A Temporal Proteomic Map of Epstein-Barr Virus Lytic Replication in B Cells

Publication date: 16 May 2017
Source:Cell Reports, Volume 19, Issue 7
Author(s): Ina Ersing, Luis Nobre, Liang Wei Wang, Lior Soday, Yijie Ma, Joao A. Paulo, Yohei Narita, Camille W. Ashbaugh, Chang Jiang, Nicholas E. Grayson, Elliott Kieff, Steven P. Gygi, Michael P. Weekes, Benjamin E. Gewurz
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.

Graphical abstract

Teaser

Ersing et al. present a temporal proteomic map of EBV B cell lytic replication. Tandem-mass-tag-based proteomics uncover extensive remodeling of the human proteome by EBV, conserved across the two major EBV strains. Cell-cycle, innate, and adaptive immune pathways are modulated, complement is upregulated, and the B cell receptor is degraded by infection.


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