Preferential Selection of Human T-Cell Leukemia Virus Type 1 Provirus Lacking the 5′ Long Terminal Repeat during Oncogenesis

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Published in:	Journal of Virology Vol. 81; no. 11; pp. 5714 - 5723
Main Authors:	MIYAZAKI, Maki, YASUNAGA, Jun-Ichirou, TANIGUCHI, Yuko, TAMIYA, Sadahiro, NAKAHATA, Tatsutoshi, MATSUOKA, Masao
Format:	Journal Article
Language:	English
Published:	Washington, DC American Society for Microbiology 01-06-2007
Subjects:	Amino Acid Sequence Base Sequence Basic-Leucine Zipper Transcription Factors - chemistry Basic-Leucine Zipper Transcription Factors - genetics Basic-Leucine Zipper Transcription Factors - metabolism Biological and medical sciences Cell Line, Tumor Fundamental and applied biological sciences. Psychology Human T-lymphotropic virus 1 Human T-lymphotropic virus 1 - genetics Humans Leukemia-Lymphoma, Adult T-Cell - virology Medical sciences Microbiology Miscellaneous Molecular Sequence Data Pathogenesis and Immunity Proviruses - genetics Retroviridae Proteins Terminal Repeat Sequences Tumors Viral Proteins - chemistry Viral Proteins - genetics Viral Proteins - metabolism Virology Virus Integration - genetics Human Virus T-Lymphocyte LTR sequence Tumor cell Provirus Virology
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Abstract	Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology. For an alternate route to JVI .asm.org, visit: JVI
AbstractList	In adult T-cell leukemia (ATL) cells, a defective human T-cell leukemia virus type 1 (HTLV-1) provirus lacking the 5′ long terminal repeat (LTR), designated type 2 defective provirus, is frequently observed. To investigate the mechanism underlying the generation of the defective provirus, we sequenced HTLV-1 provirus integration sites from cases of ATL. In HTLV-1 proviruses retaining both LTRs, 6-bp repeat sequences were adjacent to the 5′ and 3′ LTRs. In 8 of 12 cases with type 2 defective provirus, 6-bp repeats were identified at both ends. In five of these cases, a short repeat was bound to CA dinucleotides of the pol and env genes at the 5′ end, suggesting that these type 2 defective proviruses were formed before integration. In four cases lacking the 6-bp repeat, short (6- to 26-bp) deletions in the host genome were identified, indicating that these defective proviruses were generated after integration. Quantification indicated frequencies of type 2 defective provirus of less than 3.9% for two carriers, which are much lower than those seen for ATL cases (27.8%). In type 2 defective proviruses, the second exons of the tax , rex , and p30 genes were frequently deleted, leaving Tax unable to activate NF-κB and CREB pathways. The HTLV-1 bZIP factor gene, located on the minus strand, is expressed in ATL cells with this defective provirus, and its coding sequences are intact, suggesting its significance in oncogenesis. In adult T-cell leukemia (ATL) cells, a defective human T-cell leukemia virus type 1 (HTLV-1) provirus lacking the 5' long terminal repeat (LTR), designated type 2 defective provirus, is frequently observed. To investigate the mechanism underlying the generation of the defective provirus, we sequenced HTLV-1 provirus integration sites from cases of ATL. In HTLV-1 proviruses retaining both LTRs, 6-bp repeat sequences were adjacent to the 5' and 3' LTRs. In 8 of 12 cases with type 2 defective provirus, 6-bp repeats were identified at both ends. In five of these cases, a short repeat was bound to CA dinucleotides of the pol and env genes at the 5' end, suggesting that these type 2 defective proviruses were formed before integration. In four cases lacking the 6-bp repeat, short (6- to 26-bp) deletions in the host genome were identified, indicating that these defective proviruses were generated after integration. Quantification indicated frequencies of type 2 defective provirus of less than 3.9% for two carriers, which are much lower than those seen for ATL cases (27.8%). In type 2 defective proviruses, the second exons of the tax, rex, and p30 genes were frequently deleted, leaving Tax unable to activate NF- Kappa B and CREB pathways. The HTLV-1 bZIP factor gene, located on the minus strand, is expressed in ATL cells with this defective provirus, and its coding sequences are intact, suggesting its significance in oncogenesis. In adult T-cell leukemia (ATL) cells, a defective human T-cell leukemia virus type 1 (HTLV-1) provirus lacking the 5' long terminal repeat (LTR), designated type 2 defective provirus, is frequently observed. To investigate the mechanism underlying the generation of the defective provirus, we sequenced HTLV-1 provirus integration sites from cases of ATL. In HTLV-1 proviruses retaining both LTRs, 6-bp repeat sequences were adjacent to the 5' and 3' LTRs. In 8 of 12 cases with type 2 defective provirus, 6-bp repeats were identified at both ends. In five of these cases, a short repeat was bound to CA dinucleotides of the pol and env genes at the 5' end, suggesting that these type 2 defective proviruses were formed before integration. In four cases lacking the 6-bp repeat, short (6- to 26-bp) deletions in the host genome were identified, indicating that these defective proviruses were generated after integration. Quantification indicated frequencies of type 2 defective provirus of less than 3.9% for two carriers, which are much lower than those seen for ATL cases (27.8%). In type 2 defective proviruses, the second exons of the tax, rex, and p30 genes were frequently deleted, leaving Tax unable to activate NF-kappaB and CREB pathways. The HTLV-1 bZIP factor gene, located on the minus strand, is expressed in ATL cells with this defective provirus, and its coding sequences are intact, suggesting its significance in oncogenesis. Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology. For an alternate route to JVI .asm.org, visit: JVI
Author	Maki Miyazaki Yuko Taniguchi Tatsutoshi Nakahata Jun-Ichirou Yasunaga Masao Matsuoka Sadahiro Tamiya
AuthorAffiliation	Laboratory of Virus Immunology, Institute for Virus Research, 1 Department of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, 3 Department of Hematology and Department of Infectious Diseases, Graduate School of Medicine, Kumamoto University, Kumamoto 860-8556, Japan 2
AuthorAffiliation_xml	– name: Laboratory of Virus Immunology, Institute for Virus Research, 1 Department of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, 3 Department of Hematology and Department of Infectious Diseases, Graduate School of Medicine, Kumamoto University, Kumamoto 860-8556, Japan 2
Author_xml	– sequence: 1 givenname: Maki surname: MIYAZAKI fullname: MIYAZAKI, Maki organization: Laboratory of Virus Immunology, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan – sequence: 2 givenname: Jun-Ichirou surname: YASUNAGA fullname: YASUNAGA, Jun-Ichirou organization: Laboratory of Virus Immunology, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan – sequence: 3 givenname: Yuko surname: TANIGUCHI fullname: TANIGUCHI, Yuko organization: Laboratory of Virus Immunology, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan – sequence: 4 givenname: Sadahiro surname: TAMIYA fullname: TAMIYA, Sadahiro organization: Department of Hematology and Department of Infectious Diseases, Graduate School of Medicine, Kumamoto University, Kumamoto 860-8556, Japan – sequence: 5 givenname: Tatsutoshi surname: NAKAHATA fullname: NAKAHATA, Tatsutoshi organization: Department of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan – sequence: 6 givenname: Masao surname: MATSUOKA fullname: MATSUOKA, Masao organization: Laboratory of Virus Immunology, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Corresponding author. Mailing address: Laboratory of Virus Immunology, Institute for Virus Research, Kyoto University, Shogoin Kawara-cho 53, Sakyo-ku, Kyoto 606-8507, Japan. Phone: 81-75-751-4048. Fax: 81-75-751-4049. E-mail: mmatsuok@virus.kyoto-u.ac.jp
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Snippet	Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... In adult T-cell leukemia (ATL) cells, a defective human T-cell leukemia virus type 1 (HTLV-1) provirus lacking the 5' long terminal repeat (LTR), designated... In adult T-cell leukemia (ATL) cells, a defective human T-cell leukemia virus type 1 (HTLV-1) provirus lacking the 5′ long terminal repeat (LTR), designated...
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SubjectTerms	Amino Acid Sequence Base Sequence Basic-Leucine Zipper Transcription Factors - chemistry Basic-Leucine Zipper Transcription Factors - genetics Basic-Leucine Zipper Transcription Factors - metabolism Biological and medical sciences Cell Line, Tumor Fundamental and applied biological sciences. Psychology Human T-lymphotropic virus 1 Human T-lymphotropic virus 1 - genetics Humans Leukemia-Lymphoma, Adult T-Cell - virology Medical sciences Microbiology Miscellaneous Molecular Sequence Data Pathogenesis and Immunity Proviruses - genetics Retroviridae Proteins Terminal Repeat Sequences Tumors Viral Proteins - chemistry Viral Proteins - genetics Viral Proteins - metabolism Virology Virus Integration - genetics
Title	Preferential Selection of Human T-Cell Leukemia Virus Type 1 Provirus Lacking the 5′ Long Terminal Repeat during Oncogenesis
URI	http://jvi.asm.org/content/81/11/5714.abstract https://www.ncbi.nlm.nih.gov/pubmed/17344291 https://search.proquest.com/docview/20292045 https://search.proquest.com/docview/70513204 https://pubmed.ncbi.nlm.nih.gov/PMC1900290
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