Ersing, InaNobre, LuisWang, Liang WeiSoday, LiorMa, YijiePaulo, JoaoNarita, YoheiAshbaugh, Camille W.Jiang, ChangGrayson, Nicholas E.Kieff, ElliottGygi, StevenWeekes, Michael P.Gewurz, Benjamin2017-06-152017Ersing, I., L. Nobre, L. W. Wang, L. Soday, Y. Ma, J. A. Paulo, Y. Narita, et al. 2017. “A Temporal Proteomic Map of Epstein-Barr Virus Lytic Replication in B Cells.” Cell Reports 19 (7): 1479-1493. doi:10.1016/j.celrep.2017.04.062. http://dx.doi.org/10.1016/j.celrep.2017.04.062.http://nrs.harvard.edu/urn-3:HUL.InstRepos:33029761Summary Epstein-Barr virus (EBV) replication contributes to multiple human diseases, including infectious mononucleosis, nasopharyngeal carcinoma, B cell lymphomas, and oral hairy leukoplakia. We performed systematic quantitative analyses of temporal changes in host and EBV proteins during lytic replication to gain insights into virus-host interactions, using conditional Burkitt lymphoma models of type I and II EBV infection. We quantified profiles of >8,000 cellular and 69 EBV proteins, including >500 plasma membrane proteins, providing temporal views of the lytic B cell proteome and EBV virome. Our approach revealed EBV-induced remodeling of cell cycle, innate and adaptive immune pathways, including upregulation of the complement cascade and proteasomal degradation of the B cell receptor complex, conserved between EBV types I and II. Cross-comparison with proteomic analyses of human cytomegalovirus infection and of a Kaposi-sarcoma-associated herpesvirus immunoevasin identified host factors targeted by multiple herpesviruses. Our results provide an important resource for studies of EBV replication.en-USEpstein-Barr virusherpesviruslytic replicationquantitative proteomicstandem mass taghost-pathogen interactionimmune evasionB cell receptorcomplementviral evasionJournal Article2017-06-1510.1016/j.celrep.2017.04.062