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Viruses. 2015 Jan 14;7(1):116-53. doi: 10.3390/v7010116.

Molecular biology of KSHV lytic reactivation.

Author information

1
Department of Microbiology and Immunology, University of Nevada, Reno, School of Medicine, 1664 N Virginia Street, MS 320, Reno, NV 89557, USA. pravinp@medicine.nevada.edu.
2
Department of Microbiology and Immunology, University of Nevada, Reno, School of Medicine, 1664 N Virginia Street, MS 320, Reno, NV 89557, USA. tuppal@medicine.nevada.edu.
3
Department of Microbiology and Immunology, University of Nevada, Reno, School of Medicine, 1664 N Virginia Street, MS 320, Reno, NV 89557, USA. scverma@medicine.nevada.edu.

Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV) primarily persists as a latent episome in infected cells. During latent infection, only a limited number of viral genes are expressed that help to maintain the viral episome and prevent lytic reactivation. The latent KSHV genome persists as a highly ordered chromatin structure with bivalent chromatin marks at the promoter-regulatory region of the major immediate-early gene promoter. Various stimuli can induce chromatin modifications to an active euchromatic epigenetic mark, leading to the expression of genes required for the transition from the latent to the lytic phase of KSHV life cycle. Enhanced replication and transcription activator (RTA) gene expression triggers a cascade of events, resulting in the modulation of various cellular pathways to support viral DNA synthesis. RTA also binds to the origin of lytic DNA replication to recruit viral, as well as cellular, proteins for the initiation of the lytic DNA replication of KSHV. In this review we will discuss some of the pivotal genetic and epigenetic factors that control KSHV reactivation from the transcriptionally restricted latent program.

PMID:
25594835
PMCID:
PMC4306831
DOI:
10.3390/v7010116
[Indexed for MEDLINE]
Free PMC Article

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