Establishment and characterization of an in vivo model for Epstein–Barr virus positive gastric carcinoma

2007 ◽  
Vol 79 (9) ◽  
pp. 1343-1348 ◽  
Author(s):  
Sang Taek Oh ◽  
Jung-Ho Cha ◽  
Dong-Jik Shin ◽  
Sungjoo Kim Yoon ◽  
Suk Kyeong Lee
Keyword(s):  
Gastric Carcinoma ◽  
Epstein Barr Virus ◽  
In Vivo Model ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Common Epstein-Barr virus (EBV) type-1 variant strains in both malignant and benign EBV-associated disorders

Blood ◽  
1996 ◽  
Vol 87 (4) ◽  
pp. 1579-1585 ◽  
Author(s):  
V Schuster ◽  
G Ott ◽  
S Seidenspinner ◽  
HW Kreth
Keyword(s):  
Gastric Carcinoma ◽  
Epstein Barr Virus ◽  
Hodgkin's Lymphoma ◽  
Sequence Pattern ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

In the present study, Epstein-Barr virus (EBV) isolates from 18 malignant tumors (angioimmunoblastic lymphadenopathy [AILD], n = 4; Hodgkin's disease [HD], n = 3; pleomorphic T-cell non-Hodgkin's lymphoma [T-NHL], n = 1; B-cell non-Hodgkin's lymphoma [B-NHL], n = 8; gastric carcinoma, n = 2) as well as from 10 tonsils of EBV- seropositive children and from peripheral blood mononuclear cells of 12 children with uncomplicated infectious mononucleosis (IM) and of a boy with severe chronic active EBV infection were genotyped in the EBV nuclear antigen-2 (EBNA-2) gene. A total of 40 of 41 isolates harbored EBV type 1; in 1 specimen (tonsil), only EBV type 2 was found. Further molecular characterization of EBV type-1 wild-type isolates in the EBNA- 2 gene and in the 40-kb distant EBV-encoded small RNAs (EBER) region showed that different groups of stable EBV type-1 variant strains exist in vivo both in benign and malignant lymphatic tissue. Group 1 is composed of EBV type-1 isolates (B-NHL, n = 3; T-NHL, n = 1; HD, n = 1; IM, n = 4) that showed a B95–8-like DNA sequence pattern in both viral genes. Group 2 isolates (HD, n = 1; AILD, n = B-NHL, n = 1; tonsils of EBV-seropositive children, n = 9; IM, n = 20 showed a nucleotide change at position 49095 in the EBNA-2 gene, leading to an amino acid substitution (Pro-->Ser), and EBV type-2 sequences in the EBER region. EBV type-1 isolates that fall into group 3 (AILD, n = 3; HD, n = 1; B- NHL, n = 4; gastric carcinoma, n = 2; IM, n = 6; severe chronic active EBV infection, n = 1) were characterized by typical nucleotide changes and a 3-bp insertion (CTC; extra Leu residue) in the EBNA-2 gene and an EBV type-2-specific sequence pattern in the EBER region. These EBV type- 1 variant strains may represent the most prevalent circulating EBV type- 1 strains in the exposed population and seem not to be restricted to a certain EBV-associated disease or tumor type. However, analysis of more EBV isolates from benign and malignant lesions must show whether more EBV type-1 substrains exist in vivo.

Characterization of the Epstein–Barr virus BRRF1 gene, located between early genes BZLF1 and BRLF1

Microbiology ◽  
2000 ◽  
Vol 81 (7) ◽  
pp. 1791-1799 ◽  
Author(s):  
Carine Segouffin-Cariou ◽  
Géraldine Farjot ◽  
Alain Sergeant ◽  
Henri Gruffat
Keyword(s):  
Transcriptional Activation ◽  
Binding Sites ◽  
Epstein Barr Virus ◽  
Regulatory Elements ◽  
Barr Virus ◽  
Viral Genes ◽  
Epstein Barr

The switch from latency to a productive cycle in Epstein–Barr virus (EBV)-infected B cells proliferating in vitro is thought to be due to the transcriptional activation of two viral genes, BZLF1 and BRLF1, encoding two transcription factors called EB1 and R respectively. However, a third gene, BRRF1 is contained in the BZLF1/BRLF1 locus, overlapping with BRLF1 but in inverse orientation. We have characterized the 5′ end of the BRRF1 mRNA and the promoter, PNa, at which BRRF1 pre-mRNA is initiated. We show that although a single BRRF1 mRNA species is induced by 12-O-tetradecanoylphorbol 13-acetate/sodium butyrate in several EBV-infected B cell lines, in Akata cells treated with anti-IgG two BRRF1 mRNAs can be detected. Transcription initiated at the BRRF1 promoter was activated by EB1 but not by R, and EB1-binding sites which contribute to the EB1-activated transcription have been mapped to between positions −469 and +1. A 34 kDa protein could be translated from the BRRF1 mRNA both in vitro and in vivo, and was found predominantly in the nucleus of HeLa cells transfected with a BRRF1 expression vector. Thus there are three promoters in the region of the EBV chromatin containing the BZLF1/BRLF1 genes, two of which, PZ and PNa, potentially share regulatory elements.

Characterization of Epstein-Barr virus gp350/220 gene variants in virus isolates from gastric carcinoma and nasopharyngeal carcinoma

2011 ◽  
Vol 157 (2) ◽  
pp. 207-216 ◽  
Author(s):  
Bing Luo ◽  
Mengyang Liu ◽  
Yan Chao ◽  
Yun Wang ◽  
Yongzheng Jing ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Gastric Carcinoma ◽  
Epstein Barr Virus ◽  
Gene Variants ◽  
Barr Virus ◽  
Epstein Barr ◽  
Virus Isolates

Characterization of an Epstein-Barr virus-induced thymidine kinase.

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

scholarly journals EBV-LMP1 promotes radioresistance by inducing protective autophagy through BNIP3 in nasopharyngeal carcinoma

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
San Xu ◽  
Zhuan Zhou ◽  
Xingzhi Peng ◽  
Xuxiu Tao ◽  
Peijun Zhou ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Crucial Role ◽  
Epstein Barr Virus ◽  
Interacting Protein ◽  
Multiple Tumors ◽  
Barr Virus ◽  
Signaling Axis ◽  
Epstein Barr ◽  
Adenovirus E1b

AbstractStudies have indicated that dysfunction of autophagy is involved in the initiation and progression of multiple tumors and their chemoradiotherapy. Epstein–Barr virus (EBV) is a lymphotropic human gamma herpes virus that has been implicated in the pathogenesis of nasopharyngeal carcinoma (NPC). EBV encoded latent membrane protein1 (LMP1) exhibits the properties of a classical oncoprotein. In previous studies, we experimentally demonstrated that LMP1 could increase the radioresistance of NPC. However, how LMP1 contributes to the radioresistance in NPC is still not clear. In the present study, we found that LMP1 could enhance autophagy by upregulating the expression of BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3). Knockdown of BNIP3 could increase the apoptosis and decrease the radioresistance mediated by protective autophagy in LMP1-positive NPC cells. The data showed that increased BNIP3 expression is mediated by LMP1 through the ERK/HIF1α signaling axis, and LMP1 promotes the binding of BNIP3 to Beclin1 and competitively reduces the binding of Bcl-2 to Beclin1, thus upregulating autophagy. Furthermore, knockdown of BNIP3 can reduce the radioresistance promoted by protective autophagy in vivo. These data clearly indicated that, through BNIP3, LMP1 induced autophagy, which has a crucial role in the protection of LMP1-positive NPC cells against irradiation. It provides a new basis and potential target for elucidating LMP1-mediated radioresistance.

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