Epigenetic control in Kaposi sarcoma-associated herpesvirus infection and associated disease
Open Access
- 26 March 2020
- journal article
- review article
- Published by Springer Science and Business Media LLC in Seminars in Immunopathology
- Vol. 42 (2), 143-157
- https://doi.org/10.1007/s00281-020-00787-z
Abstract
Kaposi sarcoma-associated herpesvirus (KSHV) is the etiologic agent of several malignancies of endothelial and B-cell origin. The fact that latently infected tumor cells in these malignancies do not express classical viral oncogenes suggests that pathogenesis of KSHV-associated disease results from multistep processes that, in addition to constitutive viral gene expression, may require accumulation of cellular alterations. Heritable changes of the epigenome have emerged as an important co-factor that contributes to the pathogenesis of many non-viral cancers. Since KSHV encodes a number of factors that directly or indirectly manipulate host cell chromatin, it is an intriguing possibility that epigenetic reprogramming also contributes to the pathogenesis of KSHV-associated tumors. The fact that heritable histone modifications have also been shown to regulate viral gene expression programs in KSHV-infected tumor cells underlines the importance of epigenetic control during latency and tumorigenesis. We here review what is presently known about the role of epigenetic regulation of viral and host chromatin in KSHV infection and discuss how viral manipulation of these processes may contribute to the development of KSHV-associated disease.Keywords
Funding Information
- Freie und Hansestadt Hamburg (LFF-FV44 Epilog)
This publication has 150 references indexed in Scilit:
- TrxG and PcG Proteins but Not Methylated Histones Remain Associated with DNA through ReplicationCell, 2012
- Virus-encoded microRNAsVirology, 2011
- Bub1 and CENP-F Can Contribute to Kaposi's Sarcoma-Associated Herpesvirus Genome Persistence by Targeting LANA to KinetochoresJournal of Virology, 2010
- An Interleukin‐6–Related Systemic Inflammatory Syndrome in Patients Co‐Infected with Kaposi Sarcoma–Associated Herpesvirus and HIV but without Multicentric Castleman DiseaseClinical Infectious Diseases, 2010
- A viral microRNA functions as an orthologue of cellular miR-155Nature, 2007
- Kaposi's Sarcoma-Associated Herpesvirus LANA-1 Interacts with the Short Variant of BRD4 and Releases Cells from a BRD4- and BRD2/RING3-Induced G 1 Cell CycleArrestJournal of Virology, 2006
- Recruitment of the de novo DNA methyltransferase Dnmt3a by Kaposi's sarcoma-associated herpesvirus LANAProceedings of the National Academy of Sciences of the United States of America, 2006
- Kaposi's Sarcoma-Associated Herpesvirus Latency-Associated Nuclear Antigen Interacts with Bromodomain Protein Brd4 on Host Mitotic ChromosomesJournal of Virology, 2006
- Identification of microRNAs of the herpesvirus familyNature Methods, 2005
- Identification of Herpesvirus-Like DNA Sequences in AIDS-Sssociated Kaposi's SarcomaScience, 1994