Founder of Health Rising and Phoenix Rising
In conclusion, we demonstrated that inhibition of class I HDACs by romidepsin could potently induce EBV lytic cycle and mediate enhanced cell death with ganciclovir
It's a cancer study. When they added a drug called romidepsin they found they could induce death of EBV in 75% of cells. Romidepsin is an anticancer agent going through clinical trials right now. It's been approved for the treatment of T-cell lymphoma.
Unfortunately it can have quite a few side effects: most common were nausea and vomiting,fatigue, infection, loss of appetite, and blood disorders (including anemia, thrombocytopenia, and leukopenia). It has also been associated with metabolic disturbances (such as abnormal electrolyte levels), skin reactions, altered taste perception, and changes in cardiac electrical conduction.
If it knocks EBV out though it might be worth it - if its possible to get a hold of.
Int J Cancer. 2015 Jul 23. doi: 10.1002/ijc.29698. [Epub ahead of print] Inhibition of class I histone deacetylases by romidepsin potently induces Epstein-Barr virus lytic cycle and mediates enhanced cell death with ganciclovir Hui KF1, Cheung AK2, Choi CK1, Yeung PL1, Middeldorp JM3, Lung ML2,4, Tsao SW5,4, Chiang AK1,4.
Pan-histone deacetylase (HDAC) inhibitors, which inhibit eleven HDAC isoforms, are widely used to induce EBV lytic cycle in EBV-associated cancers in vitro and in clinical trials. Here, we hypothesized that inhibition of one or several specific HDAC isoforms by selective HDAC inhibitors could potently induce EBV lytic cycle in EBV-associated malignancies such as nasopharyngeal carcinoma (NPC) and gastric carcinoma (GC).
We found that inhibition of class I HDACs, particularly HDAC-1, -2 and -3, was sufficient to induce EBV lytic cycle in NPC and GC cells in vitro and in vivo. Among a panel of selective HDAC inhibitors, the FDA-approved HDAC inhibitor romidepsin was found to be the most potent lytic inducer, which could activate EBV lytic cycle at ∼0.5 to 5 nM (versus ∼800 nM achievable concentration in patients' plasma) in more than 75% of cells. Up-regulation of p21WAF1 , which is negatively regulated by class I HDACs was observed prior to the induction of EBV lytic cycle. The up-regulation of p21WAF1 and induction of lytic cycle were abrogated by a specific inhibitor of PKC-δ but not the inhibitors of PI3K, MEK, p38 MAPK, JNK, or ATM pathways.
Interestingly, inhibition of HDAC-1, -2 and -3 by romidepsin or shRNA knockdown could confer susceptibility of EBV-positive epithelial cells to the treatment with ganciclovir. In conclusion, we demonstrated that inhibition of class I HDACs by romidepsin could potently induce EBV lytic cycle and mediate enhanced cell death with ganciclovir, suggesting potential application of romidepsin for the treatment of EBV-associated cancers. This article is protected by copyright. All rights reserved.