Understanding the Role of EBV Infection in Lymphomagenesis

Hiroshi Kimura; Takayuki Murata

doi:10.1002/9781119824572.ch16

Understanding the Role of EBV Infection in Lymphomagenesis

Hiroshi Kimura
, Takayuki Murata

Research output: Chapter in Book/Report/Conference proceeding › Chapter

Abstract

Epstein-Barr virus (EBV) is associated with several lymphomas including Burkitt lymphoma; EBV-positive diffuse large B cell lymphoma, not otherwise specified; post-transplant lymphoproliferative disorders; extranodal NK/T cell lymphoma, nasal type; and chronic active EBV disease. EBV encodes several oncoproteins important in terms of B-cell immortalization; it also encodes proteins that potentiate lymphomagenesis. Host gene mutation/modification followed by EBV infection triggers lymphomas, though the host driver genes differ among lymphomas. Both congenital and acquired immunodeficiency greatly compromise cellular immunity and increase the rates of EBV-associated lymphoma. PD-1/PD-L1 pathway blockade is effective in treating EBV-associated lymphomas, as PDL-1 is overexpressed in these diseases, and is attributable to structural abnormalities in the 3' untranslated region and/or upregulation by viral genes.

Original language	English
Title of host publication	Precision Cancer Therapies
Subtitle of host publication	Volume 2: Immunologic Approaches for the Treatment of Lymphoid Malignancies: From Concept to Practice
Publisher	wiley
Pages	235-245
Number of pages	11
ISBN (Electronic)	9781119824572
ISBN (Print)	9781119824541
DOIs	https://doi.org/10.1002/9781119824572.ch16
Publication status	Published - 01-01-2024
Externally published	Yes

All Science Journal Classification (ASJC) codes

General Medicine

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10.1002/9781119824572.ch16

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title = "Understanding the Role of EBV Infection in Lymphomagenesis",

abstract = "Epstein-Barr virus (EBV) is associated with several lymphomas including Burkitt lymphoma; EBV-positive diffuse large B cell lymphoma, not otherwise specified; post-transplant lymphoproliferative disorders; extranodal NK/T cell lymphoma, nasal type; and chronic active EBV disease. EBV encodes several oncoproteins important in terms of B-cell immortalization; it also encodes proteins that potentiate lymphomagenesis. Host gene mutation/modification followed by EBV infection triggers lymphomas, though the host driver genes differ among lymphomas. Both congenital and acquired immunodeficiency greatly compromise cellular immunity and increase the rates of EBV-associated lymphoma. PD-1/PD-L1 pathway blockade is effective in treating EBV-associated lymphomas, as PDL-1 is overexpressed in these diseases, and is attributable to structural abnormalities in the 3' untranslated region and/or upregulation by viral genes.",

keywords = "EVB infection, epigenetic modification, host genes, lymphoid malignancies, lymphomagenesis, viral expression profile",

author = "Hiroshi Kimura and Takayuki Murata",

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AU - Kimura, Hiroshi

AU - Murata, Takayuki

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N2 - Epstein-Barr virus (EBV) is associated with several lymphomas including Burkitt lymphoma; EBV-positive diffuse large B cell lymphoma, not otherwise specified; post-transplant lymphoproliferative disorders; extranodal NK/T cell lymphoma, nasal type; and chronic active EBV disease. EBV encodes several oncoproteins important in terms of B-cell immortalization; it also encodes proteins that potentiate lymphomagenesis. Host gene mutation/modification followed by EBV infection triggers lymphomas, though the host driver genes differ among lymphomas. Both congenital and acquired immunodeficiency greatly compromise cellular immunity and increase the rates of EBV-associated lymphoma. PD-1/PD-L1 pathway blockade is effective in treating EBV-associated lymphomas, as PDL-1 is overexpressed in these diseases, and is attributable to structural abnormalities in the 3' untranslated region and/or upregulation by viral genes.

AB - Epstein-Barr virus (EBV) is associated with several lymphomas including Burkitt lymphoma; EBV-positive diffuse large B cell lymphoma, not otherwise specified; post-transplant lymphoproliferative disorders; extranodal NK/T cell lymphoma, nasal type; and chronic active EBV disease. EBV encodes several oncoproteins important in terms of B-cell immortalization; it also encodes proteins that potentiate lymphomagenesis. Host gene mutation/modification followed by EBV infection triggers lymphomas, though the host driver genes differ among lymphomas. Both congenital and acquired immunodeficiency greatly compromise cellular immunity and increase the rates of EBV-associated lymphoma. PD-1/PD-L1 pathway blockade is effective in treating EBV-associated lymphomas, as PDL-1 is overexpressed in these diseases, and is attributable to structural abnormalities in the 3' untranslated region and/or upregulation by viral genes.

KW - EVB infection

KW - epigenetic modification

KW - host genes

KW - lymphoid malignancies

KW - lymphomagenesis

KW - viral expression profile

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U2 - 10.1002/9781119824572.ch16

DO - 10.1002/9781119824572.ch16

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BT - Precision Cancer Therapies

PB - wiley

ER -

Understanding the Role of EBV Infection in Lymphomagenesis

Abstract

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