Manganus
Senior Member
- Messages
- 166
- Location
- Canary islands
Haven't seen this referred to.
http://www.sciencedirect.com/science/article/pii/S1879625717300275
Abstract
Like all herpesviruses, the ability of Epstein-Barr virus (EBV) to establish life-long persistent infections is related to a biphasic viral lifecycle that involves latency and reactivation/lytic replication. Memory B cells serve as the EBV latency compartment where silencing of viral gene expression allows maintenance of the viral genome, avoidance of immune surveillance, and life-long carriage. Upon viral reactivation, viral gene expression is induced for replication, progeny virion production, and viral spread. EBV uses the host epigenetic machinery to regulate its distinct viral gene expression states. However, epigenetic manipulation by EBV affects the host epigenome by reprogramming cells in ways that leave long-lasting, oncogenic phenotypes. Such virally-induced epigenetic alterations are evident in EBV-associated cancers.
Consequences of EBV-induced epigenetic reprogramming. EBV infection of B cells and epithelial cells leads to cellular epigenetic changes that involve DNA methylation and histone modifications. Such epigenetic changes also affect the host epigenome altering cellular gene expression to states that are conducive for viral latency and replication, having effects on cell growth and differentiation. However, epigenetic changes to the host persist from one generation to the next, increasing the cellular heterogeneity of the population. In the context of cancer, virally-induced epigenetic changes may act as preneoplastic lesions that are retained in virally silent states or after loss of the viral genome as a mechanism for ‘hit-and-run’ oncogenesis.
http://www.sciencedirect.com/science/article/pii/S1879625717300275
Abstract
Like all herpesviruses, the ability of Epstein-Barr virus (EBV) to establish life-long persistent infections is related to a biphasic viral lifecycle that involves latency and reactivation/lytic replication. Memory B cells serve as the EBV latency compartment where silencing of viral gene expression allows maintenance of the viral genome, avoidance of immune surveillance, and life-long carriage. Upon viral reactivation, viral gene expression is induced for replication, progeny virion production, and viral spread. EBV uses the host epigenetic machinery to regulate its distinct viral gene expression states. However, epigenetic manipulation by EBV affects the host epigenome by reprogramming cells in ways that leave long-lasting, oncogenic phenotypes. Such virally-induced epigenetic alterations are evident in EBV-associated cancers.
Consequences of EBV-induced epigenetic reprogramming. EBV infection of B cells and epithelial cells leads to cellular epigenetic changes that involve DNA methylation and histone modifications. Such epigenetic changes also affect the host epigenome altering cellular gene expression to states that are conducive for viral latency and replication, having effects on cell growth and differentiation. However, epigenetic changes to the host persist from one generation to the next, increasing the cellular heterogeneity of the population. In the context of cancer, virally-induced epigenetic changes may act as preneoplastic lesions that are retained in virally silent states or after loss of the viral genome as a mechanism for ‘hit-and-run’ oncogenesis.
