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Combining five Epstein-Barr virus (EBV) and Kaposi\u2019s sarcoma-associated herpesvirus (KSHV) reactivation systems across B cell and epithelial models with deep poly(A)+ RNA sequencing of purified lytic cells, we find that most induced isoforms are predicted to undergo nonsense-mediated decay or to lose conserved protein domains, broadly compromising cell cycle, innate immune and RNA-processing pathways. The phenotype arises independently of viral DNA replication, indicating early host remodeling. A screen of EBV early genes identifies BRRF1 as a key driver: through a CIY(Y\/E) motif conserved in KSHV ORF49, BRRF1 engages the nuclear CCR4-NOT complex through its CNOT9 and CNOT1 subunits, hijacking this canonically cytoplasmic deadenylation hub for nuclear disruption of host splicing.<\/jats:p>","DOI":"10.64898\/2026.05.20.726682","type":"posted-content","created":{"date-parts":[[2026,5,23]],"date-time":"2026-05-23T18:50:29Z","timestamp":1779562229000},"source":"Crossref","is-referenced-by-count":1,"title":["A BRRF1-CCR4-NOT axis underlies conserved transcriptome-wide loss of splicing fidelity during gammaherpesvirus reactivation"],"prefix":"10.64898","author":[{"given":"Trang T","family":"Nguyen","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA, 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