Loss of functional transforming growth factor (TGF)-β type II receptor results in insensitivity to TGF-β1-mediated apoptosis and Epstein–Barr virus reactivation

2006 ◽  
Vol 78 (11) ◽  
pp. 1456-1464 ◽  
Author(s):  
Makoto Fukuda ◽  
Hajime Kurosaki ◽  
Takeshi Sairenji
Keyword(s):  
Growth Factor ◽  
Epstein Barr Virus ◽  
Transforming Growth Factor ◽  
Type Ii ◽  
Virus Reactivation ◽  
Barr Virus ◽  
Epstein Barr ◽  
Epstein Barr Virus Reactivation ◽  
Tgf Β1

scholarly journals Transforming Growth Factor Beta 1 Stimulates Expression of the Epstein-Barr Virus BZLF1 Immediate-Early Gene Product ZEBRA by an Indirect Mechanism Which Requires the MAPK Kinase Pathway

2000 ◽  
Vol 74 (13) ◽  
pp. 5810-5818 ◽  
Author(s):  
Hassan Fahmi ◽  
Chantal Cochet ◽  
Zakariae Hmama ◽  
Paule Opolon ◽  
Irene Joab
Keyword(s):  
Growth Factor ◽  
Protein Kinase ◽  
Transforming Growth Factor Beta ◽  
Epstein Barr Virus ◽  
Transforming Growth Factor ◽  
Barr Virus ◽  
Growth Factor Beta ◽  
Epstein Barr ◽  
Bzlf1 Promoter ◽  
Tgf Β1

ABSTRACT Disruption of Epstein-Barr virus (EBV) latency is mediated by ZEBRA, the protein product of the immediate-early EBV gene, BZLF1. In vitro, phorbol 12-myristate 13-acetate (PMA), a potent activator of protein kinase C (PKC), induces reactivation of EBV. However, the physiological stimuli responsible for the disruption of viral latency are not well characterized. Transforming growth factor beta 1 (TGF-β1) has also been shown to trigger the reactivation of EBV in Burkitt lymphoma cell lines; however, the effect of TGF-β1 on ZEBRA expression has not been reported. To further understand this phenomenon, we have investigated the effect of TGF-β1 on ZEBRA expression. Our results indicate that the treatment of different EBV-positive Burkitt's lymphoma cell lines with TGF-β1 induces a time-dependent activation of BZLF1 transcription with a corresponding increase in the production of the protein ZEBRA. TGF-β1 has been shown to exert its effects through a wide range of intracellular routes; in the present study, we have explored these pathways. Transient expression of Smad proteins on their own had no effect on ZEBRA expression. A specific inhibitor of p38 mitogen-activated protein kinase (MAPK), SB203580, did not affect TGF-β1-induced ZEBRA expression, whereas treatment with the MAPK/ERK kinase inhibitors, PD98059 and U0126, dramatically decreased this induction. This suggests that TGF-β1 effect on BZLF1 expression requires the MAPK pathway. However, in Raji and B95-8 cells additional routes can be used, as (i) the inhibition of ZEBRA induction by PD98059 or U0126 was incomplete, whereas these inhibitors completely abolished PMA-induced ZEBRA expression, (ii) TGF-β1 induction of ZEBRA expression occurs in PKC-depleted cells, (iii) in Raji and in B95-8 cells, the effect of TGF-β1 and PMA are additive. Transient transfection of the EBV-negative B-cell line DG75 with a BZLF1 promoter-fusion construct (Zp-CAT) showed that under conditions where the BZLF1 promoter is activated by PMA treatment, TGF-β1 had no significant effect on the expression of the chloramphenicol acetyltransferase gene. Furthermore, TGF-β1 induction of BZLF1 transcripts is dependent on de novo protein synthesis, which suggests that TGF-β1 induces BZLF1 expression by an indirect mechanism.

Valganciclovir suppressed Epstein Barr virus reactivation during immunosuppression with alemtuzumab

2014 ◽  
Vol 59 (4) ◽  
pp. 255-258 ◽  
Author(s):  
Harinder Gill ◽  
Yu-Yan Hwang ◽  
Thomas S.Y. Chan ◽  
Annie W.K. Pang ◽  
Anskar Y.H. Leung ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Virus Reactivation ◽  
Barr Virus ◽  
Epstein Barr ◽  
Epstein Barr Virus Reactivation

scholarly journals Elevated Serum Transforming Growth Factor β1 Levels in Epstein-Barr Virus-Associated Diseases and Their Correlation with Virus-Specific Immunoglobulin A (IgA) and IgM

2000 ◽  
Vol 74 (5) ◽  
pp. 2443-2446 ◽  
Author(s):  
Jingwu Xu ◽  
Ali Ahmad ◽  
James F. Jones ◽  
Riccardo Dolcetti ◽  
Emanuela Vaccher ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epstein Barr Virus ◽  
Transforming Growth Factor ◽  
Immunoglobulin A ◽  
Elevated Serum ◽  
Transforming Growth Factor Β ◽  
Serum Levels ◽  
Barr Virus ◽  
Associated Diseases ◽  
Epstein Barr

ABSTRACT Transforming growth factor β (TGF-β) is an immunosuppressive cytokine which can induce immunoglobulin A (IgA) switch and Epstein-Barr virus (EBV) replication in latently infected cells. Here we report elevated serum levels of TGF-β in various EBV-associated diseases correlating positively with EBV-specific IgA titers and negatively with IgM titers, suggesting a role for this cytokine in the pathogenesis of these diseases.

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