Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas

ABSTRACT Avian leukosis virus (ALV) induces B-cell lymphoma and other neoplasms in chickens by integrating within or near cancer genes and perturbing their expression. Four genes—MYC, MYB, Mir-155, and TERT—have previously been identified as common integration sites in these virus-induced lymphomas...

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Autores principales:	James F. Justice, Robin W. Morgan, Karen L. Beemon
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2015
Materias:	Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/dcdad5b0aa2942b3b15d2d683935fb92
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spelling	oai:doaj.org-article:dcdad5b0aa2942b3b15d2d683935fb922021-11-15T15:41:24ZCommon Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas10.1128/mBio.01863-152150-7511https://doaj.org/article/dcdad5b0aa2942b3b15d2d683935fb922015-12-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.01863-15https://doaj.org/toc/2150-7511ABSTRACT Avian leukosis virus (ALV) induces B-cell lymphoma and other neoplasms in chickens by integrating within or near cancer genes and perturbing their expression. Four genes—MYC, MYB, Mir-155, and TERT—have previously been identified as common integration sites in these virus-induced lymphomas and are thought to play a causal role in tumorigenesis. In this study, we employ high-throughput sequencing to identify additional genes driving tumorigenesis in ALV-induced B-cell lymphomas. In addition to the four genes implicated previously, we identify other genes as common integration sites, including TNFRSF1A, MEF2C, CTDSPL, TAB2, RUNX1, MLL5, CXorf57, and BACH2. We also analyze the genome-wide ALV integration landscape in vivo and find increased frequency of ALV integration near transcriptional start sites and within transcripts. Previous work has shown ALV prefers a weak consensus sequence for integration in cultured human cells. We confirm this consensus sequence for ALV integration in vivo in the chicken genome. IMPORTANCE Avian leukosis virus induces B-cell lymphomas in chickens. Earlier studies showed that ALV can induce tumors through insertional mutagenesis, and several genes have been implicated in the development of these tumors. In this study, we use high-throughput sequencing to reveal the genome-wide ALV integration landscape in ALV-induced B-cell lymphomas. We find elevated levels of ALV integration near transcription start sites and use common integration site analysis to greatly expand the number of genes implicated in the development of these tumors. Interestingly, we identify several genes targeted by viral insertions that have not been previously shown to be involved in cancer.James F. JusticeRobin W. MorganKaren L. BeemonAmerican Society for MicrobiologyarticleMicrobiologyQR1-502ENmBio, Vol 6, Iss 6 (2015)
institution	DOAJ
collection	DOAJ
language	EN
topic	Microbiology QR1-502
spellingShingle	Microbiology QR1-502 James F. Justice Robin W. Morgan Karen L. Beemon Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas
description	ABSTRACT Avian leukosis virus (ALV) induces B-cell lymphoma and other neoplasms in chickens by integrating within or near cancer genes and perturbing their expression. Four genes—MYC, MYB, Mir-155, and TERT—have previously been identified as common integration sites in these virus-induced lymphomas and are thought to play a causal role in tumorigenesis. In this study, we employ high-throughput sequencing to identify additional genes driving tumorigenesis in ALV-induced B-cell lymphomas. In addition to the four genes implicated previously, we identify other genes as common integration sites, including TNFRSF1A, MEF2C, CTDSPL, TAB2, RUNX1, MLL5, CXorf57, and BACH2. We also analyze the genome-wide ALV integration landscape in vivo and find increased frequency of ALV integration near transcriptional start sites and within transcripts. Previous work has shown ALV prefers a weak consensus sequence for integration in cultured human cells. We confirm this consensus sequence for ALV integration in vivo in the chicken genome. IMPORTANCE Avian leukosis virus induces B-cell lymphomas in chickens. Earlier studies showed that ALV can induce tumors through insertional mutagenesis, and several genes have been implicated in the development of these tumors. In this study, we use high-throughput sequencing to reveal the genome-wide ALV integration landscape in ALV-induced B-cell lymphomas. We find elevated levels of ALV integration near transcription start sites and use common integration site analysis to greatly expand the number of genes implicated in the development of these tumors. Interestingly, we identify several genes targeted by viral insertions that have not been previously shown to be involved in cancer.
format	article
author	James F. Justice Robin W. Morgan Karen L. Beemon
author_facet	James F. Justice Robin W. Morgan Karen L. Beemon
author_sort	James F. Justice
title	Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas
title_short	Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas
title_full	Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas
title_fullStr	Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas
title_full_unstemmed	Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas
title_sort	common viral integration sites identified in avian leukosis virus-induced b-cell lymphomas
publisher	American Society for Microbiology
publishDate	2015
url	https://doaj.org/article/dcdad5b0aa2942b3b15d2d683935fb92
work_keys_str_mv	AT jamesfjustice commonviralintegrationsitesidentifiedinavianleukosisvirusinducedbcelllymphomas AT robinwmorgan commonviralintegrationsitesidentifiedinavianleukosisvirusinducedbcelllymphomas AT karenlbeemon commonviralintegrationsitesidentifiedinavianleukosisvirusinducedbcelllymphomas
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Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas

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