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Article: Epstein-Barr virus protein EBNA-LP engages YY1 through leucine-rich motifs to promote naïve B cell transformation.

Cable, Jana M / Reinoso-Vizcaino, Nicolás M / White, Robert E / Luftig, Micah A

bioRxiv : the preprint server for biology

2024

Abstract: Epstein-Barr Virus (EBV) is associated with numerous cancers including B cell lymphomas. ...

Abstract	Epstein-Barr Virus (EBV) is associated with numerous cancers including B cell lymphomas.
Language	English
Publishing date	2024-01-08
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.07.574580
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Article ; Online: The Role of EBV-Induced Hypermethylation in Gastric Cancer Tumorigenesis.

Stanland, Lyla J / Luftig, Micah A

Viruses

2020 Volume 12, Issue 11

Abstract: Epstein-Barr-virus-associated Gastric Cancer (EBVaGC) comprises approximately 10% of global gastric cancers and is known to be the most hypermethylated of all tumor types. EBV infection has been shown to directly induce the hypermethylation of both the ... ...

Abstract	Epstein-Barr-virus-associated Gastric Cancer (EBVaGC) comprises approximately 10% of global gastric cancers and is known to be the most hypermethylated of all tumor types. EBV infection has been shown to directly induce the hypermethylation of both the host and viral genome following initial infection of gastric epithelial cells. Many studies have been completed in an attempt to identify genes that frequently become hypermethylated and therefore significant pathways that become silenced to promote tumorigenesis. It is clear that EBV-induced hypermethylation silences key tumor suppressor genes, cell cycle genes and cellular differentiation factors to promote a highly proliferative and poorly differentiated cell population. EBV infection has been shown to induce methylation in additional malignancies including Nasopharyngeal Carcinoma and Burkitt's Lymphoma though not to the same level as in EBVaGC. Lastly, some genes silenced in EBVaGC are common to other heavily methylated tumors such as colorectal and breast tumors; however, some genes are unique to EBVaGC and can provide insights into the major pathways involved in tumorigenesis.
MeSH term(s)	Carcinogenesis/genetics ; CpG Islands ; DNA Methylation/genetics ; Epstein-Barr Virus Infections/complications ; Gene Expression Regulation, Neoplastic ; Genome ; Herpesvirus 4, Human/pathogenicity ; Humans ; Stomach Neoplasms/genetics ; Stomach Neoplasms/physiopathology ; Tumor Suppressor Proteins/genetics
Chemical Substances	Tumor Suppressor Proteins
Language	English
Publishing date	2020-10-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v12111222
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Article ; Online: Reprogramming of cellular metabolic pathways by human oncogenic viruses.

Purdy, John G / Luftig, Micah A

Current opinion in virology

2019 Volume 39, Page(s) 60–69

Abstract: Oncogenic viruses, like all viruses, relies on host metabolism to provide the metabolites and energy needed for virus replication. Many DNA tumor viruses and retroviruses will reprogram metabolism during infection. Additionally, some viral oncogenes may ... ...

Abstract	Oncogenic viruses, like all viruses, relies on host metabolism to provide the metabolites and energy needed for virus replication. Many DNA tumor viruses and retroviruses will reprogram metabolism during infection. Additionally, some viral oncogenes may alter metabolism independent of virus replication. Virus infection and cancer development share many similarities regarding metabolic reprogramming as both processes demand increased metabolic activity to produce biomass: cell proliferation in the case of cancer and virion production in the case of infection. This review discusses the parallels in metabolic reprogramming between human oncogenic viruses and oncogenesis.
MeSH term(s)	Biomass ; Carcinogenesis ; Cell Proliferation ; Cellular Reprogramming ; Hepacivirus/physiology ; Hepatitis B virus/physiology ; Herpesviridae/physiology ; Humans ; Merkel cell polyomavirus/physiology ; Metabolic Networks and Pathways ; Neoplasms/metabolism ; Oncogenic Viruses/physiology ; Papillomaviridae/physiology ; Retroviridae ; Virion/metabolism ; Virus Replication
Language	English
Publishing date	2019-11-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2611378-8
ISSN	1879-6265 ; 1879-6257
ISSN (online)	1879-6265
ISSN	1879-6257
DOI	10.1016/j.coviro.2019.11.002
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Article: Viruses and the DNA Damage Response: Activation and Antagonism.

Luftig, Micah A

Annual review of virology

2014 Volume 1, Issue 1, Page(s) 605–625

Abstract: Viruses must interact with their hosts in order to replicate; these interactions often provoke the evolutionarily conserved response to DNA damage, known as the DNA damage response (DDR). The DDR can be activated by incoming viral DNA, during the ... ...

Abstract	Viruses must interact with their hosts in order to replicate; these interactions often provoke the evolutionarily conserved response to DNA damage, known as the DNA damage response (DDR). The DDR can be activated by incoming viral DNA, during the integration of retroviruses, or in response to the aberrant DNA structures generated upon replication of DNA viruses. Furthermore, DNA and RNA viral proteins can induce the DDR by promoting inappropriate S phase entry, by modifying cellular DDR factors directly, or by unintentionally targeting host DNA. The DDR may be antiviral, although viruses often require proximal DDR activation of repair and recombination factors to facilitate replication as well as downstream DDR signaling suppression to ensure cell survival. An unintended consequence of DDR attenuation during infection is the long-term survival and proliferation of precancerous cells. Therefore, the molecular basis for DDR activation and attenuation by viruses remains an important area of study that will likely provide key insights into how viruses have evolved with their hosts.
Language	English
Publishing date	2014-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2764224-0
ISSN	2327-0578 ; 2327-056X
ISSN (online)	2327-0578
ISSN	2327-056X
DOI	10.1146/annurev-virology-031413-085548
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Article: Molecular features and translational outlook for Epstein-Barr virus-associated gastric cancer.

Stanland, Lyla J / Luftig, Micah A

Future virology

2018 Volume 13, Issue 11, Page(s) 803–818

Abstract: Epstein-Barr Virus (EBV) was the first discovered human tumor virus and is the etiological agent of B cell lymphomas and also epithelial cancers. Indeed, nearly 10% of gastric cancers worldwide are EBV-positive and display unique molecular, epigenetic, ... ...

Abstract	Epstein-Barr Virus (EBV) was the first discovered human tumor virus and is the etiological agent of B cell lymphomas and also epithelial cancers. Indeed, nearly 10% of gastric cancers worldwide are EBV-positive and display unique molecular, epigenetic, and clinicopathological features. EBV-positive gastric cancers display the highest rate of host genome methylation of all tumor types studied and harbor recurrent mutations activating PI3Kα, silencing ARID1A, and amplifying PD-L1. While EBV infection of B cells can be studied efficiently,
Language	English
Publishing date	2018-10-24
Publishing country	England
Document type	Journal Article
ZDB-ID	2254606-6
ISSN	1746-0808 ; 1746-0794
ISSN (online)	1746-0808
ISSN	1746-0794
DOI	10.2217/fvl-2018-0071
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Article ; Online: Intracellular BH3 Profiling Reveals Shifts in Antiapoptotic Dependency in Human B Cell Maturation and Mitogen-Stimulated Proliferation.

Dai, Joanne / Luftig, Micah A

Journal of immunology (Baltimore, Md. : 1950)

2018 Volume 200, Issue 5, Page(s) 1727–1736

Abstract: Apoptosis is critical to B cell maturation, but studies of apoptotic regulation in primary human B cells is lacking. In this study, we sought to better understand the mechanisms of apoptotic regulation in normal and activated B cells. Using intracellular ...

Abstract	Apoptosis is critical to B cell maturation, but studies of apoptotic regulation in primary human B cells is lacking. In this study, we sought to better understand the mechanisms of apoptotic regulation in normal and activated B cells. Using intracellular BH3 profiling, we defined the Bcl2 dependency of B cell subsets from human peripheral blood and tonsillar lymphoid tissue as well as mitogen-activated B cells. We found that naive and memory B cells were BCL-2-dependent, whereas germinal center B cells were MCL-1-dependent and plasma cells were BCL-X
MeSH term(s)	Apoptosis/drug effects ; Apoptosis/immunology ; Apoptosis Regulatory Proteins/metabolism ; B-Lymphocytes/drug effects ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Cell Line ; Cell Proliferation/drug effects ; Cell Proliferation/physiology ; Germinal Center/drug effects ; Germinal Center/immunology ; Germinal Center/metabolism ; Humans ; Immunologic Memory/drug effects ; Immunologic Memory/immunology ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/immunology ; Mitogens/pharmacology ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Plasma Cells/drug effects ; Plasma Cells/immunology ; Plasma Cells/metabolism ; bcl-X Protein/metabolism
Chemical Substances	Apoptosis Regulatory Proteins ; Mitogens ; Myeloid Cell Leukemia Sequence 1 Protein ; bcl-X Protein
Language	English
Publishing date	2018-01-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1701473
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Article: The Role of EBV-Induced Hypermethylation in Gastric Cancer Tumorigenesis

Stanland, Lyla J / Luftig, Micah A

Viruses. 2020 Oct. 28, v. 12, no. 11

2020

Abstract: Epstein–Barr-virus-associated Gastric Cancer (EBVaGC) comprises approximately 10% of global gastric cancers and is known to be the most hypermethylated of all tumor types. EBV infection has been shown to directly induce the hypermethylation of both the ... ...

Abstract	Epstein–Barr-virus-associated Gastric Cancer (EBVaGC) comprises approximately 10% of global gastric cancers and is known to be the most hypermethylated of all tumor types. EBV infection has been shown to directly induce the hypermethylation of both the host and viral genome following initial infection of gastric epithelial cells. Many studies have been completed in an attempt to identify genes that frequently become hypermethylated and therefore significant pathways that become silenced to promote tumorigenesis. It is clear that EBV-induced hypermethylation silences key tumor suppressor genes, cell cycle genes and cellular differentiation factors to promote a highly proliferative and poorly differentiated cell population. EBV infection has been shown to induce methylation in additional malignancies including Nasopharyngeal Carcinoma and Burkitt’s Lymphoma though not to the same level as in EBVaGC. Lastly, some genes silenced in EBVaGC are common to other heavily methylated tumors such as colorectal and breast tumors; however, some genes are unique to EBVaGC and can provide insights into the major pathways involved in tumorigenesis.
Keywords	breast neoplasms ; carcinogenesis ; carcinoma ; cell cycle ; cell differentiation ; epithelial cells ; gastric mucosa ; lymphoma ; methylation ; stomach neoplasms ; tumor suppressor genes
Language	English
Dates of publication	2020-1028
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v12111222
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Epstein-Barr virus perpetuates B cell germinal center dynamics and generation of autoimmune-associated phenotypes

SoRelle, Elliott D / Reinoso-Vizcaino, Nicolás M / Horn, Gillian Q / Luftig, Micah A

Frontiers in immunology

2022 Volume 13, Page(s) 1001145

Abstract: Human B cells encompass functionally diverse lineages and phenotypic states that contribute to protective as well as pathogenic responses. Epstein-Barr virus (EBV) provides a unique lens for studying heterogeneous B cell responses, given its adaptation ... ...

Abstract	Human B cells encompass functionally diverse lineages and phenotypic states that contribute to protective as well as pathogenic responses. Epstein-Barr virus (EBV) provides a unique lens for studying heterogeneous B cell responses, given its adaptation to manipulate intrinsic cell programming. EBV promotes the activation, proliferation, and eventual outgrowth of host B cells as immortalized lymphoblastoid cell lines (LCLs)
MeSH term(s)	Autoimmunity ; B-Lymphocytes ; Epstein-Barr Virus Infections ; Germinal Center ; Herpesvirus 4, Human ; Humans ; Immunoglobulin D/genetics ; Phenotype ; Toll-Like Receptor 7/genetics
Chemical Substances	Immunoglobulin D ; Toll-Like Receptor 7
Language	English
Publishing date	2022-09-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1001145
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Article ; Online: Epstein-Barr virus induces germinal center light zone chromatin architecture and promotes survival through enhancer looping at the

Dai, Joanne / SoRelle, Elliott D / Heckenberg, Emma / Song, Lingyun / Cable, Jana M / Crawford, Gregory E / Luftig, Micah A

mBio

2023 Volume 15, Issue 1, Page(s) e0244423

Abstract: Importance: Epstein-Barr virus has evolved with its human host leading to an intimate relationship where infection of antibody-producing B cells mimics the process by which these cells normally recognize foreign antigens and become activated. Virtually ... ...

Abstract	Importance: Epstein-Barr virus has evolved with its human host leading to an intimate relationship where infection of antibody-producing B cells mimics the process by which these cells normally recognize foreign antigens and become activated. Virtually everyone in the world is infected by adulthood and controls this virus pushing it into life-long latency. However, immune-suppressed individuals are at high risk for EBV+ cancers. Here, we isolated B cells from tonsils and compare the underlying molecular genetic differences between these cells and those infected with EBV. We find similar regulatory mechanism for expression of an important cellular protein that enables B cells to survive in lymphoid tissue. These findings link an underlying relationship at the molecular level between EBV-infected B cells in vitro with normally activated B cells
MeSH term(s)	Adult ; Humans ; Chromatin ; Epstein-Barr Virus Infections ; Epstein-Barr Virus Nuclear Antigens ; Germinal Center ; Herpesvirus 4, Human/genetics ; Herpesvirus 4, Human/metabolism ; Virus Latency ; Proto-Oncogene Proteins c-bcl-2/genetics
Chemical Substances	Chromatin ; Epstein-Barr Virus Nuclear Antigens ; BCL2-related protein A1 ; Proto-Oncogene Proteins c-bcl-2
Language	English
Publishing date	2023-12-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.02444-23
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Article: Recent advances in understanding Epstein-Barr virus.

Stanfield, Brent A / Luftig, Micah A

F1000Research

2017 Volume 6, Page(s) 386

Abstract: Epstein-Barr virus (EBV) is a common human herpes virus known to infect the majority of the world population. Infection with EBV is often asymptomatic but can manifest in a range of pathologies from infectious mononucleosis to severe cancers of ... ...

Abstract	Epstein-Barr virus (EBV) is a common human herpes virus known to infect the majority of the world population. Infection with EBV is often asymptomatic but can manifest in a range of pathologies from infectious mononucleosis to severe cancers of epithelial and lymphocytic origin. Indeed, in the past decade, EBV has been linked to nearly 10% of all gastric cancers. Furthermore, recent advances in high-throughput next-generation sequencing and the development of humanized mice, which effectively model EBV pathogenesis, have led to a wealth of knowledge pertaining to strain variation and host-pathogen interaction. This review highlights some recent advances in our understanding of EBV biology, focusing on new findings on the early events of infection, the role EBV plays in gastric cancer, new strain variation, and humanized mouse models of EBV infection.
Language	English
Publishing date	2017
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2699932-8
ISSN	2046-1402
ISSN	2046-1402
DOI	10.12688/f1000research.10591.1
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