Activation of TRAF5 and TRAF6 signal cascades negatively regulates the latent replication origin of Epstein-Barr virus through p38 mitogen-activated protein kinase

Journal of Virology
M ShirakataK Hirai

Abstract

Latent Epstein-Barr virus (EBV) is maintained by the virus replication origin oriP that initiates DNA replication with the viral oriP-binding factor EBNA1. However, it is not known whether oriP's replicator activity is regulated by virus proteins or extracellular signals. By using a transient replication assay, we found that a low level of expression of viral signal transduction activator latent membrane protein 1 (LMP1) suppressed oriP activity. The binding site of the tumor necrosis factor receptor-associated factor (TRAF) of LMP1 was essential for this suppressive effect. Activation of the TRAF signal cascade by overexpression of TRAF5 and/or TRAF6 also suppressed oriP activity. Conversely, blocking of TRAF signaling with dominant negative mutants of TRAF5 and TRAF6, as well as inhibition of a downstream signal mediator p38 MAPK, released the LMP1-induced oriP suppression. Furthermore, activation of TRAF6 signal cascade by lipopolysaccharides (LPS) resulted in loss of EBV from Burkitt's lymphoma cell line Akata, and inhibition of p38 MAPK abolished the suppressive effect of LPS. These results suggested that the level of oriP activity is regulated by LMP1 and extracellular signals through TRAF5- and TRAF6-mediated signal casc...Continue Reading

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Citations

Jun 23, 2004·PLoS Biology·Paolo Norio, Carl L Schildkraut
Feb 14, 2016·Biochemical and Biophysical Research Communications·Meng LiHua Du
Oct 28, 2003·BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology·Hao Wu, Joseph R Arron
Oct 9, 2018·Frontiers in Immunology·Sining ZhuPing Xie
Sep 24, 2013·The Journal of Immunology : Official Journal of the American Association of Immunologists·Gail A Bishop
Dec 1, 2018·Future Virology·Mujeeb R Cheerathodi, David G Meckes

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