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Updated: Jun 2, 2025

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
Published on: August 25, 2017
Modulation of Cell Cycle Kinases by Kaposi's Sarcoma-Associated Herpesvirus
Steven Longworth1,2, Blossom Damania1,2
1Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Abstract:
The cell cycle is governed by kinase activity that coordinates progression through a series of regulatory checkpoints, preventing the division of damaged cells. The Kaposi's sarcoma-associated herpesvirus (KSHV) encodes multiple genes that modulate or co-opt the activity of these kinases, shaping the cellular environment to promote viral persistence. By advancing the cell cycle, KSHV facilitates latent replication and subsequent transmission of viral genomes to daughter cells, while also contributing to the establishment of multiple cancer types. Conversely, during viral lytic replication, KSHV extends the resting phase of the cell cycle to prevent cellular DNA synthesis that would otherwise compete for essential replication precursors. This review will examine the mechanisms KSHV has evolved to control the kinase activity regulating host cell cycle progression.
Insights
Kaposi
Area of Science:
- Virology and molecular biology, focusing on viral manipulation of host cellular processes.
Background:
- Cell cycle regulation by kinase activity is crucial for preventing division of damaged cells.
- Kaposi's sarcoma-associated herpesvirus (KSHV) encodes proteins that interact with host cell cycle machinery.
Purpose of the Study:
- To review the mechanisms KSHV employs to control host cell cycle kinase activity.
- To understand how KSHV manipulates the cell cycle for viral persistence and pathogenesis.
Main Methods:
- This is a review article, synthesizing existing research on KSHV and cell cycle control.
- Analysis of viral genes and their known interactions with host cell cycle regulators.
Main Results:
- KSHV advances the cell cycle for latent replication and transmission.
- KSHV extends the resting phase during lytic replication to inhibit host DNA synthesis.
- KSHV's manipulation of cell cycle kinases contributes to cancer development.
Conclusions:
- KSHV has evolved sophisticated strategies to hijack host cell cycle kinases.
- These viral strategies are essential for KSHV replication, persistence, and oncogenesis.
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