<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yan B</submitter><funding>Intramural NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>e28362</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10027397</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>95(1)</volume><pubmed_abstract>We probed the lifecycle of Epstein-Barr virus (EBV) on a cell-by-cell basis using single cell RNA sequencing (scRNA-seq) data from nine publicly available lymphoblastoid cell lines (LCLs). While the majority of LCLs comprised cells containing EBV in the latent phase, two other clusters of cells were clearly evident and were distinguished by distinct expression of host and viral genes. Notably, both were high expressors of EBV LMP1/BNLF2 and BZLF1 compared to another cluster that expressed neither gene. The two novel clusters differed from each other in their expression of EBV lytic genes, including glycoprotein gene GP350. The first cluster, comprising GP350&lt;sup>-&lt;/sup> LMP1&lt;sup>hi&lt;/sup> cells, expressed high levels of HIF1A and was transcriptionally regulated by HIF1-α. Treatment of LCLs </pubmed_abstract><journal>Journal of medical virology</journal><pubmed_title>A comprehensive single cell data analysis of lymphoblastoid cells reveals the role of super-enhancers in maintaining EBV latency.</pubmed_title><pmcid>PMC10027397</pmcid><funding_grant_id>ZIA/DK075149</funding_grant_id><funding_grant_id>ZIA DK075149</funding_grant_id><funding_grant_id>P30 CA023168</funding_grant_id><funding_grant_id>R01 CA047006</funding_grant_id><funding_grant_id>R35 GM138283</funding_grant_id><funding_grant_id>R01 AI136995</funding_grant_id><funding_grant_id>R01 AI123420</funding_grant_id><funding_grant_id>R35GM138283; 5R01AI123420 and 5R01CA047006</funding_grant_id><funding_grant_id>P30CA023168</funding_grant_id><pubmed_authors>Sahoo SS</pubmed_authors><pubmed_authors>Hu Y</pubmed_authors><pubmed_authors>Zhao B</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Shao K</pubmed_authors><pubmed_authors>Briggs SD</pubmed_authors><pubmed_authors>Afzali B</pubmed_authors><pubmed_authors>Zhuang Y</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Trujillo-Ochoa JL</pubmed_authors><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Chakravorty S</pubmed_authors><pubmed_authors>Anderson NL</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Sirit I</pubmed_authors><pubmed_authors>Olson MR</pubmed_authors><pubmed_authors>Yan B</pubmed_authors><pubmed_authors>Jung M</pubmed_authors><pubmed_authors>Kazemian M</pubmed_authors><pubmed_authors>Kadadi SD</pubmed_authors></additional><is_claimable>false</is_claimable><name>A comprehensive single cell data analysis of lymphoblastoid cells reveals the role of super-enhancers in maintaining EBV latency.</name><description>We probed the lifecycle of Epstein-Barr virus (EBV) on a cell-by-cell basis using single cell RNA sequencing (scRNA-seq) data from nine publicly available lymphoblastoid cell lines (LCLs). While the majority of LCLs comprised cells containing EBV in the latent phase, two other clusters of cells were clearly evident and were distinguished by distinct expression of host and viral genes. Notably, both were high expressors of EBV LMP1/BNLF2 and BZLF1 compared to another cluster that expressed neither gene. The two novel clusters differed from each other in their expression of EBV lytic genes, including glycoprotein gene GP350. The first cluster, comprising GP350&lt;sup>-&lt;/sup> LMP1&lt;sup>hi&lt;/sup> cells, expressed high levels of HIF1A and was transcriptionally regulated by HIF1-α. Treatment of LCLs </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2026-07-14T20:14:08.952Z</modification><creation>2025-04-05T19:40:35.702Z</creation></dates><accession>S-EPMC10027397</accession><cross_references><pubmed>36453088</pubmed><doi>10.1002/jmv.28362</doi></cross_references></HashMap>