{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["SoRelle ED"],"funding":["American Cancer Society","NIDCR NIH HHS","St. Baldrick's Foundation","NIDCR","National Science Foundation Graduate Research Fellowship Program","National Cancer Institute","NCI NIH HHS"],"pagination":["e1012341"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11563402"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(10)"],"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 "],"journal":["PLoS pathogens"],"pubmed_title":["Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression."],"pmcid":["PMC11563402"],"funding_grant_id":["GRFP #1644868","T32 CA009111","R01CA215185","F31 DE033216","PF-21-084-01-DMC","R01 DE025994","1F31DE033216","R01DE025994","T32CA009111","U01 CA275306"],"pubmed_authors":["Luftig MA","Haynes LE","SoRelle ED","Willard KA","Chang B","Ch'ng J","Christofk H"],"additional_accession":[]},"is_claimable":false,"name":"Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.","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 ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-07-16T21:45:22.118Z","creation":"2025-04-06T01:46:00.336Z"},"accession":"S-EPMC11563402","cross_references":{"pubmed":["39446925"],"doi":["10.1371/journal.ppat.1012341"]}}