ArticleMedical microbiology and immunology2006
Reactivation of the Epstein-Barr virus from viral latency by an S-adenosylhomocysteine hydrolase/14-3-3 zeta/PLA2-dependent pathway.
Article in Medical microbiology and immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- The biography of the immune system and the control of cancer: from St Peregrine to contemporary vaccination strategies.BMC cancer · 2014Review
- Is a hypothetical melanoma-like neuromelanin the underlying factor essential for the aetiopathogenesis and clinical manifestations of multiple sclerosis?BMC neurology · 2013Article
- Glial cell type-specific subcellular localization of 14-3-3 zeta: an implication for JCV tropism.Glia · 2009Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The S-adenosylhomocysteine hydrolase (SAH) and 14-3-3 zeta/phospholipase A2 (PLA2) are transcriptionally activated in parallel to the induction of the Epstein-Barr virus (EBV) lytic cycle by the ganglioside IV(3)NeuAc-nLcOse(4)Cer. For analysis of the initiation of the viral reactivation, SAH and 14-3-3 zeta/PLA2 were overexpressed. Expression of EA-D, BZLF1, and BHRF1 was increased in response to both, SAH- and 14-3-3 zeta/PLA2 overexpression indicating the initiation of the EBV lytic cycle. Expression of 14-3-3 zeta/PLA2 was shown to be increased in SAH overexpressing cells. Additionally, SAH-triggered initiation of viral reactivation could be inhibited by PLA2-specific inhibitors. The phosphorylation status of protein kinase C (PKC) was shown to be increased in SAH-overexpressing cells. PKC-specific inhibitors arrested SAH-triggered initiation of viral reactivation. Surprisingly, 14-3-3 zeta/PLA2-induced initiation of viral reactivation did not correlate with PKC activation. PKC-specific inhibitors were of no influence. SAH initiated EBV reactivation via the BZLF1-Zp and the BZLF1-Rp promoter, whereas 14-3-3 zeta/PLA2 was connected to the promoter Rp only. Our results suggest two routes of viral reactivation involving SAH, one associated with PKC and BZLF1-Zp, the other associated with 14-3-3 zeta/PLA2 and BZLF1-Rp.
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