The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-β/Smad signaling pathway-Reference-Cited by-同舟云学术

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The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-β/Smad signaling pathway

Published:2018-04-02 Issue:1 Volume:15 Page:
ISSN:1743-422X
Container-title:Virology Journal
language:en
Short-container-title:Virol J

Author:

Wang Meng-Lan,Wu Dong-Bo,Tao Ya-Chao,Chen Lan-Lan,Liu Cui-Ping,Chen En-Qiang,Tang Hong

Funder

National Natural Science Foundation of China

Publisher

Springer Science and Business Media LLC

Subject

Infectious Diseases,Virology

Link

http://link.springer.com/content/pdf/10.1186/s12985-018-0972-0.pdf

Reference18 articles.

1. Sundaram V, Kowdley K. Management of chronic hepatitis B infection. BMJ. 2015;351:h4263.

2. Deng L, Tang H. Hepatitis B virus drug resistance to current nucleos(t)ide analogs: mechanisms and mutation sites. Hepatol Res. 2011;41:1017–24.

3. Terrault NA, Bzowej NH, Chang KM, Hwang JP, Jonas MM, Murad MH. American Association for the Study of liver D: AASLD guidelines for treatment of chronic hepatitis B. Hepatology. 2016;63:261–83.

4. Wang ML, Tang H. Nucleos(t)ide analogues causes HBV S gene mutations and carcinogenesis. Hepatobiliary Pancreat Dis Int. 2016;15:579–86.

5. Warner N, Locarnini S. The antiviral drug selected hepatitis B virus rtA181T/sW172* mutant has a dominant negative secretion defect and alters the typical profile of viral rebound. Hepatology. 2008;48:88–98.

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