Characterization of Epstein-Barr virus (EBV) BZLF1 gene promoter variants and comparison of cellular gene expression profiles in Japanese patients with infectious mononucleosis, chronic active EBV infection, and EBV-associated hemophagocytic lymphohistioc

2012 ◽  
Vol 84 (6) ◽  
pp. 940-946 ◽  
Author(s):  
Masayuki Imajoh ◽  
Yumiko Hashida ◽  
Masanao Murakami ◽  
Akihiko Maeda ◽  
Tetsuya Sato ◽  
...  
2012 ◽  
Vol 84 (10) ◽  
pp. 1697-1697
Author(s):  
Mario Alejandro Lorenzetti ◽  
Marina Inés Gutiérrez ◽  
Jaime Altcheh ◽  
Guillermo Moscatelli ◽  
Samanta Moroni ◽  
...  

2014 ◽  
Vol 16 (7) ◽  
pp. 581-586 ◽  
Author(s):  
Masanao Murakami ◽  
Yumiko Hashida ◽  
Masayuki Imajoh ◽  
Akihiko Maeda ◽  
Mikio Kamioka ◽  
...  

2009 ◽  
Vol 81 (11) ◽  
pp. 1912-1917 ◽  
Author(s):  
Mario Alejandro Lorenzetti ◽  
Marina Inés Gutiérrez ◽  
Jaime Altcheh ◽  
Guillermo Moscatelli ◽  
Samanta Moroni ◽  
...  

2020 ◽  
Author(s):  
Joanne Dai ◽  
Emma Heckenberg ◽  
Lingyun Song ◽  
Gregory E. Crawford ◽  
Micah A. Luftig

ABSTRACTBFL-1 is an understudied anti-apoptotic protein upregulated in cancer and Epstein-Barr virus (EBV)-immortalized lymphoblastoid cell lines (LCLs). We have previously shown that BFL-1 is regulated through viral EBNA3A-mediated alterations in B-cell chromatin conformation (Price et al., 2017). Here, we extend those findings to define cis- and trans-acting factors that regulate BFL-1 in LCLs and reliance on BFL-1 for survival from extrinsic apoptosis. Beyond LCLs, BFL-1 is expressed in B cells maturing in the germinal center (GC). We therefore characterized the gene expression profiles and chromatin landscape of maturing human tonsillar B-cell subsets. While chromatin accessibility at the BFL-1 locus increases as naïve B cells enter the GC reaction, BFL-1 expression increases during the transition from dark zone to light zone (LZ) correlating with association between enhancer regions and the transcriptional start site. The relationship between LCLs and LZ B cells suggests that EBV phenocopies GC biology to enhance their survival in establishing latent infection.


1998 ◽  
Vol 72 (10) ◽  
pp. 8230-8239 ◽  
Author(s):  
Pingfan Liu ◽  
Shaofan Liu ◽  
Samuel H. Speck

ABSTRACT The Epstein-Barr virus (EBV) lytic switch gene, BZLF1, is tightly regulated in latently infected B cells. The BZLF1 gene promoter (Zp) contains several cis elements that have been previously shown to respond to inducers of the viral lytic cycle. These include four copies of an element referred to as the ZI domains and an element that contains a consensus CRE/AP-1 motif (ZII domain). In addition, Zp is autoregulated through two sites that bind the BZLF1 gene product Zta. The ZI domains have been shown to bind the ubiquitous cellular transcription factors Sp1 and Sp3 and/or the myocyte enhancer factor 2D (Liu et al., EMBO J. 16:143–153, 1997; Liu et al., Virology 228:9–16, 1997). Here we present a functional analysis of the ZII domain and show: (i) ATF-1 and ATF-2 appear to be the predominant cellular factors that bind to the CRE/AP-1 motif present in the ZII domain; and (ii) the region immediately upstream of the CRE/AP-1 motif contains a potent negative cis element, mutation of which results in a >10-fold increase in Zp activity. The negative cis element (ZIIR) in the ZII domain decreases both basal and induced Zp activity and thus is likely to play an important role in regulating reactivation of EBV. In addition, analysis of heterologous promoter constructs indicates that the function of ZIIR is context sensitive. Attempts to demonstrate a cellular factor binding to ZIIR have been unsuccessful, leaving unresolved the mechanism by which repression is mediated.


1986 ◽  
Vol 57 (3) ◽  
pp. 1105-1112 ◽  
Author(s):  
M de Turenne-Tessier ◽  
T Ooka ◽  
G de The ◽  
J Daillie

Sign in / Sign up

Export Citation Format

Share Document