Hepatitis B Virus (HBV) Genotype: A Significant Risk Factor in Determining which Patients with Chronic HBV Infection should Undergo Surveillance for Hepatocellular Carcinoma: The Hepatitis B Alaska (HEP‐B‐AK) Study

Hepatology ◽  
2021 ◽  
Author(s):  
Brian J McMahon ◽  
Solu Nolen ◽  
Mary Snowball ◽  
Chriss Homan ◽  
Susan Negus ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
Hbv Genotype ◽  
Chronic Hbv Infection ◽  
B Virus ◽  
Chronic Hbv ◽  
Hep B ◽  
Genotype A

scholarly journals Association of STAT3 and STAT4 polymorphisms with susceptibility to chronic hepatitis B virus infection and risk of hepatocellular carcinoma: a meta-analysis

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Han Shi ◽  
Hongyan He ◽  
Suvash Chandra Ojha ◽  
Changfeng Sun ◽  
Juan Fu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Chronic Hepatitis ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Meta Analysis ◽  
Hbv Infection ◽  
Chronic Hbv Infection ◽  
B Virus ◽  
Chronic Hbv

Abstract Background: It has been reported that polymorphisms of signal transducer and activator of transcription (STAT) 3 and STAT4 might be associated with susceptibility to hepatitis B virus (HBV) infection and risk of chronic hepatocellular carcinoma (HCC). Owing to limitation of sample size and inconclusive results, we conducted a meta-analysis to clarify the association. Methods: We identified relevant studies by a systematic search of Medline/PubMed, Embase, Web of Science and the Cochrane Library up to 20 February 2019. The strength of the association measured by odds ratios (OR) with 95% confidence intervals (CIs) was studied. All the statistical analyses were conducted based on Review Manager 5.3 software. Results: A total of 5242 cases and 2717 controls from five studies were included for the STAT3 polymorphism, 5902 cases and 7867 controls from nine studies for the STAT4 polymorphism. Our results suggested that STAT3 rs1053004 polymorphism was a significant risk factor of chronic HBV infection (C vs. T: OR = 1.17, 95% CI: 1.07–1.29, PA=0.0007; CC + CT vs. TT: OR = 1.38, 95% CI: 1.09–1.76, PA=0.008). Validation with all the genetic models revealed that rs7574865 polymorphism of STAT4 gene was closely associated with chronic HBV infection (PA<0.01) and chronic hepatitis B (CHB)-related HCC (PA<0.05). Meanwhile, the authenticity of the above meta-analysis results was confirmed by trial sequential analysis (TSA). Conclusions: The meta-analysis showed that STAT3 rs1053004 polymorphism may be the risk for developing chronic HBV infection but not associated with HCC. The present study also indicates that STAT4 rs7574865 polymorphism increased the risk of chronic HBV infection and HCC.

scholarly journals Impact of Hepatitis B Virus (HBV) X Gene Mutations on Hepatocellular Carcinoma Development in Chronic HBV Infection

2013 ◽  
Vol 20 (1) ◽  
pp. 127-127 ◽  
Author(s):  
Jong-Han Lee ◽  
Kwang-Hyub Han ◽  
Jae Myun Lee ◽  
Jeon Han Park ◽  
Hyon-Suk Kim
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Gene Mutations ◽  
Hbv Infection ◽  
Chronic Hbv Infection ◽  
B Virus ◽  
Chronic Hbv ◽  
X Gene

Hepatitis B Virus

2021 ◽  
Author(s):  
Ming V. Lin ◽  
April Wall
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Infection ◽  
Treatment Options ◽  
Hbv Infection ◽  
Chronic Hbv Infection ◽  
Chronic Hepatitis B Virus ◽  
B Virus ◽  
Chronic Hbv

Chronic hepatitis B virus (HBV) infection is a major health burden worldwide, with approximately 257 million people with chronic infection. HBV is a small partially double-stranded DNA virus that replicates within the nucleus of the hepatocyte and commonly leads to chronic infection. Chronic HBV infection can cause cirrhosis, hepatocellular carcinoma, and extrahepatic manifestations such as glomerulonephritis or vasculitis. The latter is due to deposition of circulating immune complex in the different tissues. The natural history of HBV infection can be conceptualized as a spectrum encompassing different phases, including immune tolerance, immune clearance, inactive carrier, and reactivation and resolution. The diagnosis of the different phases of chronic HBV infection relies on various HBV serologies, liver enzyme levels, and histology findings. There are currently eight therapies approved for the treatment of HBV. Tenofovir alafenamide was the most recently approved therapy with a better side effect profile compared with tenofovir disoproxil fumarate. With the recent advances in the basic research in hepatitis B, new treatment options may become available in the near-future. This review contains 9 figures, 11 tables and 80 references Key words: cirrhosis, entecavir, Hepadnaviridae, hepatitis B virus, hepatocellular carcinoma, precore mutation, tenofovir

Hepatitis B Virus

2021 ◽  
Author(s):  
Ming V. Lin ◽  
April Wall
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Infection ◽  
Treatment Options ◽  
Hbv Infection ◽  
Chronic Hbv Infection ◽  
Chronic Hepatitis B Virus ◽  
B Virus ◽  
Chronic Hbv

Chronic hepatitis B virus (HBV) infection is a major health burden worldwide, with approximately 257 million people with chronic infection. HBV is a small partially double-stranded DNA virus that replicates within the nucleus of the hepatocyte and commonly leads to chronic infection. Chronic HBV infection can cause cirrhosis, hepatocellular carcinoma, and extrahepatic manifestations such as glomerulonephritis or vasculitis. The latter is due to deposition of circulating immune complex in the different tissues. The natural history of HBV infection can be conceptualized as a spectrum encompassing different phases, including immune tolerance, immune clearance, inactive carrier, and reactivation and resolution. The diagnosis of the different phases of chronic HBV infection relies on various HBV serologies, liver enzyme levels, and histology findings. There are currently eight therapies approved for the treatment of HBV. Tenofovir alafenamide was the most recently approved therapy with a better side effect profile compared with tenofovir disoproxil fumarate. With the recent advances in the basic research in hepatitis B, new treatment options may become available in the near-future. This review contains 9 figures, 11 tables and 80 references Key words: cirrhosis, entecavir, Hepadnaviridae, hepatitis B virus, hepatocellular carcinoma, precore mutation, tenofovir

scholarly journals Enhancers and attenuators of risk associations of chronic hepatitis B virus infection with hepatocellular carcinoma in type 2 diabetes

2012 ◽  
Vol 20 (2) ◽  
pp. 161-171 ◽  
Author(s):  
Xilin Yang ◽  
Ying Wang ◽  
Andrea O Y Luk ◽  
Wing Yee So ◽  
Ronald C W Ma ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Type 2 Diabetes ◽  
Hepatitis B ◽  
Hbv Infection ◽  
Promoting Effect ◽  
Chronic Hbv Infection ◽  
Chronic Hepatitis B Virus ◽  
B Virus ◽  
Chronic Hbv

Chronic hepatitis B virus (HBV) infection promotes hepatocellular carcinoma (HCC) risk. In type 2 diabetes (T2D), use of insulin and statins was associated with reduced cancer risk while co-presence of low LDL cholesterol (LDLC <2.8 mmol/l) plus low triglyceride (TG; <1.7 mmol/l) increased cancer risk. There is experimental evidence showing that insulin insufficiency might promote HCC. In this study, we examined whether this lipid subphenotype and use of insulin or statins might modify the promoting effect of chronic HBV infection (indicated by the presence of hepatitis B surface antigen) on HCC. We analyzed data of 1319 T2D patients enrolled into the Hong Kong Diabetes Registry from December 1996 to January 2005 and followed up to 2005. Additive interaction was estimated using relative excess risk due to interaction and attributable proportion due to interaction. During 5782 person-years of follow-up, 1.74% (n=23) of patients developed HCC (incidence, 3.98; 95% confidence interval, 2.36–5.60/1000 person-years). HbA1c ≥7.0% and the lipid phenotype (LDLC <2.8 mmol/l plus TG <1.7 mmol/l) increased the hazard ratios (HRs) of chronic HBV infection for HCC from 3.74 to 74.96 and from 11.01 to 89.82 respectively with significant interactions. Use of insulin or statins decreased the HRs from 37.51 to 5.87 and from 64.94 to 16.99 respectively with significant interactions (allPvalues <0.05). These findings support our hypothesis that hyperglycemia and co-presence of low LDLC plus low TG might enhance, while insulin or statin usage might attenuate the promoting effect of chronic HBV infection on HCC in T2D.

scholarly journals Progress of research on the immune tolerance of chronic HBV infection

2018 ◽  
Vol 7 (3) ◽  
pp. 88-93
Author(s):  
Xuemei Li ◽  
Xiaoxia Li
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Immune Tolerance ◽  
The Body ◽  
Hbv Infection ◽  
Research Progress ◽  
Hbv Genotype ◽  
Chronic Hbv Infection ◽  
B Virus ◽  
Chronic Hbv

Abstract Immune tolerance is a specific lack or negative response of T and B lymphocytes to antigen. According to different formation periods, immune tolerance can be divided into central and peripheral tolerances. The immune tolerance of the body to hepatitis B virus (HBV) after infection is the main cause of chronic HBV infection. In this paper, the functional defects of hepatitis B virus e antigen and dendritic cells, hyporesponsiveness of cytotoxic T lymphocyte, variation of helper T lymphocytes and cytokines, HBV genotype and genome, and the role of host gene polymorphism in the formation of immune tolerance in chronic HBV infection and its related research progress are introduced briefly.

scholarly journals Impact of Hepatitis B Virus (HBV) X Gene Mutations on Hepatocellular Carcinoma Development in Chronic HBV Infection

2011 ◽  
Vol 18 (6) ◽  
pp. 914-921 ◽  
Author(s):  
Jong-Han Lee ◽  
Kwang-Hyub Han ◽  
Jae Myun Lee ◽  
Jeon Han Park ◽  
Hyon-Suk Kim
Keyword(s):  
Hepatocellular Carcinoma ◽  
Risk Factor ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hbv Infection ◽  
Regulatory Pathways ◽  
Chronic Hbv Infection ◽  
B Virus ◽  
Chronic Hbv ◽  
The Impact

ABSTRACTThe hepatitis B virus (HBV) PreS mutations C1653T, T1753V, and A1762T/G1764A were reported as a strong risk factor of hepatocellular carcinoma (HCC) in a meta-analysis. HBV core promoter overlaps partially with HBx coding sequence, so the nucleotide 1762 and 1764 mutations induce HBV X protein (HBx) 130 and 131 substitutions. We sought to elucidate the impact of HBx mutations on HCC development. Chronically HBV-infected patients were enrolled in this study: 42 chronic hepatitis B (CHB) patients, 23 liver cirrhosis (LC) patients, and 31 HCC patients. Direct sequencing showed HBx131, HBx130, HBx5, HBx94, and HBx38 amino acid mutations were common in HCC patients. Of various mutations, HBx130+HBx131 (double) mutations and HBx5+HBx130+HBx131 (triple) mutations were significantly high in HCC patients. Double and triple mutations increased the risk for HCC by 3.75-fold (95% confidence interval [CI] = 1.101 to 12.768,P= 0.033) and 5.34-fold (95% CI = 1.65 to 17.309,P= 0.005), respectively, when HCC patients were compared to CHB patients. Functionally, there were significantly higher levels of NF-κB activity in cells with the HBx5 mutant and with the double mutants than that of wild-type cells and the triple-mutant cells. The triple mutation did not increase NF-κB activity. Other regulatory pathways seem to exist for NF-κB activation. In conclusion, a specific HBx mutation may contribute to HCC development by activating NF-κB activity. The HBx5 mutation in genotype C2 HBV appears to be a risk factor for the development of HCC and may be used to predict the clinical outcomes of patients with chronic HBV infection.

Hepatitis B Virus

2021 ◽  
Author(s):  
Ming V. Lin ◽  
April Wall
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Infection ◽  
Treatment Options ◽  
Hbv Infection ◽  
Chronic Hbv Infection ◽  
Chronic Hepatitis B Virus ◽  
B Virus ◽  
Chronic Hbv

Chronic hepatitis B virus (HBV) infection is a major health burden worldwide, with approximately 257 million people with chronic infection. HBV is a small partially double-stranded DNA virus that replicates within the nucleus of the hepatocyte and commonly leads to chronic infection. Chronic HBV infection can cause cirrhosis, hepatocellular carcinoma, and extrahepatic manifestations such as glomerulonephritis or vasculitis. The latter is due to deposition of circulating immune complex in the different tissues. The natural history of HBV infection can be conceptualized as a spectrum encompassing different phases, including immune tolerance, immune clearance, inactive carrier, and reactivation and resolution. The diagnosis of the different phases of chronic HBV infection relies on various HBV serologies, liver enzyme levels, and histology findings. There are currently eight therapies approved for the treatment of HBV. Tenofovir alafenamide was the most recently approved therapy with a better side effect profile compared with tenofovir disoproxil fumarate. With the recent advances in the basic research in hepatitis B, new treatment options may become available in the near-future. This review contains 9 figures, 11 tables and 80 references Key words: cirrhosis, entecavir, Hepadnaviridae, hepatitis B virus, hepatocellular carcinoma, precore mutation, tenofovir

scholarly journals Hepatitis B Virus Demethylates PD-1 and Modulates the Changes of the Tumor Microenvironment in Hepatocellular Carcinoma Patients

2021 ◽  
Author(s):  
Weiguang Lian ◽  
Ruixue Lai ◽  
Jianhua Wu ◽  
Jingjing Zhang ◽  
Shengchao Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Dna Methylation ◽  
T Cells ◽  
Hepatitis B Virus ◽  
Tumor Microenvironment ◽  
Hepatitis B ◽  
Hbv Infection ◽  
Chronic Hbv Infection ◽  
B Virus ◽  
Chronic Hbv

Abstract Background: Hepatitis B virus (HBV) constitutes a major global health burden. Previously study has found the expression of programmed cell death 1 (PD-1) is up-regulated during the chronic HBV infection. However, the mechanism of how HBV infection modulates the expression of PD-1 on CD8+T cells are not well understood. In the present study, we aimed to analyzed the role of DNA methylation in regulating the expression of PD-1 on CD8+T cells during HBV infection, we also aimed to evaluate the HBV induced changes of tumor microenvironment (TME).Methods: The methylation microarray was used to assess the profile changes of gene methylation upon chronic HBV infection. CD8+T cells were separated from peripheral blood of health volunteers and HCC patients including HBV related HCC (HBV-HCC) and non-viral HCC. The immune microenvironments of hepatocellular carcinoma (HCC) was interrogated by using Immunofluorescence staining. The PD-1 expression of CD8+T cells from peripheral blood were examined by western blot and flow cytometry. T cells function was determined by cytokine measurement. Sequenom MassARRAY platform was used to detected the DNA methylation status of PD-1 promoter.Results: HBV could drive 413 genes methylated while 3,023 genes including PD-1 demethylated, the reduced PD-1 expression and increased PD-1 demethylation was proved in HBV-HCC tissue. The subsequent analysis indicate that the expression of PD-1 differed by stages of HBV infection, it reduced on the cell membrane of HBV-transfected CD8+T cells upon transient HBV plasmid transfection which might mimic acute HBV infection, while upregulated on the HBV specific CD8+T cells by demethylation during chronic HBV infection. Interferon-gamma increased in the medium of HBV transfected CD8+T cells and interleukin-10 increased in the blood of chronic HBV infection patients. Increased tumor associated macrophage (TAM) cells and T regulatory cells (Tregs) invasion was identified in HBV-HCC tissue when compared with those from non-viral HCC tissue Conclusion: Our data suggested that the expression of PD-1 varies upon the stage of HBV infection, chronic HBV infection could drove the TME more immunosuppressive through PD-1 demethylation related CD8+T cells exhaustion as well as promotion of invaded Treg and TAM cells thereby to attenuating therapy of immune checkpoint inhibitors.

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