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发表于 2009-7-17 00:10
新的一篇关于抑制cccdna的文章。
这个文章看上去只是综述性质的,而不是提供新的研究结果。
哪位网友能找到原文帮忙发上来,大家看看?谢谢了
Control of cccDNA function in hepatitis B virus infection
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Massimo Levrero1, 2, 3, , , , Teresa Pollicino4, Jorg Petersen5, Lucia Belloni6, Giovanni Raimondo4 and Maura Dandri7
1Department of Internal Medicine, Sapienza University of Rome, Policlinico Umberto I, Viale del Policlinico 155, 0061 Rome, Italy
2Oncogenomic Center, Andrea Cesalpino Foundation, Laboratory of Gene Expression, Regina Elena Cancer Institute, Rome, Italy
3Laboratory of Gene Expression, Cenci Bolognetti Foundation, Sapienza University, Rome, Italy
4Department of Internal Medicine, Unit of Clinical and Molecular Hepatology, University Hospital of Messina, Messina, Italy
5Liver Centre Hamburg, IFI Institute for Interdisciplinary Medicine at Asclepius Klinik S. Georg, Hamburg, Germany
6Department of Gene Expression, Sapienza University of Rome, Rome, Italy
7Department of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Associate Editor: F. Zoulim. Available online 10 June 2009.
The template of hepatitis B virus (HBV) transcription, the covalently closed circular DNA (cccDNA), plays a key role in the life-cycle of the virus and permits the persistence of infection. Novel molecular techniques have opened new possibilities to investigate the organization and the activity of the cccDNA minichromosome in vivo, and recent advances have started to shed light on the complexity of the mechanisms controlling cccDNA function. Nuclear cccDNA accumulates in hepatocyte nuclei as a stable minichromosome organized by histone and non-histone viral and cellular proteins. Identification of the molecular mechanisms regulating cccDNA stability and its transcriptional activity at the RNA, DNA and epigenetic levels in the course of chronic hepatitis B (CH-B) infection may reveal new potential therapeutic targets for anti-HBV drugs and hence assist in the design of strategies aimed at silencing and eventually depleting the cccDNA reservoir. Infection with hepatitis B virus (HBV) continues to be a major health problem with about 400 million people chronically infected worldwide who are at high risk of developing liver cirrhosis and hepatocellular carcinoma (HCC) [Shepard CW, Simard EP, Finelli L, Fiore AE, Bell BP. Hepatitis B virus infection: epidemiology and vaccination. Epidemiol Rev 2006;28:112–25]. HBV is a member of the Hepadnaviridae family, that includes small enveloped DNA viruses infecting primates, rodents, and birds. One common characteristic of these viruses is their high species and cell-type specificity, as well as a unique genomic organization and replication mechanism.
Keywords: Hepatitis B virus; Covalently closed circular DNA; Chronic hepatitis B infection; cccDNA function
Abbreviations: HBV, hepatitis B virus; CH-B, chronic hepatitis B; HCC, hepatocellular carcinoma; RC, relaxed circular; PF-RC DNA, protein free relaxed circular; cccDNA, covalently closed circular DNA; NHEJ, nonhomologous end joining; DLS, double-stranded linear (DSL); pgRNA, pregenomic RNA; LS, viral large surface protein; ChIP, chromatin immuno-precipitation
Article Outline
1. cccDNA and HBV replication
2. Control of cccDNA pool in hepadnavirus infection
3. Structure of the cccDNA minichromosome
4. cccDNA quantification and activity in HBV chronic carriers
5. Factors regulating cccDNA activity
5.1. Immune-mediated factors
5.2. Virological factors
5.3. Epigenetic factors
6. cccDNA is “suppressed” in occult hepatitis B
7. Conclusions
8. Uncited reference
Acknowledgements
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