Year: 2017
Type: article
Abstract: 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.
Source: Cell Reports
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $5,620
Funders: Burroughs Wellcome Fund, Wellcome Trust, Agency for Science, Technology and Research, National Institutes of Health, Cambridge Institute for Medical Research, University of Cambridge, National Cancer Institute, National Institute of General Medical Sciences, National Institute of Diabetes and Digestive and Kidney Diseases
Awards: Functional proteomic analysis of innate immune subversion by human cytomegalovirus., Genetic and Proteomic Analysis of Epstein-Barr Virus LMP1 Activation of NF-kB, New Sample Multiplexing Technologies to Identify Chemical Probes and Illuminate Ubiquitin Biology, G3170305048, G4273598029, Cellular Medicine at the Cambridge Institute for Medical Research., Resolving the role of nicotine-mediated phosphorylation on pancreatic fibrosis, Epstein-Barr Virus LMP1-Mediated Oncogenecity, G6868616705, Cellular Medicine at the Cambridge Institute for Medical Research., G8351965958, G8703993721
OpenAlex ID: W2616410853