ppat.1012058.ref002","doi-asserted-by":"crossref","first-page":"355","DOI":"10.1002\/rmv.544","article-title":"New estimates of the prevalence of neurological and sensory sequelae and mortality associated with congenital cytomegalovirus infection.","volume":"17","author":"SC Dollard","year":"2007","journal-title":"Rev Med Virol"},{"key":"ppat.1012058.ref003","doi-asserted-by":"crossref","first-page":"12","DOI":"10.1016\/j.antiviral.2013.10.011","article-title":"Resistance of human cytomegalovirus to ganciclovir\/valganciclovir: a comprehensive review of putative resistance pathways","volume":"101","author":"TE Komatsu","year":"2014","journal-title":"Antiviral Res"},{"issue":"6","key":"ppat.1012058.ref004","doi-asserted-by":"crossref","first-page":"859","DOI":"10.2165\/00003495-200565060-00012","article-title":"Valganciclovir: a review of its use in the management of CMV infection and disease in immunocompromised patients.","volume":"65","author":"RS Cvetkovic","year":"2005","journal-title":"Drugs."},{"issue":"1","key":"ppat.1012058.ref005","doi-asserted-by":"crossref","first-page":"4","DOI":"10.1016\/j.vaccine.2013.09.042","article-title":"Priorities for CMV vaccine development","volume":"32","author":"PR Krause","year":"2013","journal-title":"Vaccine"},{"issue":"20","key":"ppat.1012058.ref006","doi-asserted-by":"crossref","first-page":"4589","DOI":"10.1242\/jcs.02579","article-title":"The NF- B pathway","volume":"118","author":"PN Moynagh","year":"2005","journal-title":"Journal of cell science"},{"key":"ppat.1012058.ref007","doi-asserted-by":"crossref","first-page":"225","DOI":"10.1146\/annurev.immunol.16.1.225","article-title":"NF-kappa B and Rel proteins: evolutionarily conserved mediators of immune responses","volume":"16","author":"S Ghosh","year":"1998","journal-title":"Annual review of immunology"},{"key":"ppat.1012058.ref008","unstructured":"Gilmore TG. 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