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Cancers 2015, 7(1), 112-142; doi:10.3390/cancers7010112

Chromatinization of the KSHV Genome During the KSHV Life Cycle

1
Department of Microbiology and Immunology, School of Medicine, University of Nevada, 1664 N Virginia Street, MS 320, Reno, NV 89557, USA
2
Department of Microbiology and the Tumor Virology Program of the Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, 201E Johnson Pavilion, 3610 Hamilton Walk, Philadelphia, PA 19104, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Elena Kashuba
Received: 28 October 2014 / Accepted: 7 January 2015 / Published: 14 January 2015
(This article belongs to the Special Issue DNA Viruses in Human Cancer)
View Full-Text   |   Download PDF [1115 KB, uploaded 14 January 2015]   |  

Abstract

Kaposi’s sarcoma-associated herpesvirus (KSHV) belongs to the gamma herpesvirus family and is the causative agent of various lymphoproliferative diseases in humans. KSHV, like other herpesviruses, establishes life-long latent infection with the expression of a limited number of viral genes. Expression of these genes is tightly regulated by both the viral and cellular factors. Recent advancements in identifying the expression profiles of viral transcripts, using tilling arrays and next generation sequencing have identified additional coding and non-coding transcripts in the KSHV genome. Determining the functions of these transcripts will provide a better understanding of the mechanisms utilized by KSHV in altering cellular pathways involved in promoting cell growth and tumorigenesis. Replication of the viral genome is critical in maintaining the existing copies of the viral episomes during both latent and lytic phases of the viral life cycle. The replication of the viral episome is facilitated by viral components responsible for recruiting chromatin modifying enzymes and replication factors for altering the chromatin complexity and replication initiation functions, respectively. Importantly, chromatin modification of the viral genome plays a crucial role in determining whether the viral genome will persist as latent episome or undergo lytic reactivation. Additionally, chromatinization of the incoming virion DNA, which lacks chromatin structure, in the target cells during primary infection, helps in establishing latent infection. Here, we discuss the recent advancements on our understating of KSHV genome chromatinization and the consequences of chromatin modifications on viral life cycle. View Full-Text
Keywords: KSHV; oncogenic virus; LANA; RTA; epigenetics; viral chromatin; histone modifications; DNA methylation; PAN RNA; de novo infection KSHV; oncogenic virus; LANA; RTA; epigenetics; viral chromatin; histone modifications; DNA methylation; PAN RNA; de novo infection
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Uppal, T.; Jha, H.C.; Verma, S.C.; Robertson, E.S. Chromatinization of the KSHV Genome During the KSHV Life Cycle. Cancers 2015, 7, 112-142.

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