Next Article in Journal
Cell Penetrable Human scFv Specific to Middle Domain of Matrix Protein-1 Protects Mice from Lethal Influenza
Next Article in Special Issue
Multiple Regions of Kaposi’s Sarcoma-Associated Herpesvirus ORF59 RNA are Required for Its Expression Mediated by Viral ORF57 and Cellular RBM15
Previous Article in Journal / Special Issue
KSHV Reactivation and Novel Implications of Protein Isomerization on Lytic Switch Control
Review

Molecular Biology of KSHV Lytic Reactivation

Department of Microbiology and Immunology, University of Nevada, Reno, School of Medicine, 1664 N Virginia Street, MS 320, Reno, NV 89557, USA
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Zhi-Ming Zheng
Viruses 2015, 7(1), 116-153; https://doi.org/10.3390/v7010116
Received: 31 October 2014 / Accepted: 5 January 2015 / Published: 14 January 2015
(This article belongs to the Special Issue Kaposi's Sarcoma-Associated Herpesvirus)
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. View Full-Text
Keywords: KSHV; reactivation; Lytic DNA replication; hypoxia; RTA; LANA KSHV; reactivation; Lytic DNA replication; hypoxia; RTA; LANA
Show Figures

Figure 1

MDPI and ACS Style

Purushothaman, P.; Uppal, T.; Verma, S.C. Molecular Biology of KSHV Lytic Reactivation. Viruses 2015, 7, 116-153. https://doi.org/10.3390/v7010116

AMA Style

Purushothaman P, Uppal T, Verma SC. Molecular Biology of KSHV Lytic Reactivation. Viruses. 2015; 7(1):116-153. https://doi.org/10.3390/v7010116

Chicago/Turabian Style

Purushothaman, Pravinkumar, Timsy Uppal, and Subhash C. Verma. 2015. "Molecular Biology of KSHV Lytic Reactivation" Viruses 7, no. 1: 116-153. https://doi.org/10.3390/v7010116

Find Other Styles

Article Access Map by Country/Region

1
Only visits after 24 November 2015 are recorded.
Back to TopTop