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Published on: March 30, 2018
Clinical-Stage Nanatinostat Triggers Productive Epstein-Barr Virus Lytic Replication
Ibukun A Akinyemi1, Travis M Zeigler2, Griffin H Willman2
1Child Health Research Institute, Department of Pediatrics, University of Florida, Gainesville, Florida, USA.
Journal of Medical Virology
|July 28, 2026
Summary
Nanatinostat, an HDAC1/3 inhibitor, effectively triggers Epstein-Barr virus (EBV) replication and cell death in EBV-positive lymphomas. This supports the "kick-and-kill" strategy for treating EBV-driven cancers.
Area of Science:
- Oncology
- Virology
- Epigenetics
Background:
- Epstein-Barr virus (EBV)-associated lymphomas are challenging to treat.
- The
Purpose of the Study:
- To elucidate the mechanistic effects of nanatinostat on EBV and cell death.
- To understand the role of nanatinostat metabolites in EBV reactivation.
Main Methods:
- Treatment of EBV-positive lymphoma cell lines with nanatinostat.
- Analysis of EBV lytic cycle gene transcription, viral replication, and virion release.
- Assessment of nanatinostat metabolite activity on EBV and histone acetylation.
Main Results:
- Nanatinostat robustly induced the full EBV lytic cycle, including gene transcription and viral replication.
- Nanatinostat demonstrated nanomolar cytotoxicity against EBV-positive cells.
- Nanatinostat metabolites were found to be biologically inert regarding EBV activity.
Conclusions:
- Nanatinostat effectively reactivates EBV, leading to cell death in EBV-driven malignancies.
- Valganciclovir's role is to prevent viral dissemination, not enhance cytotoxicity.
- These findings support the clinical development of nanatinostat-based
