EBV and Apoptosis: The Viral Master Regulator of Cell Fate?

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EBV and Apoptosis: The Viral Master Regulator of Cell Fate? / Fitzsimmons, Leah; Kelly, Gemma L.

In: Viruses, Vol. 9, No. 11, 13.11.2017.

Research output: Contribution to journalReview articlepeer-review

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@article{2c1c0b8b1ba44a3988b58b9ccc036d29,
title = "EBV and Apoptosis:: The Viral Master Regulator of Cell Fate?",
abstract = "Epstein-Barr virus (EBV) was first discovered in cells from a patient with Burkitt lymphoma (BL), and is now known to be a contributory factor in 1-2% of all cancers, for which there are as yet, no EBV-targeted therapies available. Like other herpesviruses, EBV adopts a persistent latent infection in vivo and only rarely reactivates into replicative lytic cycle. Although latency is associated with restricted patterns of gene expression, genes are never expressed in isolation; always in groups. Here, we discuss (1) the ways in which the latent genes of EBV are known to modulate cell death, (2) how these mechanisms relate to growth transformation and lymphomagenesis, and (3) how EBV genes cooperate to coordinately regulate key cell death pathways in BL and lymphoblastoid cell lines (LCLs). Since manipulation of the cell death machinery is critical in EBV pathogenesis, understanding the mechanisms that underpin EBV regulation of apoptosis therefore provides opportunities for novel therapeutic interventions.",
keywords = "Journal Article, Review, EBV , apoptosis , genetic cooperation , latency , virus cancers , p53 , BCL-2 family , growth transformation",
author = "Leah Fitzsimmons and Kelly, {Gemma L.}",
year = "2017",
month = nov,
day = "13",
doi = "10.3390/v9110339",
language = "English",
volume = "9",
journal = "Viruses",
issn = "1999-4915",
publisher = "MDPI",
number = "11",

}

RIS

TY - JOUR

T1 - EBV and Apoptosis:

T2 - The Viral Master Regulator of Cell Fate?

AU - Fitzsimmons, Leah

AU - Kelly, Gemma L.

PY - 2017/11/13

Y1 - 2017/11/13

N2 - Epstein-Barr virus (EBV) was first discovered in cells from a patient with Burkitt lymphoma (BL), and is now known to be a contributory factor in 1-2% of all cancers, for which there are as yet, no EBV-targeted therapies available. Like other herpesviruses, EBV adopts a persistent latent infection in vivo and only rarely reactivates into replicative lytic cycle. Although latency is associated with restricted patterns of gene expression, genes are never expressed in isolation; always in groups. Here, we discuss (1) the ways in which the latent genes of EBV are known to modulate cell death, (2) how these mechanisms relate to growth transformation and lymphomagenesis, and (3) how EBV genes cooperate to coordinately regulate key cell death pathways in BL and lymphoblastoid cell lines (LCLs). Since manipulation of the cell death machinery is critical in EBV pathogenesis, understanding the mechanisms that underpin EBV regulation of apoptosis therefore provides opportunities for novel therapeutic interventions.

AB - Epstein-Barr virus (EBV) was first discovered in cells from a patient with Burkitt lymphoma (BL), and is now known to be a contributory factor in 1-2% of all cancers, for which there are as yet, no EBV-targeted therapies available. Like other herpesviruses, EBV adopts a persistent latent infection in vivo and only rarely reactivates into replicative lytic cycle. Although latency is associated with restricted patterns of gene expression, genes are never expressed in isolation; always in groups. Here, we discuss (1) the ways in which the latent genes of EBV are known to modulate cell death, (2) how these mechanisms relate to growth transformation and lymphomagenesis, and (3) how EBV genes cooperate to coordinately regulate key cell death pathways in BL and lymphoblastoid cell lines (LCLs). Since manipulation of the cell death machinery is critical in EBV pathogenesis, understanding the mechanisms that underpin EBV regulation of apoptosis therefore provides opportunities for novel therapeutic interventions.

KW - Journal Article

KW - Review

KW - EBV

KW - apoptosis

KW - genetic cooperation

KW - latency

KW - virus cancers

KW - p53

KW - BCL-2 family

KW - growth transformation

U2 - 10.3390/v9110339

DO - 10.3390/v9110339

M3 - Review article

C2 - 29137176

VL - 9

JO - Viruses

JF - Viruses

SN - 1999-4915

IS - 11

ER -