{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T09:29:25Z","timestamp":1785403765053,"version":"3.56.0"},"reference-count":57,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T00:00:00Z","timestamp":1784592000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T00:00:00Z","timestamp":1784592000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100018542","name":"Natural Science Foundation of Sichuan Province","doi-asserted-by":"publisher","award":["2025ZNSFSC0208"],"award-info":[{"award-number":["2025ZNSFSC0208"]}],"id":[{"id":"10.13039\/501100018542","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["32573410"],"award-info":[{"award-number":["32573410"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100010038","name":"Earmarked Fund for China Agriculture Research System","doi-asserted-by":"publisher","award":["CARS-42-17"],"award-info":[{"award-number":["CARS-42-17"]}],"id":[{"id":"10.13039\/501100010038","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Program Sichuan Veterinary Medicine and Drug Innovation Group Of the China Agricultural Research System","award":["SCCXTD-2025-18"],"award-info":[{"award-number":["SCCXTD-2025-18"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2026,7,21]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Herpesviruses employ sophisticated immune evasion strategies to establish lifelong infections, subverting type I interferon (IFN-I) responses critical for antiviral defense. However, their adaptive mechanisms across species remain poorly characterized. Using duck plague virus (DPV)\u2014an avian alphaherpesvirus model\u2014we identify a cooperative immune evasion axis wherein ICP27 orchestrates UL55-mediated immunosuppression through dual regulatory mechanisms: its RNA-binding domain (RGG) facilitates UL55 mRNA nuclear export, while its C-terminal domain (CTD) stabilizes UL55 protein via direct interaction. This partnership enables synergistic suppression of IFN-I signaling\u2014co-expression of ICP27 and UL55 inhibits Poly(I:C)-induced immune genes (IFN-\u03b2, Mx, OASL, IL-6) more potently than either protein alone. UL55 functions as a precision-targeted IFN-I antagonist, selectively degrading RIG-I and IRF7 through proteasomal pathways\u2014confirmed by proteasome inhibitor rescue (MG132), structural modeling (AlphaFold), and binding assays (Co-IP). Evolutionarily, UL55 homologs (DPV, Herpes simplex virus type 1 [HSV-1], Varicella zoster virus [VZV]) conserve RIG-I targeting but diverge in IRF3\/IRF7 regulation\u2014adaptations shaped by UL55 sequence divergence (38.68% identity) and host biology (e.g., waterfowl IRF3 deficiency). This work establishes ICP27-UL55 as a key regulatory axis in herpesviral immune evasion and redefines UL55 as a conserved yet adaptable immunosuppressor in\n                      <jats:italic toggle=\"yes\">Alphaherpesvirinae<\/jats:italic>\n                      .\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>This study fundamentally advances herpesvirology by defining a novel immune evasion paradigm in duck plague virus. We reveal ICP27 as a master regulator that coordinates UL55 immunosuppression through a two-tiered mechanism: RGG domain-mediated mRNA nuclear export and CTD-dependent protein stabilization\u2014an unreported strategy in herpesviruses. UL55 selectively degrades RIG-I and IRF7 via proteasomal pathways, enabling precise IFN-I suppression with minimal immune activation. Crucially, ICP27-UL55 synergy inhibits Poly(I:C)-induced immune genes (IFN-\u03b2, Mx, OASL, IL-6) more effectively than individual proteins. Evolutionary analyses demonstrate conserved targeting of RIG-I across alphaherpesvirus UL55 homologs (DPV, HSV-1, VZV) but host-adapted divergence in IRF3\/IRF7 regulation, shaped by UL55 sequence variation (38.68% identity) and host biology (e.g., avian IRF3 deficiency). These findings provide the first evidence of effector coordination through integrated transcriptional\/post-translational regulation in herpesviruses. Disrupting ICP27-UL55 interaction offers new antiviral targets, while UL55-deficient strains serve as vaccine candidates for poultry disease control.<\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/jvi.00653-26","type":"journal-article","created":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T18:16:18Z","timestamp":1782843378000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Alpha-herpesvirus UL55 synergizes with ICP27 to suppress type I interferon production through conserved and host-adapted mechanisms"],"prefix":"10.1128","volume":"100","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0103-6446","authenticated-orcid":false,"given":"Ying","family":"Wu","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01mv9t934","id-type":"ROR","asserted-by":"publisher"}],"name":"Engineering Research Center of Southwest Animal Disease Prevention and 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