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Who found some new mechanisms of HBV virulence?

February 22, 2008

This dreadful HBV is small in size. The genome of this virus is a partial double stranded circle. When made fully double stranded, this genome carries about 3000 base pairs, compared to 200 kilo base pairs of the genome of the smallpox virus. These 3000 base pairs encode an envelope protein, a core protein, a polymerase essential for virus replication and a very special X protein, named such because its function was not known when it was named.

A research article to be published on January 28, 2008 in the World Journal of Gastroenterology addresses this question. Dr Kremsdorf and her associates have been trying to elucidate some of the functions of this X protein involved in liver pathogenesis during HBV infection. They first established a system in which the gene for X protein is permanently incorporated into mouse genome. With transgenic mice expressing X protein, they could research many different impacts of the protein on the host.

Their first exciting discovery was the inhibition of liver cell proliferation by X protein. This discovery raised a novel mechanism on how HBV causes liver diseases. Recently, the team further investigated how X protein inhibited the liver cell proliferation. These groundbreaking discoveries were published in the January 28 issue of the World Journal of Gastroenterology. In this report, Dr Kremsdorf et al looked at the expression level of 5376 genes in the transgenic mice. This seemingly daunting work was made possible when Dr Kremsdorf took advantage of the DNA microarray technique, which allowed simultaneous analysis of all 5376 genes. Their results indicated a decreased activity of those genes required for gene transcription and cholesterol metabolic pathway. This not only confirmed the previous observation, but showed how the molecular mechanism of how Hepatitis B virus X protein inhibits the liver regeneration.

These new discoveries should improve our knowledge of the implication of the viral proteins in the pathogenesis of HBV infection. This should allow participation in the design of new and more effective treatments for HBV patients.
-end-
Reference: Sidorkiewicz M, Jais JP, Tralhao G, Morosan S, Giannini C, Brezillon N, Soussan P, Delpuech O, Kremsdorf D. Gene modulation associated with inhibition of liver regeneration in hepatitis B virus X transgenic mice. World J Gastroenterol 2008; 14(4): 574-581
http://www.wjgnet.com/1007-9327/14/574.asp

Correspondence to: Dina Kremsdorf, INSERM (Institut National de la Sante et de la Recherche Medicale) U845, CHU Necker; 156 Rue de Vaugirard, Paris 75015, France. kremsdor@necker.fr
Telephone: +33-1-40615343 Fax: +33-1-40615581

About World Journal of Gastroenterology

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

World Journal of Gastroenterology

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