scholarly journals Association of hepatitis B virus mutations in basal core promoter and precore regions with severity of liver disease: an investigation of 793 Chinese patients with mild and severe chronic hepatitis B and acute-on-chronic liver failure

2010 ◽  
Vol 46 (3) ◽  
pp. 391-400 ◽  
Author(s):  
Zhihui Xu ◽  
Xiaoqiang Ren ◽  
Yan Liu ◽  
Xiaodong Li ◽  
Siyu Bai ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Liver Disease ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Chinese Patients ◽  
Basal Core Promoter ◽  
Chronic Liver Failure ◽  
B Virus ◽  
Severe Chronic Hepatitis

T1762/A1764variants of the basal core promoter of hepatitis B virus; serological and clinical correlations in Chinese patients

1999 ◽  
Vol 19 (5) ◽  
pp. 411-417 ◽  
Author(s):  
Jinlin Hou ◽  
George K. K. Lau ◽  
Jinjun Cheng ◽  
Chi Chung Cheng ◽  
Kangxian Luo ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Chinese Patients ◽  
Basal Core Promoter ◽  
B Virus ◽  
Clinical Correlations

scholarly journals Effects of Hepatitis B Virus Mutations on its Replication and Liver Disease Severity

2013 ◽  
Vol 7 (1) ◽  
pp. 12-18 ◽  
Author(s):  
Abdulrahim Hakami ◽  
Abdelwahid Ali ◽  
Ahmed Hakami
Keyword(s):  
Liver Disease ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Disease Severity ◽  
Chronic Infection ◽  
Core Promoter ◽  
Basal Core Promoter ◽  
Double Mutation ◽  
B Virus ◽  
Genotype C

Hepatitis B virus (HBV), nowadays, is one of the major human pathogens worldwide. Approximately, 400 million people worldwide have chronic HBV infection. Only 5% of persons infected during adulthood develop chronic infection. The reverse is true for those infected at birth or in early childhood, i.e. more than 90% of these persons progress to chronic infection. Currently, eight different genotypes o f HBV have been identified, differing in nucleotide sequence by greater than 8%. In addition, numerous subgenotypes have a l s o been recognized based on the nucleotide sequence variability of 4- 8%. It has invariably been found that these genotypes and mutations play a pivotal role in the liver disease aggravation and virus replication. The precore mutations (G1896A) and the double mutation (T1762/A1764) in the basal core promoter are important mutations that alter expression of the hepatitis B e antigen (HBeAg). The HBeAg is important for establishing viral persistence. The precore G1896A mutation abrogates the expression of HBeAg. Numerous other mutations alter the disease severity and progression. It is predictive that the infected patient has high risk of hepatocellular carcinoma if the genotype C is incriminated or if HBV possesses basal core promoter double mutation. Association of the remaining genotypes have been noted but with less degree than genotype C. Phenotypic assays of the different HBV protein markers with different molecular techniques illustrate the replication efficiency of the virus in cell lines. This review will discuss various mutations into their association with liver disease severity and progression as well as virus replication.

scholarly journals Specific mutations of basal core promoter are associated with chronic liver disease in hepatitis B virus subgenotype D1 prevalent in Turkey

2013 ◽  
Vol 57 (2) ◽  
pp. 122-129 ◽  
Author(s):  
Mustafa Sunbul ◽  
Masaya Sugiyama ◽  
Fuat Kurbanov ◽  
Hakan Leblebicioglu ◽  
Anis Khan ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Liver Disease ◽  
Core Promoter ◽  
Chronic Liver ◽  
Basal Core Promoter ◽  
B Virus

scholarly journals Basal Core Promoter and Precore Mutations in the Hepatitis B Virus Genome Enhance Replication Efficacy of Lamivudine-Resistant Mutants

2004 ◽  
Vol 78 (16) ◽  
pp. 8524-8535 ◽  
Author(s):  
Frank Tacke ◽  
Christina Gehrke ◽  
Tom Luedde ◽  
Albert Heim ◽  
Michael P. Manns ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Virus Replication ◽  
Drug Sensitivity ◽  
Core Promoter ◽  
Basal Core Promoter ◽  
B Virus ◽  
Resistant Mutants

ABSTRACT During chronic hepatitis B virus (HBV) infection, mutations in the precore (PC) or basal core promoter (BCP) region affecting HBV e antigen (HBeAg) expression occur commonly and represent the predominant virus species in patients with HBeAg-negative chronic hepatitis B. The PC mutation (G1896A+C1858T) creates a translational stop codon resulting in absent HBeAg expression, whereas BCP mutations (A1762T/G1764A) reduce HBeAg expression by transcriptional mechanisms. Treatment of chronic HBV infection with lamivudine (LMV) often selects drug-resistant strains with single (rtM204I) or double (rtL180M+rtM204V) point mutations in the YMDD motif of HBV reverse transcriptase. We cloned replication-competent HBV vectors (genotype A, adw2) combining mutations in the core (wild type [wt], PC, and BCP) and polymerase gene (wt, rtM204I, and rtL180M/M204V) and analyzed virus replication and drug sensitivity in vitro. Resistance to LMV (rtM204I/rtL180M+rtM204V) was accompanied by a reduced replication efficacy as evidenced by reduced pregenomic RNA, encapsidated progeny DNA, polymerase activity, and virion release. PC mutations alone did not alter virus replication but restored replication efficacy of the LMV-resistant mutants without affecting drug resistance. BCP mutants had higher replication capacities than did the wt, also in combination with LMV resistance mutations. All nine HBV constructs showed similar sensitivities to adefovir. In conclusion, BCP-PC mutations directly impact the replication capacity of LMV-resistant mutants. PC mutations compensated for replication inefficiency of LMV-resistant mutants, whereas BCP mutations increased viral replication levels to above the wt baseline values, even in LMV-resistant mutants, without affecting drug sensitivity in vitro. Adefovir may be an effective treatment when combinations of core and polymerase mutations occur.

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