Viruses 2013, 5(5), 1346-1373; doi:10.3390/v5051346

The Chromatin Landscape of Kaposi’s Sarcoma-Associated Herpesvirus

Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Harlyne J. Norris Cancer Research Tower, 1450 Biggy Street, Los Angeles, CA 90033, USA
* Author to whom correspondence should be addressed.
Received: 24 April 2013; in revised form: 17 May 2013 / Accepted: 17 May 2013 / Published: 23 May 2013
(This article belongs to the Special Issue Chromatin Control of Viral Infection)
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Abstract: Kaposi’s sarcoma-associated herpesvirus is an oncogenic γ-herpesvirus that causes latent infection in humans. In cells, the viral genome adopts a highly organized chromatin structure, which is controlled by a wide variety of cellular and viral chromatin regulatory factors. In the past few years, interrogation of the chromatinized KSHV genome by whole genome-analyzing tools revealed that the complex chromatin landscape spanning the viral genome in infected cells has important regulatory roles during the viral life cycle. This review summarizes the most recent findings regarding the role of histone modifications, histone modifying enzymes, DNA methylation, microRNAs, non-coding RNAs and the nuclear organization of the KSHV epigenome in the regulation of latent and lytic viral gene expression programs as well as their connection to KSHV-associated pathogenesis.
Keywords: Kaposi’s sarcoma-associated herpesvirus; KSHV; KS; viral chromatin; polycomb; EZH2; minichromosome; histone modifications; MLL/Set1; JMJD2A

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MDPI and ACS Style

Toth, Z.; Brulois, K.; Jung, J.U. The Chromatin Landscape of Kaposi’s Sarcoma-Associated Herpesvirus. Viruses 2013, 5, 1346-1373.

AMA Style

Toth Z, Brulois K, Jung JU. The Chromatin Landscape of Kaposi’s Sarcoma-Associated Herpesvirus. Viruses. 2013; 5(5):1346-1373.

Chicago/Turabian Style

Toth, Zsolt; Brulois, Kevin; Jung, Jae U. 2013. "The Chromatin Landscape of Kaposi’s Sarcoma-Associated Herpesvirus." Viruses 5, no. 5: 1346-1373.

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