Chemical carcinogen epstein-barr virus (ebv) synergism: Ebv genome amplification and site-specific mutation during transformation

1989 ◽  
Vol 43 (1) ◽  
pp. 72-79 ◽  
Author(s):  
Earl E. Henderson ◽  
Carol Franks ◽  
Gerald Fronko
2007 ◽  
Vol 88 (9) ◽  
pp. 2463-2472 ◽  
Author(s):  
Ya-Fang Chiu ◽  
Chao-Ping Tung ◽  
Yu-Hisu Lee ◽  
Wen-Hung Wang ◽  
Ching Li ◽  
...  

A mutant library of 249 mutants with mutations that span the entire Epstein–Barr virus (EBV) genome was generated by transposition with EZ : : TN <KAN-2> and insertion with an apramycin resistance gene by a PCR-targeting method. This study also demonstrates the feasibility of generating deletions and site-specific mutations in the BRLF1 promoter on the EBV genome to determine the regions in the promoter that are crucial to transcription. Analysing BZLF1 and BRLF1 mutants by microarray analysis revealed that these two genes regulate the transcription of EBV lytic genes differently. A BZLF1 mutation affects global expression of EBV lytic genes; almost no lytic gene is expressed by the mutant after lytic induction. However, although a BRLF1 mutant still transcribes most lytic genes, the expression of these lytic genes is inefficient. Furthermore, this study shows that the proximal Zta-response element in the BRLF1 promoter is crucial to BRLF1 transcription from the EBV genome, despite the fact that another work demonstrated that this site was unimportant in transient transfection analysis. Furthermore, mutants with a mutation in BDLF1 and BORF1 cannot assemble viral capsids. Results of this study demonstrate the usefulness of a comprehensive mutant library in genetic analyses of EBV.


1998 ◽  
Vol 89 (5) ◽  
pp. 510-515 ◽  
Author(s):  
Shizuo Kojya ◽  
Tetsuo Itokazu ◽  
Yutaka Noda ◽  
Mitsuhiko Ezaki ◽  
Yasuhiko Tomita ◽  
...  

2001 ◽  
Vol 75 (6) ◽  
pp. 3010-3015 ◽  
Author(s):  
Baozhong Xin ◽  
Zhimin He ◽  
Xinhai Yang ◽  
Ching-Ping Chan ◽  
Mun-Hon Ng ◽  
...  

ABSTRACT Mutation analysis of latent membrane protein 1 (LMP1) in Epstein-Barr virus (EBV)-induced B-cell immortalization revealed two transformation effector sites, TES1 and TES2. TES2 mediates the interaction with tumor necrosis factor receptor-associated death domain protein (TRADD) and plays a key role in transactivating NF-κB and AP-1. Recombinant EBV containing LMP1 with TES2 deleted induces a limited proliferation of B cells. The present study shows that a mutant with an LMP1 site-specific mutation at TES2, LMP1TRADD, initially stimulates cell growth and significantly extends the life span of MEF. However, it is not sufficient for the immortalization of MEF, and MEF-LMP1TRADD cells eventually enter growth arrest. Further analysis reveals that although LMP1TRADDpromotes cell growth, it does not prevent the eventual onset of senescence and the expression of tumor suppressor p16Ink4a.


1998 ◽  
Vol 72 (7) ◽  
pp. 6195-6198 ◽  
Author(s):  
Julie Dyall ◽  
Kenneth I. Berns

ABSTRACT Five site-specific adeno-associated virus integrants generated in a model system with an Epstein-Barr virus- based shuttle vector have been characterized. The results suggest a deletion-substitution mechanism of recombination.


Author(s):  
C. M. Payne ◽  
P. M. Tennican

In the normal peripheral circulation there exists a sub-population of lymphocytes which is ultrastructurally distinct. This lymphocyte is identified under the electron microscope by the presence of cytoplasmic microtubular-like inclusions called parallel tubular arrays (PTA) (Figure 1), and contains Fc-receptors for cytophilic antibody. In this study, lymphocytes containing PTA (PTA-lymphocytes) were quantitated from serial peripheral blood specimens obtained from two patients with Epstein -Barr Virus mononucleosis and two patients with cytomegalovirus mononucleosis. This data was then correlated with the clinical state of the patient.It was determined that both the percentage and absolute number of PTA- lymphocytes was highest during the acute phase of the illness. In follow-up specimens, three of the four patients' absolute lymphocyte count fell to within normal limits before the absolute PTA-lymphocyte count.In one patient who was followed for almost a year, the absolute PTA- lymphocyte count was consistently elevated (Figure 2). The estimation of absolute PTA-lymphocyte counts was determined to be valid after a morphometric analysis of the cellular areas occupied by PTA during the acute and convalescent phases of the disease revealed no statistical differences.


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