<HashMap><database>biostudies-literature</database><scores/><additional><submitter>SoRelle ED</submitter><funding>American Cancer Society</funding><funding>NIDCR NIH HHS</funding><funding>St. Baldrick&amp;apos;s Foundation</funding><funding>NIDCR</funding><funding>National Science Foundation Graduate Research Fellowship Program</funding><funding>National Cancer Institute</funding><funding>NCI NIH HHS</funding><pagination>e1012341</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11563402</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(10)</volume><pubmed_abstract>Viral infection leads to heterogeneous cellular outcomes ranging from refractory to abortive and fully productive states. Single cell transcriptomics enables a high resolution view of these distinct post-infection states. Here, we have interrogated the host-pathogen dynamics following reactivation of Epstein-Barr virus (EBV). While benign in most people, EBV is responsible for infectious mononucleosis, up to 2% of human cancers, and is a trigger for the development of multiple sclerosis. Following latency establishment in B cells, EBV reactivates and is shed in saliva to enable infection of new hosts. Beyond its importance for transmission, the lytic cycle is also implicated in EBV-associated oncogenesis. Conversely, induction of lytic reactivation in latent EBV-positive tumors presents a </pubmed_abstract><journal>PLoS pathogens</journal><pubmed_title>Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.</pubmed_title><pmcid>PMC11563402</pmcid><funding_grant_id>GRFP #1644868</funding_grant_id><funding_grant_id>T32 CA009111</funding_grant_id><funding_grant_id>R01CA215185</funding_grant_id><funding_grant_id>F31 DE033216</funding_grant_id><funding_grant_id>PF-21-084-01-DMC</funding_grant_id><funding_grant_id>R01 DE025994</funding_grant_id><funding_grant_id>1F31DE033216</funding_grant_id><funding_grant_id>R01DE025994</funding_grant_id><funding_grant_id>T32CA009111</funding_grant_id><funding_grant_id>U01 CA275306</funding_grant_id><pubmed_authors>Luftig MA</pubmed_authors><pubmed_authors>Haynes LE</pubmed_authors><pubmed_authors>SoRelle ED</pubmed_authors><pubmed_authors>Willard KA</pubmed_authors><pubmed_authors>Chang B</pubmed_authors><pubmed_authors>Ch'ng J</pubmed_authors><pubmed_authors>Christofk H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.</name><description>Viral infection leads to heterogeneous cellular outcomes ranging from refractory to abortive and fully productive states. Single cell transcriptomics enables a high resolution view of these distinct post-infection states. Here, we have interrogated the host-pathogen dynamics following reactivation of Epstein-Barr virus (EBV). While benign in most people, EBV is responsible for infectious mononucleosis, up to 2% of human cancers, and is a trigger for the development of multiple sclerosis. Following latency establishment in B cells, EBV reactivates and is shed in saliva to enable infection of new hosts. Beyond its importance for transmission, the lytic cycle is also implicated in EBV-associated oncogenesis. Conversely, induction of lytic reactivation in latent EBV-positive tumors presents a </description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-07-16T21:45:22.118Z</modification><creation>2025-04-06T01:46:00.336Z</creation></dates><accession>S-EPMC11563402</accession><cross_references><pubmed>39446925</pubmed><doi>10.1371/journal.ppat.1012341</doi></cross_references></HashMap>