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Review
. 2013 Jun 27;5(7):1607-32.
doi: 10.3390/v5071607.

Histone deacetylases in herpesvirus replication and virus-stimulated host defense

Amanda J Guise  1 , Hanna G Budayeva, Benjamin A Diner, Ileana M Cristea
Affiliations
Review

Histone deacetylases in herpesvirus replication and virus-stimulated host defense

Amanda J Guise et al. Viruses. .

Abstract

Emerging evidence highlights a critical role for protein acetylation during herpesvirus infection. As prominent modulators of protein acetylation, histone deacetylases (HDACs) are essential transcriptional and epigenetic regulators. Not surprisingly, viruses have evolved a wide array of mechanisms to subvert HDAC functions. Here, we review the mechanisms underlying HDAC regulation during herpesvirus infection. We next discuss the roles of acetylation in host defense against herpesvirus infection. Finally, we provide a perspective on the contribution of current mass spectrometry-based "omic" technologies to infectious disease research, offering a systems biology view of infection.

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Figures

Figure 1
Figure 1
Summary of HDAC functions during herpesvirus infection. (A) Response to alpha-herpesvirus infection (HSV-1); (B) response to beta-herpesvirus infection (HCMV); (C) response to gamma-herpesvirus infection (EBV and KSHV).
Figure 2
Figure 2
Host response to viral DNA is mediated by IFI16. Acetylation-dependent localization of IFI16 allows dual-compartment sensing of viral DNA, promoting pro-inflammatory response and innate immune signaling during herpesvirus infection. (A) IFI16 senses HSV-1 DNA within the nucleus. (B) IFI16 senses cytoplasmic DNA resulting from transient transfection or viral capsid degradation.
Figure 3
Figure 3
Assessing HDAC functions during infection through integrative omic approaches. A combination of multi-disciplinary approaches, including metabolomics, proteomics and chemoproteomics, can provide information for comprehensive characterization of the roles that HDACs play during herpesvirus infection.
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