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Epstein-Barr virus ensures B cell survival by uniquely modulating apoptosis at early and late times after infection.

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Date
2017-04-20
Authors
Price, Alexander M
Dai, Joanne
Bazot, Quentin
Patel, Luv
Nikitin, Pavel A
Djavadian, Reza
Winter, Peter S
Salinas, Cristina A
Barry, Ashley Perkins
Wood, Kris C
Johannsen, Eric C
Letai, Anthony
Allday, Martin J
Luftig, Micah A
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(14 total)
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Abstract
Latent Epstein-Barr virus (EBV) infection is causally linked to several human cancers. EBV expresses viral oncogenes that promote cell growth and inhibit the apoptotic response to uncontrolled proliferation. The EBV oncoprotein LMP1 constitutively activates NFκB and is critical for survival of EBV-immortalized B cells. However, during early infection EBV induces rapid B cell proliferation with low levels of LMP1 and little apoptosis. Therefore, we sought to define the mechanism of survival in the absence of LMP1/NFκB early after infection. We used BH3 profiling to query mitochondrial regulation of apoptosis and defined a transition from uninfected B cells (BCL-2) to early-infected (MCL-1/BCL-2) and immortalized cells (BFL-1). This dynamic change in B cell survival mechanisms is unique to virus-infected cells and relies on regulation of MCL-1 mitochondrial localization and BFL-1 transcription by the viral EBNA3A protein. This study defines a new role for EBNA3A in the suppression of apoptosis with implications for EBV lymphomagenesis.
Type
Journal article
Subject
B cell
BH3 Profiling
Epstein-Barr virus
apoptosis
cancer biology
enhancer
human
infectious disease
microbiology
virus
Permalink
https://hdl.handle.net/10161/14611
Published Version (Please cite this version)
10.7554/eLife.22509
Publication Info
Price, Alexander M; Dai, Joanne; Bazot, Quentin; Patel, Luv; Nikitin, Pavel A; Djavadian, Reza; ... Luftig, Micah A (2017). Epstein-Barr virus ensures B cell survival by uniquely modulating apoptosis at early and late times after infection. Elife, 6. 10.7554/eLife.22509. Retrieved from https://hdl.handle.net/10161/14611.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Luftig

Micah Alan Luftig

Associate Professor of Molecular Genetics and Microbiology
The Luftig laboratory studies viruses that cause cancer with an overarching goal of defining the basic molecular mechanisms underlying pathogenesis and leveraging these findings for diagnostic value and therapeutic intervention. Our work primarily focuses on the common herpesvirus, Epstein-Barr virus (EBV). This virus latently infects virtually all adults worldwide being acquired early in life. In the immune suppressed, EBV promotes lymphomas in the B cells that it naturally infects. However, EB
Wood

Kris Cameron Wood

Associate Professor of Pharmacology and Cancer Biology
Our laboratory uses genomic and pharmacological approaches to understand how tumor dependencies are shaped by cell intrinsic factors, environmental factors, and drug treatments during the dynamic process of tumor evolution. To learn more, please visit our laboratory website: https://sites.duke.edu/woodlab/.
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