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Epstein-Barr Virus Infection Precedes Clonal Expansion in Burkitt's and Acquired Immunodeficiency Syndrome-Associated Lymphoma
The Epstein-Barr virus (EBV) is associated with distinct forms of human lymphoid malignancies, including the endemic (eBL) and sporadic forms of Burkitt's lymphoma (sBL) and acquired immunodeficiency syndrome-associated non-Hodgkin lymphoma (AIDS-NHL). However, whether EBV has a pathogenetic ro...
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Published in: | Blood 1991-03, Vol.77 (5), p.1092-1095 |
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creator | Neri, Antonino Barriga, Francisco Inghirami, Giorgio Knowles, Daniel M. Neequaye, Janet Magrath, Ian T. Dalla-Favera, Riccardo |
description | The Epstein-Barr virus (EBV) is associated with distinct forms of human lymphoid malignancies, including the endemic (eBL) and sporadic forms of Burkitt's lymphoma (sBL) and acquired immunodeficiency syndrome-associated non-Hodgkin lymphoma (AIDS-NHL). However, whether EBV has a pathogenetic role in these tumors or is a passenger virus has not been conclusively demonstrated. One element to distinguish between these two possibilities is to determine whether EBV infection has preceded and, thus, possibly contributed to clonal expansion, or whether infection has occurred after clonal expansion and thus is unlikely to contribute to pathogenesis. Toward this end we analyzed the structure of the heterogeneous genomic termini of EBV as markers of clonal infection in a panel of eBL (11 cases), sBL (9 cases), and AIDS-NHL (10 cases) biopsies. We show that EBV termini are uniformly clonal in sBL, eBL, and AIDS-NHL, strongly suggesting that EBV infection has preceded and, thus, most likely contributed to clonal expansion in these malignancies. |
doi_str_mv | 10.1182/blood.V77.5.1092.1092 |
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We show that EBV termini are uniformly clonal in sBL, eBL, and AIDS-NHL, strongly suggesting that EBV infection has preceded and, thus, most likely contributed to clonal expansion in these malignancies.</description><subject>Acquired Immunodeficiency Syndrome - complications</subject><subject>Acquired Immunodeficiency Syndrome - pathology</subject><subject>AIDS/HIV</subject><subject>Blotting, Southern</subject><subject>Burkitt Lymphoma - microbiology</subject><subject>Burkitt Lymphoma - pathology</subject><subject>DNA, Viral - analysis</subject><subject>Herpesvirus 4, Human - genetics</subject><subject>Herpesvirus 4, Human - pathogenicity</subject><subject>Humans</subject><subject>Lymphoma, Non-Hodgkin - microbiology</subject><subject>Lymphoma, Non-Hodgkin - pathology</subject><subject>Neoplastic Stem Cells - microbiology</subject><subject>Neoplastic Stem Cells - pathology</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><recordid>eNqFkE-P0zAQxS0EWroLH2Eln-CUYjt24pxQtypLpUogAXu1_GcsDImdtRNEL3x20nYljlxmNHpv5ml-CN1SsqZUsnemT8mtH9p2LdaUdOxcnqEVFUxWhDDyHK0IIU3Fu5a-RNel_CCE8pqJK3RFJW9rSlboz24sE4RY3emc8UPIc8H76MFOIUX8OYMFBwVv-xR1j3e_Rx3LSQkR3835Z5imtwXr6PDGPs4hg8P7YZhjcuCDDRDtEX85RpfTANWmlGSDnhbT4TiM39OgX6EXXvcFXj_1G_Ttw-7r9mN1-HS_324Ola2lZFXTCcc88cZII710rex8V9eam7bxpiHUUUq87oznnInG04YtU-MayaSg3NQ36M3l7pjT4wxlUkMoFvpeR0hzUZJw3gjCFqO4GG1OpWTwasxh0PmoKFEn7urMXS3clVAn5Oey7N0-BcxmAPdv6wJ60d9fdFi-_BUgq3LGA26BZiflUvhPwl-RepcH</recordid><startdate>19910301</startdate><enddate>19910301</enddate><creator>Neri, Antonino</creator><creator>Barriga, Francisco</creator><creator>Inghirami, Giorgio</creator><creator>Knowles, Daniel M.</creator><creator>Neequaye, Janet</creator><creator>Magrath, Ian T.</creator><creator>Dalla-Favera, Riccardo</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19910301</creationdate><title>Epstein-Barr Virus Infection Precedes Clonal Expansion in Burkitt's and Acquired Immunodeficiency Syndrome-Associated Lymphoma</title><author>Neri, Antonino ; 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However, whether EBV has a pathogenetic role in these tumors or is a passenger virus has not been conclusively demonstrated. One element to distinguish between these two possibilities is to determine whether EBV infection has preceded and, thus, possibly contributed to clonal expansion, or whether infection has occurred after clonal expansion and thus is unlikely to contribute to pathogenesis. Toward this end we analyzed the structure of the heterogeneous genomic termini of EBV as markers of clonal infection in a panel of eBL (11 cases), sBL (9 cases), and AIDS-NHL (10 cases) biopsies. We show that EBV termini are uniformly clonal in sBL, eBL, and AIDS-NHL, strongly suggesting that EBV infection has preceded and, thus, most likely contributed to clonal expansion in these malignancies.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>1847310</pmid><doi>10.1182/blood.V77.5.1092.1092</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acquired Immunodeficiency Syndrome - complications Acquired Immunodeficiency Syndrome - pathology AIDS/HIV Blotting, Southern Burkitt Lymphoma - microbiology Burkitt Lymphoma - pathology DNA, Viral - analysis Herpesvirus 4, Human - genetics Herpesvirus 4, Human - pathogenicity Humans Lymphoma, Non-Hodgkin - microbiology Lymphoma, Non-Hodgkin - pathology Neoplastic Stem Cells - microbiology Neoplastic Stem Cells - pathology |
title | Epstein-Barr Virus Infection Precedes Clonal Expansion in Burkitt's and Acquired Immunodeficiency Syndrome-Associated Lymphoma |
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