How Histone Acetylation Affects Murine Gammaherpesvirus Reactivation
Author Information
Author(s): Yang Zhang, Tang Haidong, Huang Hai, Deng Hongyu
Primary Institution: Center for Infection and Immunity and National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China
Hypothesis
The study investigates the role of DNA demethylation and histone acetylation in the reactivation of murine gammaherpesvirus 68 (MHV-68).
Conclusion
Histone acetylation, but not DNA demethylation, is sufficient for effective reactivation of MHV-68 from latency in S11E cells.
Supporting Evidence
- Histone acetylation was shown to significantly increase during MHV-68 reactivation.
- 5-AzaC treatment led to weak reactivation of MHV-68 despite demethylation of the RTA promoter.
- TSA treatment resulted in the removal of HDAC3 from the RTA promoter, facilitating reactivation.
Takeaway
This study found that changing how certain proteins attach to DNA can help a virus wake up from sleep, but just changing the DNA itself isn't enough.
Methodology
The study used S11E cells to analyze the effects of DNA demethylation and histone acetylation on MHV-68 reactivation through various chemical treatments.
Limitations
The study primarily focuses on a single cell line and may not fully represent other contexts of MHV-68 infection.
Digital Object Identifier (DOI)
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