{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T17:02:53Z","timestamp":1786122173201,"version":"build-2736575974"},"reference-count":121,"publisher":"Wiley","issue":"44","license":[{"start":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T00:00:00Z","timestamp":1778803200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T00:00:00Z","timestamp":1778803200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Herpes simplex virus type\u20101 (HSV\u20101) affects over 60% of the human population and increasingly develops resistance to antiviral therapies. Efficient HSV\u20101 replication requires host\u2010derived deoxynucleotide triphosphates and the manipulation of cellular DNA replication and repair. This work positions the protein phosphatase 2A (PP2A) regulatory subunit PR130 (PPP2R3A) as cellular factor that suppresses the replication of laboratory strains and clinical isolates of HSV\u20101 in epithelial and neuronal cells. HSV\u20101 infection in turn decreases PR130 levels. Global proteome and phosphoproteome profiling combined with functional assays demonstrate that PR130 modulates key regulators of the cell cycle and DNA repair. PR130 controls the expression and phosphorylation of the cyclin\u2010dependent kinase (CDK) inhibitor p21 (CDKN1A) at serine 130 (S130) which CDK2 catalyzes. The levels and activities of p21, which HSV\u20101 infection attenuates, and CDK2 are decisive factors for HSV\u20101 replication. Inhibition of the ubiquitin\u2010specific protease USP7 stabilizes the p53\u2010p21 axis and reduces HSV\u20101 viral titers. Additionally, PR130 depletion enhances signaling of the DNA damage\u2010responsive checkpoint kinase ataxia\u2010telangiectasia mutated (ATM) upon HSV\u20101 infection and creates a dependency of HSV\u20101 replication on ATM activity. These findings uncover host\u2010intrinsic mechanisms regulating HSV\u20101 replication and highlight PR130 as central hub regulator of HSV\u20101 infection.<\/jats:p>","DOI":"10.1002\/advs.202523697","type":"journal-article","created":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T15:25:13Z","timestamp":1778858713000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The Host Cell Factor Phosphatase\u20102A Subunit PR130 Restricts Replication of Herpes Simplex Virus Type\u20101"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-5917-9527","authenticated-orcid":false,"given":"Johannes","family":"Jungwirth","sequence":"first","affiliation":[{"name":"Section of Experimental Virology Institute of Medical Microbiology Center for Molecular Biomedicine (CMB) Jena University Hospital  Jena Germany"},{"name":"Institute of Toxicology University Medical Center of the Johannes Gutenberg 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