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The role of Epstein-Barr virus in mo...

Snow, Andrew Linnell.

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The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas.

Record Type:	Electronic resources : Monograph/item
Title/Author:	The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas./
Author:	Snow, Andrew Linnell.
Description:	105 p.
Notes:	Source: Dissertation Abstracts International, Volume: 66-04, Section: B, page: 1971.
Contained By:	Dissertation Abstracts International66-04B.
Subject:	Health Sciences, Immunology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3171722
ISBN:	0542084759

The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas.
Snow, Andrew Linnell.

The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas. - 105 p.

Source: Dissertation Abstracts International, Volume: 66-04, Section: B, page: 1971.

Thesis (Ph.D.)--Stanford University, 2005.

Epstein-Barr virus (EBV) is an oncogenic herpesvirus associated with several B cell malignancies. Previous studies suggest that latent EBV infection contributes to lymphomagenesis by protecting B cell hosts from apoptosis. However, the relationship between EBV infection and sensitivity to death receptor (DR)-induced apoptosis is poorly understood. In this study, we provide the first evidence demonstrating EBV can protect a latently infected B cell lymphoma from apoptosis triggered through DRs. We showed that unlike uninfected control cells, BJAB lymphoma cells latently infected with the B95.8 strain of EBV (BJAB_B95) are completely resistant to apoptosis triggered through Fas or the TRAIL receptors DR4 and DR5. Caspase 8 activation was impaired and cFLIP recruitment was enriched in death inducing signaling complexes (DISCS) formed in EBV-infected BJAB cells relative to parent BJAB cells. Furthermore, the expression of the EBV latent membrane protein 1 (LMP1) alone could reduce caspase activation and confer partial resistance to death receptor apoptosis in BJAB cells. This protective effect was dependent on LMP1-induced NF-kappaB activation, which in turn upregulated cFLIP expression in LMP1+ BJAB cells. Finally, we showed that inhibition of NF-kappaB blocked cFLIP upregulation, reversed LMP1-mediated protection from DR apoptosis and sensitized BJAB_B95 cells to DR apoptosis as well. Thus, latent EBV can block DR apoptosis in host B cells, in part through the anti-apoptosic function of LMP1. Understanding the mechanisms by which latent EBV infection contributes to apoptosis resistance will hopefully improve our understanding and treatment of various EBV-associated neoplasms.

ISBN: 0542084759Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas.
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520 $a Epstein-Barr virus (EBV) is an oncogenic herpesvirus associated with several B cell malignancies. Previous studies suggest that latent EBV infection contributes to lymphomagenesis by protecting B cell hosts from apoptosis. However, the relationship between EBV infection and sensitivity to death receptor (DR)-induced apoptosis is poorly understood. In this study, we provide the first evidence demonstrating EBV can protect a latently infected B cell lymphoma from apoptosis triggered through DRs. We showed that unlike uninfected control cells, BJAB lymphoma cells latently infected with the B95.8 strain of EBV (BJAB_B95) are completely resistant to apoptosis triggered through Fas or the TRAIL receptors DR4 and DR5. Caspase 8 activation was impaired and cFLIP recruitment was enriched in death inducing signaling complexes (DISCS) formed in EBV-infected BJAB cells relative to parent BJAB cells. Furthermore, the expression of the EBV latent membrane protein 1 (LMP1) alone could reduce caspase activation and confer partial resistance to death receptor apoptosis in BJAB cells. This protective effect was dependent on LMP1-induced NF-kappaB activation, which in turn upregulated cFLIP expression in LMP1+ BJAB cells. Finally, we showed that inhibition of NF-kappaB blocked cFLIP upregulation, reversed LMP1-mediated protection from DR apoptosis and sensitized BJAB_B95 cells to DR apoptosis as well. Thus, latent EBV can block DR apoptosis in host B cells, in part through the anti-apoptosic function of LMP1. Understanding the mechanisms by which latent EBV infection contributes to apoptosis resistance will hopefully improve our understanding and treatment of various EBV-associated neoplasms.
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