Basal core‐promoter mutant of hepatitis B virus and progression of liver disease in hepatitis B e antigen‐negative chronic hepatitis B

Lin, Chih–Lin; Liao, Li‐Ying; Wang, Chaur‐Shine; Chen, Pei‐Jer; Lai, Ming‐Yang; Chen, Ding‐Shinn; Kao, Jia‐Horng

doi:10.1111/j.1478-3231.2005.01041.x

Cited by 73 publications

(58 citation statements)

References 35 publications

(40 reference statements)

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“…HBV precore nucleotide 1,896 mutation from guanine (G) to adenine (A) as well as changes of two nucleotides, an adenine (A) to thymine (T) transversion at nucleotide 1,762 together with a guanine (G) to adenine (A) transition at nucleotide 1,764 within the BCP, lead to a proportion of HBeAg-negative patients who continue to have moderate levels of HBV replication and active liver disease [71][72][73]. Although these mutants can also be found in asymptomatic hepatitis B carriers, the BCP T1762/A1764 mutation has been shown to increase the risk of liver disease progression and HCC development for both genotypes B and C infection [74][75][76][77][78]. In HBV-related acute fulminant hepatitis, universally specific genomic mutational pattern of HBV has not yet been defined.…”

Section: Naturally Occurring Mutantsmentioning

confidence: 99%

Role of viral factors in the natural course and therapy of chronic hepatitis B

Kao

2007

Hepatol Int

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Hepatitis B virus (HBV) infection is a global health problem that causes a wide spectrum of liver disease, including acute or fulminant hepatitis, inactive carrier state, chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). The pathogenesis of hepatocyte damage associated with HBV is mainly through immune-mediated mechanisms. On the basis of the virus and host interactions, the natural history of HBV carriers who are infected in early life can be divided into four dynamic phases. The frequency, extent, and severity of hepatitis flares or acute exacerbation in the second immune clearance and/or fourth reactivation phase predict liver disease progression in HBV carriers. In the past decade, hepatitis B viral factors including serum HBV DNA level, genotype, and naturally occurring mutants predictive of clinical outcomes have been identified. The higher the serum HBV DNA level after the immune clearance phase, the higher the incidence of adverse outcomes over time. In addition, high viral load, genotype C, basal core promoter mutation, and pre-S deletion correlate with increased risk of cirrhosis and HCC development. As to the treatment of chronic hepatitis B, patients with high HBV DNA level and genotype C or D infection are shown to have a worse response to interferon therapy. In conclusion, serum HBV DNA level, genotype, and naturally occurring mutants are identified to influence liver disease progression and therapy of chronic hepatitis B. More investigations are needed to clarify the molecular mechanisms of the viral factors involved in the pathogenesis of each stage of liver disease and the response to antiviral treatments.

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Section: Naturally Occurring Mutantsmentioning

confidence: 99%

Role of viral factors in the natural course and therapy of chronic hepatitis B

Kao

2007

Hepatol Int

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“…In addition to genotype, a pathogenic role has been proposed for the common viral mutants associated with HBeAg-negative CHB. HBeAg-negative disease has been associated with severe and progressive disease; a significant proportion of patients have been found to have established cirrhosis on liver biopsy (Chu et al 2003;Lin et al 2005). The BCP mutation has been identified as a risk factor for cirrhosis (Fattovich et al 1995).…”

Section: Cirrhosismentioning

confidence: 99%

Viral Hepatitis B: Clinical and Epidemiological Characteristics

Burns

Thompson

2014

Cold Spring Harbor Perspectives in Medicine

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“…These changes are associated with alterations in the expression or formation of an oncogene or a tumor suppressor gene (Patil et al, 2009). In addition, several previous studies have also reported associations between genetic polymorphisms and the risk of HCC and/or HBV clearance, e.g., histone deacetylase-10 (HDAC10 ) and secreted phosphoprotein-1 (SPP1) polymorphisms, and interleukin-10 (IL10) haplotypes were also shown to be associated with HBV clearance and/or HCC development (Lin et al, 2005;Park et al, 2007;Shin et al, 2003;Shin et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

“…Continuous HBV infection can cause liver cirrhosis (LC) and hepatocellular carcinoma (HCC) (Lin et al, 2005). HCC is the most widespread and severe form of malignancies that are diagnosed in adults.…”

Section: Introductionmentioning

confidence: 99%

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Putative Association of ITGB1 Haplotype with the Clearance of HBV Infection

Park¹,

Chun²,

Bae³

et al. 2010

Genomics & Informatics

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Integrins are transmembrane receptor proteins that mediate cell-cell adhesion and cell-extracellular matrix (ECM) adhesion. The deregulation of cell-ECM adhesion and the abnormal expression of beta1 (β1) integrins (ITGB1s) are involved in tumor development and metastasis. In the liver, the expression of integrins and ECM proteins can be a cause of hepatocellular carcinoma (HCC) development. We performed direct DNA sequencing of 24 individuals, and identified 23 sequence variants of ITGB1 polymorphisms. Among these 23 variants, 7 common variants were selected based on frequencies and linkage disequilibrium, and then genotyped in a larger-scale group of subjects (n=1,103). The genetic associations of ITGB1 polymorphisms with the clearance of HBV and HCC outcome of HBV patients were analyzed using logistic regression models and Cox relative hazard models. Although there was no significant association observed between the polymorphisms and the HCC outcome of HBV patients, the second most common haplotype (ITGB1 haplotype-2 [C-C-C-C-T-C-T ]) was putatively associated with HBV clearance (OR=0.75, p=0.008 and P corr =0.05). The minor allele frequency (MAF) of ITGB1 haplotype-2 of the spontaneously recovered (SR) group was significantly higher than that of the chronic carrier group (CC) (freq. = 0.248 vs. 0.199). The information derived from this study could be valuable for understanding the genetic factors involved in the clearance of HBV.

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Basal core‐promoter mutant of hepatitis B virus and progression of liver disease in hepatitis B e antigen‐negative chronic hepatitis B

Cited by 73 publications

References 35 publications

Role of viral factors in the natural course and therapy of chronic hepatitis B

Role of viral factors in the natural course and therapy of chronic hepatitis B

Viral Hepatitis B: Clinical and Epidemiological Characteristics

Putative Association of ITGB1 Haplotype with the Clearance of HBV Infection

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