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Advances in Virology
Volume 2011 (2011), Article ID 193860, 19 pages
http://dx.doi.org/10.1155/2011/193860
Review Article

Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus Latency and Reactivation

Fengchun Ye,1,2,3 Xiufen Lei,1,2,3 and Shou-Jiang Gao1,2,3

1Tumor Virology Program, Greehey Children's Cancer Research Institute, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA
2Department of Pediatrics, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA
3Cancer Therapy and Research Center, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA

Received 16 November 2010; Revised 6 March 2011; Accepted 7 March 2011

Academic Editor: Eric O. Freed

Copyright © 2011 Fengchun Ye et al. 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.

Abstract

The life cycle of Kaposi's sarcoma-associated herpesvirus (KSHV) consists of latent and lytic replication phases. During latent infection, only a limited number of KSHV genes are expressed. However, this phase of replication is essential for persistent infection, evasion of host immune response, and induction of KSHV-related malignancies. KSHV reactivation from latency produces a wide range of viral products and infectious virions. The resulting de novo infection and viral lytic products modulate diverse cellular pathways and stromal microenvironment, which promote the development of Kaposi's sarcoma (KS). The mechanisms controlling KSHV latency and reactivation are complex, involving both viral and host factors, and are modulated by diverse environmental factors. Here, we review the cellular and molecular basis of KSHV latency and reactivation with a focus on the most recent advancements in the field.