The YMDD and rtA194T Mutations Result in Decreased Replication Capacity in Wild-Type HBV as well as in HBV with Precore and Basal Core Promoter Mutations

2011 ◽  
Vol 22 (1) ◽  
pp. 13-22 ◽  
Author(s):  
Yuao Zhu ◽  
Maria Curtis ◽  
Katyna Borroto-Esoda
Keyword(s):  
Core Promoter ◽  
Replication Capacity ◽  
Basal Core Promoter ◽  
Wild Type ◽  
Promoter Mutations

Basal core promoter mutations of hepatitis B virus increase the risk of hepatocellular carcinoma in hepatitis B carriers

2003 ◽  
Vol 124 (2) ◽  
pp. 327-334 ◽  
Author(s):  
Jia–Horng Kao ◽  
Pei–Jer Chen ◽  
Ming–Yang Lai ◽  
Ding–Shinn Chen
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Basal Core Promoter ◽  
B Virus ◽  
Promoter Mutations

Hepatitis B virus subgenotypes and basal core promoter mutations in Indonesia

2009 ◽  
Vol 15 (32) ◽  
pp. 3428
Author(s):  
Andi Utama ◽  
Sigit Purwantomo ◽  
Marlinang Diarta Siburian ◽  
Rama Dhenni ◽  
Rino Alvani Gani ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Basal Core Promoter ◽  
B Virus ◽  
Promoter Mutations

scholarly journals Correlation Between Viral Load of HBV in Chronic Hepatitis B Patients and Precore and Basal Core Promoter Mutations

2013 ◽  
Vol 13 (2) ◽  
Author(s):  
Soad Ghabeshi ◽  
Zohreh Sharifi ◽  
Seyed Masoud Hosseini ◽  
Mahmood Mahmoodian Shooshtari
Keyword(s):  
Chronic Hepatitis ◽  
Viral Load ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Core Promoter ◽  
Basal Core Promoter ◽  
Promoter Mutations

Effects of hepatitis B virus precore and basal core promoter mutations on the expression of viral antigens: genotype B vs C

2011 ◽  
Vol 18 (10) ◽  
pp. e482-e490 ◽  
Author(s):  
C.-J. Liu ◽  
H.-R. Cheng ◽  
C.-L. Chen ◽  
T.-C. Chen ◽  
T.-C. Tseng ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Basal Core Promoter ◽  
Viral Antigens ◽  
B Virus ◽  
Promoter Mutations

scholarly journals Genome Replication, Virion Secretion, and e Antigen Expression of Naturally Occurring Hepatitis B Virus Core Promoter Mutants

2003 ◽  
Vol 77 (12) ◽  
pp. 6601-6612 ◽  
Author(s):  
Sameer Parekh ◽  
Fabien Zoulim ◽  
Sang Hoon Ahn ◽  
Adrienne Tsai ◽  
Jisu Li ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Viral Genome ◽  
Core Promoter ◽  
Hepatoma Cell ◽  
Genome Replication ◽  
Wild Type ◽  
Naturally Occurring ◽  
B Virus ◽  
Promoter Mutations

ABSTRACT The core promoter mutants of hepatitis B virus (HBV) emerge as the dominant viral population at the late HBeAg and the anti-HBe stages of HBV infection, with the A1762T/G1764A substitutions as the hotspot mutations. The double core promoter mutations were found by many investigators to moderately enhance viral genome replication and reduce hepatitis B e antigen (HBeAg) expression. A much higher replication capacity was reported for a naturally occurring core promoter mutant implicated in the outbreak of fulminant hepatitis, which was caused by the neighboring C1766T/T1768A mutations instead. To systemically study the biological properties of naturally occurring core promoter mutants, we amplified full-length HBV genomes by PCR from sera of HBeAg+ individuals infected with genotype A. All 12 HBV genomes derived from highly viremic sera (5 × 109 to 5.7 × 109 copies of viral genome/ml) harbored wild-type core promoter sequence, whereas 37 of 43 clones from low-viremia samples (0.2 × 107 to 4.6 × 107 copies/ml) were core promoter mutants. Of the 11 wild-type genomes and 14 core promoter mutants analyzed by transfection experiments in human hepatoma cell lines, 6 core promoter mutants but none of the wild-type genomes replicated at high levels. All had 1762/1764 mutations and an additional substitution at position 1753 (T to C), at position 1766 (C to T), or both. Moreover, these HBV clones varied greatly in their ability to secrete enveloped viral particles irrespective of the presence of core promoter mutations. High-replication clones with 1762/1764/1766 or 1753/1762/1764/1766 mutations expressed very low levels of HBeAg, whereas high-replication clones with 1753/1762/1764 triple mutations expressed high levels of HBeAg. Experiments with site-directed mutants revealed that both 1762/1764/1766 and 1753/1762/1764/1766 mutations conferred significantly higher viral replication and lower HBeAg expression than 1762/1764 mutations alone, whereas the 1753/1762/1764 triple mutant displayed only mild reduction in HBeAg expression similar to the 1762/1764 mutant. Thus, core promoter mutations other than those at positions 1762 and 1764 can have major impact on viral DNA replication and HBeAg expression.

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