{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T17:54:28Z","timestamp":1791136468913,"version":"4.1.0"},"reference-count":31,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2004,2,13]],"date-time":"2004-02-13T00:00:00Z","timestamp":1076630400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2004,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>It has been reported recently that the U leader exon located within the 5\u2032 untranslated region of Epstein\u2013Barr nuclear antigen 1 (EBNA1) gene contains an internal ribosome entry site (IRES) element. Sequence analysis of the U leader exon was undertaken in samples from 19 patients with infectious mononucleosis and 19 patients with lethal lymphoproliferative diseases and in 15 spontaneously established lymphoblastoid cell lines. The sequence was conserved except for a single base substitution (T\u2010C) at position 67,585. Although the mutation was detected in only one case of infectious mononucleosis, it was found in more than half of the lethal lymphoproliferative diseases and all lymphoblastoid cell lines. The results suggest that a mutation in the IRES element affects EBNA1 gene expression at the translational level and provides Epstein\u2013Barr virus (EBV)\u2010infected cells with a growth advantage, leading to immortalization of cells in vitro and to the development of lethal lymphoproliferative diseases in vivo. J. Med. Virol. 72:630\u2013634, 2004. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jmv.20022","type":"journal-article","created":{"date-parts":[[2004,2,19]],"date-time":"2004-02-19T10:00:24Z","timestamp":1077184824000},"page":"630-634","source":"Crossref","is-referenced-by-count":3,"title":["Possible involvement in oncogenesis of a single base mutation in an internal ribosome entry site of Epstein\u2013Barr nuclear antigen 1 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