{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,24]],"date-time":"2025-09-24T10:30:21Z","timestamp":1758709821618},"reference-count":83,"publisher":"American Society for Microbiology","issue":"21","license":[{"start":{"date-parts":[[2011,11,1]],"date-time":"2011-11-01T00:00:00Z","timestamp":1320105600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            An ordered silencing of Epstein-Barr virus (EBV) latency gene transcription is critical for establishment of persistent infection within B lymphocytes, yet the mechanisms responsible and the role that the virus itself may play are unclear. Here we describe two B-cell superinfection models with which to address these problems. In the first, Burkitt lymphoma (BL) cells that maintain latency I, when superinfected, initially supported transcription from the common\n            <jats:italic>EBNA<\/jats:italic>\n            promoters Wp and Cp (latency III) but ultimately transitioned to latency I (Cp\/Wp silent), an essential requirement for establishment of EBV latency\n            <jats:italic>in vivo<\/jats:italic>\n            . We used this model to test whether the early lytic-cycle gene\n            <jats:italic>BHLF1<\/jats:italic>\n            , implicated in silencing of the Cp\/Wp locus, is required to establish latency I. Upon superinfection with EBV deleted for the\n            <jats:italic>BHLF1<\/jats:italic>\n            locus, however, we have demonstrated that\n            <jats:italic>BHLF1<\/jats:italic>\n            is not essential for this aspect of EBV latency. In the second model, BL cells that maintain Wp-restricted latency, a variant program in which Cp is silent but Wp remains active, sustained the latency III program of transcription from the superinfecting-virus genomes, failing to transition to latency I. Importantly, there was substantial reduction in Wp-mediated protein expression from endogenous EBV genomes, in the absence of Cp reactivation, that could occur independent of a parallel decrease in mRNA. Thus, our data provide evidence of a novel, potentially posttranscriptional mechanism for\n            <jats:italic>trans<\/jats:italic>\n            -repression of Wp-dependent gene expression. We suggest that this may ensure against overexpression of the EBV nuclear antigens (EBNAs) prior to the transcriptional repression of Wp in\n            <jats:italic>cis<\/jats:italic>\n            that occurs upon activation of Cp.\n          <\/jats:p>","DOI":"10.1128\/jvi.05158-11","type":"journal-article","created":{"date-parts":[[2011,8,25]],"date-time":"2011-08-25T03:34:25Z","timestamp":1314243265000},"page":"11435-11447","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":14,"title":["<i>trans<\/i>\n            -Repression of Protein Expression Dependent on the Epstein-Barr Virus Promoter Wp during Latency"],"prefix":"10.1128","volume":"85","author":[{"given":"David J.","family":"Hughes","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, and the Penn State Hershey Cancer Institute, Hershey, Pennsylvania"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carol A.","family":"Dickerson","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, and the Penn State Hershey Cancer Institute, Hershey, Pennsylvania"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marie S.","family":"Shaner","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, and the Penn State Hershey Cancer Institute, Hershey, Pennsylvania"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Clare E.","family":"Sample","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, and the Penn State Hershey Cancer Institute, Hershey, Pennsylvania"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffery T.","family":"Sample","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, and the Penn State Hershey Cancer Institute, Hershey, Pennsylvania"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.64.5.2126-2134.1990"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0042-6822(91)90893-G"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1099\/0022-1317-74-3-361"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)00049-2"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1006\/viro.1998.9440"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.61.11.3424-3430.1987"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.00025-06"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.73.4.3154-3161.1999"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.virol.2006.01.015"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1006\/viro.1995.1009"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.61.12.3870-3878.1987"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.50.1.248-254.1984"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1099\/0022-1317-71-7-1481"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2237267100"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.65.3.1245-1254.1991"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.01204-06"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.66.1.62-69.1992"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.48.1.135-148.1983"},{"key":"e_1_3_2_20_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.66.5.2846-2852.1992"},{"key":"e_1_3_2_21_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.78.13.7004-7015.2004"},{"key":"e_1_3_2_22_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0408774102"},{"key":"e_1_3_2_23_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.02596-07"},{"key":"e_1_3_2_24_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm758"},{"key":"e_1_3_2_25_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1000341"},{"key":"e_1_3_2_26_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.16.10709-10717.2005"},{"key":"e_1_3_2_27_2","first-page":"2603","volume-title":"Fields virology","author":"Kieff E. 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