Viral resistance in hepatitis B: Prevalence and management

被引：12

作者：

Poordad F. ^{[1
,2
]}

Chee G.M. ^{[2
]}

机构：

[1] David Geffen School of Medicine at UCLA, Hepatology and Liver Transplantation, Cedars-Sinai Medical Center, Los Angeles, CA 90048

[2] Hepatology and Liver Transplantation, Cedars-Sinai Medical Center, Los Angeles, CA 90048

来源：

Current Gastroenterology Reports | 2010年 / 12卷 / 1期

关键词：

Genotypic mutation; Genotypic resistance; Hepatitis B; Nucleoside analog; Phenotypic resistance;

D O I：

10.1007/s11894-009-0088-1

中图分类号：

学科分类号：

摘要：

Hepatitis B is a DNA virus affecting hundreds of millions of individuals worldwide. As the clinical sequelae of cirrhosis and hepatocellular cancer are increasingly recognized to be related to viral levels, the impetus increases to offer treatment to those previously not treated. With the development of more robust antivirals with reasonable safety profiles, long-term treatment is becoming more common. The oral nucleos(t)ide analogs have become the preferred first-line therapies for most genotypes of hepatitis B. Five are now available, all with different potencies and resistance profiles. Long-term data spanning several years are now available for most compounds in this arena. This article focuses on the common natural variants and those secondary to nucleos(t)ide therapy, as well as diagnostic methods to detect resistance. © 2010 Springer Science+Business Media, LLC.

引用

页码：62 / 69

页数：7

共 32 条

[1]

Myers R., Clark C., Khan A., Kellam P., Tedder R., Genotyping hepatitis B virus from whole- and sub-genomic fragments using position-specific scoring matrices in HBV STAR, Journal of General Virology, 87, 6, pp. 1459-1464, (2006)

[2]

Schaefer S., Hepatitis B virus taxonomy and hepatitis B virus genotypes, World J Gastroenterol, 13, pp. 14-21, (2007)

[3]

Demeyer S., Gong J.Z., Suwandhi W., Et al., Organ and species specificity of hepatitis B virus (HBV) infection: A review of literature with a special reference to preferential attachment of HBV to human hepatocytes, J Viral Hepatol, 4, pp. 145-153, (1997)

[4]

Zoulim F., Saputelli J., Seeger C., Woodchuck hepatitis virus X protein is required for viral infection in vivo, J Virol, 68, pp. 2026-2030, (1994)

[5]

Takada S., Tsuchida N., Kobayashi M., Et al., Disruption of the function of tumor-suppressor gene p53 by the hepatitis B virus X protein and hepatocarcinogenesis, J Cancer Res Clin Oncol, 121, pp. 593-601, (1995)

[6]

Gunther S., Fischer L., Pult I., Et al., Naturally occurring variants of hepatitis B virus, Adv Virus Res, 52, pp. 25-137, (1999)

[7]

Lok A.S., McMahon B.J., Chronic hepatitis B: Update 2009, Hepatology, 50, pp. 661-662, (2009)

[8]

Zheng Y., Li J., Ou J.-H., Regulation of hepatitis B virus core promoter by transcription factors HNF1 and HNF4 and the viral X protein, Journal of Virology, 78, 13, pp. 6908-6914, (2004)

[9]

Yang H.I., Yeh S.H., Chen P.J., Et al., Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma, J Natl Cancer Inst, 100, pp. 1134-1143, (2008)

[10]

Grottola A., Buttafoco P., Del Buono M.G., Cremonini C., Colantoni A., Gelmini R., Morelli C., Masetti M., Jovine E., Fruet F., Pinna A., Manenti F., Villa E., Pretransplantation pre-S2 and S protein heterogeneity predisposes to hepatitis B virus recurrence after liver transplantation, Liver Transplantation, 8, 5, pp. 443-448, (2002)

← 1 2 3 4 →