爱泼斯坦-巴尔病毒即刻早期蛋白BZLF1通过下调肿瘤坏死因子受体1来抑制肿瘤坏死因子α诱导的信号传导和细胞凋亡。
Epstein-Barr virus immediate-early protein BZLF1 inhibits tumor necrosis factor alpha-induced signaling and apoptosis by downregulating tumor necrosis factor receptor 1.
作者信息
Morrison Thomas E, Mauser Amy, Klingelhutz Aloysius, Kenney Shannon C
机构信息
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
出版信息
J Virol. 2004 Jan;78(1):544-9. doi: 10.1128/jvi.78.1.544-549.2004.
Abstract
Tumor necrosis factor alpha (TNF-alpha) is a key mediator of host immune and inflammatory responses and inhibits herpesvirus replication by cytolytic and noncytolytic mechanisms. TNF-alpha effects are primarily mediated through the major TNF-alpha receptor, TNF-R1, which is constitutively expressed in most cell types. Here we show that the Epstein-Barr virus (EBV) immediate-early protein BZLF1 prevents TNF-alpha activation of target genes and TNF-alpha-induced cell death. These effects are mediated by down-regulation of the promoter for TNF-R1. Additionally, we demonstrate that expression of TNF-R1 is downregulated during the EBV lytic replication cycle. Thus, EBV has developed a novel mechanism for evading TNF-alpha antiviral effects during lytic reactivation or primary infection.
摘要
肿瘤坏死因子α（TNF-α）是宿主免疫和炎症反应的关键介质，可通过细胞溶解和非细胞溶解机制抑制疱疹病毒复制。TNF-α的作用主要通过主要的TNF-α受体TNF-R1介导，TNF-R1在大多数细胞类型中组成性表达。在这里，我们表明爱泼斯坦-巴尔病毒（EBV）立即早期蛋白BZLF1可阻止TNF-α激活靶基因和TNF-α诱导的细胞死亡。这些作用是由TNF-R1启动子的下调介导的。此外，我们证明在EBV裂解复制周期中TNF-R1的表达下调。因此，EBV已经开发出一种新机制，在裂解再激活或原发性感染期间逃避TNF-α的抗病毒作用。
相似文献
1
Epstein-Barr virus immediate-early protein BZLF1 inhibits tumor necrosis factor alpha-induced signaling and apoptosis by downregulating tumor necrosis factor receptor 1.
J Virol. 2004 Jan;78(1):544-9. doi: 10.1128/jvi.78.1.544-549.2004.
2
Epstein-Barr Virus BZLF1-Mediated Downregulation of Proinflammatory Factors Is Essential for Optimal Lytic Viral Replication.
J Virol. 2015 Nov 4;90(2):887-903. doi: 10.1128/JVI.01921-15. Print 2016 Jan 15.
3
BZLF1 Attenuates Transmission of Inflammatory Paracrine Senescence in Epstein-Barr Virus-Infected Cells by Downregulating Tumor Necrosis Factor Alpha.
J Virol. 2016 Aug 12;90(17):7880-93. doi: 10.1128/JVI.00999-16. Print 2016 Sep 1.
4
BZLF1, an Epstein-Barr virus immediate-early protein, induces p65 nuclear translocation while inhibiting p65 transcriptional function.
Virology. 2004 Oct 25;328(2):219-32. doi: 10.1016/j.virol.2004.07.020.
5
Identification of protein tyrosine kinases required for B-cell- receptor-mediated activation of an Epstein-Barr Virus immediate-early gene promoter.
J Virol. 2004 Aug;78(16):8543-51. doi: 10.1128/JVI.78.16.8543-8551.2004.
6
Epstein-Barr virus BZLF1 gene, a switch from latency to lytic infection, is expressed as an immediate-early gene after primary infection of B lymphocytes.
J Virol. 2007 Jan;81(2):1037-42. doi: 10.1128/JVI.01416-06. Epub 2006 Nov 1.
7
Epstein-Barr virus (EBV) EB1/Zta protein provided in trans and competent for the activation of productive cycle genes does not activate the BZLF1 gene in the EBV genome.
J Gen Virol. 1996 Mar;77 ( Pt 3):501-9. doi: 10.1099/0022-1317-77-3-501.
8
Use of adenovirus vectors expressing Epstein-Barr virus (EBV) immediate-early protein BZLF1 or BRLF1 to treat EBV-positive tumors.
J Virol. 2002 Nov;76(21):10951-9. doi: 10.1128/jvi.76.21.10951-10959.2002.
9
Interferon regulatory factor 7 is negatively regulated by the Epstein-Barr virus immediate-early gene, BZLF-1.
J Virol. 2005 Aug;79(15):10040-52. doi: 10.1128/JVI.79.15.10040-10052.2005.
10
Epstein-barr virus immediate-early protein BZLF1 is SUMO-1 modified and disrupts promyelocytic leukemia bodies.
J Virol. 2001 Mar;75(5):2388-99. doi: 10.1128/JVI.75.5.2388-2399.2001.
引用本文的文献
1
Apoptosis and Phagocytosis as Antiviral Mechanisms.
Subcell Biochem. 2023;106:77-112. doi: 10.1007/978-3-031-40086-5_3.
2
Dendrosomal nanocurcumin prevents EBV-associated cell transformation by targeting the lytic cycle genes of the Epstein-Barr virus in the generation of lymphoblastoid cell line.
Iran J Basic Med Sci. 2023;26(10):1220-1226. doi: 10.22038/IJBMS.2023.69839.15199.
3
Contribution of Epstein-Barr Virus Lytic Proteins to Cancer Hallmarks and Implications from Other Oncoviruses.
Cancers (Basel). 2023 Apr 2;15(7):2120. doi: 10.3390/cancers15072120.
4
Oncogenic Viruses as Entropic Drivers of Cancer Evolution.
Front Virol. 2021 Nov;1. doi: 10.3389/fviro.2021.753366. Epub 2021 Nov 15.
5
Identification of an N6-methyladenosine-mediated positive feedback loop that promotes Epstein-Barr virus infection.
J Biol Chem. 2021 Jan-Jun;296:100547. doi: 10.1016/j.jbc.2021.100547. Epub 2021 Mar 16.
6
Epstein-Barr virus inactivates the transcriptome and disrupts the chromatin architecture of its host cell in the first phase of lytic reactivation.
Nucleic Acids Res. 2021 Apr 6;49(6):3217-3241. doi: 10.1093/nar/gkab099.
7
Viral Infections: Negative Regulators of Apoptosis and Oncogenic Factors.
Biochemistry (Mosc). 2020 Oct;85(10):1191-1201. doi: 10.1134/S0006297920100077.
8
Epstein-Barr Virus Promotes B Cell Lymphomas by Manipulating the Host Epigenetic Machinery.
Cancers (Basel). 2020 Oct 19;12(10):3037. doi: 10.3390/cancers12103037.
9
Ubiquitin Modification of the Epstein-Barr Virus Immediate Early Transactivator Zta.
J Virol. 2020 Oct 27;94(22). doi: 10.1128/JVI.01298-20.
10
Lytic Induction Therapy against Epstein-Barr Virus-Associated Malignancies: Past, Present, and Future.
Cancers (Basel). 2020 Aug 2;12(8):2142. doi: 10.3390/cancers12082142.
本文引用的文献
1
Murine cytomegalovirus infection inhibits tumor necrosis factor alpha responses in primary macrophages.
J Virol. 2003 Sep;77(18):10125-30. doi: 10.1128/jvi.77.18.10125-10130.2003.
2
Human cytomegalovirus infection inhibits tumor necrosis factor alpha (TNF-alpha) signaling by targeting the 55-kilodalton TNF-alpha receptor.
J Virol. 2003 Jun;77(12):7007-16. doi: 10.1128/jvi.77.12.7007-7016.2003.
3
A novel function for the Epstein-Barr virus transcription factor EB1/Zta: induction of transcription of the hIL-10 gene.
J Gen Virol. 2003 Apr;84(Pt 4):965-974. doi: 10.1099/vir.0.18845-0.
4
The Epstein-Barr virus immediate-early protein BZLF1 regulates p53 function through multiple mechanisms.
J Virol. 2002 Dec;76(24):12503-12. doi: 10.1128/jvi.76.24.12503-12512.2002.
5
To kill or be killed: viral evasion of apoptosis.
Nat Immunol. 2002 Nov;3(11):1013-8. doi: 10.1038/ni1102-1013.
6
The lytic cycle of Epstein-Barr virus is associated with decreased expression of cell surface major histocompatibility complex class I and class II molecules.
J Virol. 2002 Aug;76(16):8179-88. doi: 10.1128/jvi.76.16.8179-8188.2002.
7
The human papillomavirus 16 E6 protein binds to tumor necrosis factor (TNF) R1 and protects cells from TNF-induced apoptosis.
J Biol Chem. 2002 Jun 14;277(24):21730-9. doi: 10.1074/jbc.M200113200. Epub 2002 Apr 4.
8
Vaccinia virus CrmE encodes a soluble and cell surface tumor necrosis factor receptor that contributes to virus virulence.
Virology. 2002 Jan 20;292(2):285-98. doi: 10.1006/viro.2001.1236.
9
Evidence of lytic infection of Epstein-Barr virus (EBV) in EBV-positive gastric carcinoma.
J Med Virol. 2002 Mar;66(3):351-9. doi: 10.1002/jmv.2152.
10
Inhibition of IFN-gamma signaling by an Epstein-Barr virus immediate-early protein.
Immunity. 2001 Nov;15(5):787-99. doi: 10.1016/s1074-7613(01)00226-6.
Zotero 插件