Мақола

Viral exploitation of p300/CBP at the virus-cancer interface: Chromatin regulation, oncogenesis, immune evasion, and therapeutic targeting

Ali M. AtoomFaculty of Allied Medical Sciences, Hourani Center for Applied Scientific Research, Al-Ahliyya Amman University, Amman, Jordan. Electronic address: [email protected]Jasur RizaevSamarkand State Medical InstituteD. PolatovaScientific-Practical Medical Center for Pediatric Oncology, Hematology and Immunology, Tashkent, Uzbekistan. Electronic address: [email protected]Pareshkumar N. PatelK.V. JamunaDepartment of Forensic Science, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India. Electronic address: [email protected]Laxmidhar MaharanaDepartment of Pharmaceutical Sciences, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, Odisha, 751030, India. Electronic address: [email protected]Neeraj BainsalUniversity Institute of Pharma Sciences, Chandigarh University, Mohali, Punjab, India. Electronic address: [email protected]Divya SinghalCentre for Research Impact and Outcome, Chitkara University, Rajpura, Punjab, India; Sharda School of Bio-Science & Technology, Sharda University, Greater Noida, India. Electronic address: [email protected]

2026en

ABI

Аннотация

The transcriptional coactivators p300 and CREB-binding protein (CBP) integrate chromatin remodeling, enhancer activity, lysine acetylation, immune signaling, and tumor-suppressor control, making them recurrent targets of viral proteins. This narrative review examines p300/CBP at the virus-cancer interface, prioritizing HTLV-1, high-risk HPV, EBV, KSHV, HBV, and HCV. We distinguish physical interaction, biochemical modulation, functional reliance, and therapeutic confirmation and compare how viral factors recruit, inhibit, degrade, or redistribute these coactivators during persistence, immune evasion, and malignant progression. Evidence from non-oncogenic viruses is retained only when it clarifies conserved mechanisms or therapeutic liabilities. Preclinical studies support catalytic, interaction-selective, and virus-specific targeting strategies, but human evidence is limited to early-phase PRI-724/OP-724 antifibrotic studies in viral cirrhosis. Because p300/CBP also support normal transcription and antiviral immunity, systemic inhibition may cause substantial toxicity. Overall, p300/CBP are best viewed as context-dependent regulatory hubs, and translation will require paralog-, domain-, and disease-specific validation.

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DOI: 10.1016/j.ctarc.2026.101448

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