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Published on: February 1, 2017
Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients
Narjes Shokatpour1, Maryam Vaezjalali2,3, Graham R Foster4
1Department of Microbiology, Faculty of Biological Sciences, Shahid Beheshti University, Tehran, Iran.
Insights
Mutations in hepatitis B virus (HBV) S gene, pre-core, and basic core promoter regions are common in chronic hepatitis B patients. These mutations, particularly G1896A in the pre-core region, are frequent and can impact immune epitopes.
Area of Science:
- Virology
- Hepatology
- Molecular Biology
Background:
- Mutations in the hepatitis B virus (HBV) S gene, pre-core (PC), and basic core promoter (BCP) regions are linked to disease progression.
- Understanding these mutations is crucial for managing chronic hepatitis B (CHB) infection.
Purpose of the Study:
- To determine the frequency of mutations in the S gene, PC, and BCP regions of HBV in CHB patients.
- To analyze the distribution and characteristics of these mutations.
Main Methods:
- Analysis of 104 CHB patients' samples from Tehran Hepatitis centers.
- Viral load determination using the TaqMan method.
- Nested PCR amplification and sequencing of S gene, PC, and BCP regions.
Main Results:
- All sequenced S gene regions belonged to genotype D (ayw2 and ayw1 subtypes).
- Mutations were prevalent in HBsAg (51.0%) and Major Hydrophilic Region (18.0%), with many in immune epitopes (B cell and Th).
- High mutation rates were observed in PC and BCP regions (84.6%), with G1896A being the most common (61.0%).
Conclusions:
- Common mutations in HBsAg, particularly within immune epitopes, were identified.
- A high frequency of G1896A mutations in the PC region was noted.
- A negative correlation was found between A1762T/G1764A and G1764T/C1766G mutations in the BCP region.
Background:
Mutations in the S gene (HBsAg), pre-core (PC), and basic core promoter (BCP) of the hepatitis B virus (HBV) infection are correlated with disease progression. This study assessed the frequency of mutations in the S gene, PC, and BCP regions in chronic hepatitis B (CHB) patients.
Methods:
104 formerly known CHB patients who visited Tehran Hepatitis centers, were included. The viral load of samples was determined based on the TaqMan method. Regions of the S gene, PC and BCP were amplified by the nested PCR. Positive PCR products were sequenced and analyzed.
Results:
33 successfully sequenced S gene region revealed all the derived strains were genotype D, with the majority (90.9%) belonging to the ayw2 subtype, and the rest (9.1%) to the ayw1 subtype. The prevalence of mutations was found to be 51.0% and 18.0% in the HBsAg and the Major Hydrophilic Region, respectively. 70.0% of amino acid changes within HBsAg occurred in different immune epitopes, of which 27.0% and 72.0% were located in B cell and Th epitopes, respectively. 26 successfully sequenced PC and BCP regions showed at least one mutation in 84.6% of the HBV strains. The PC and BCP mutations were G1896A (61.0%), G1899A (23.0%), A1762T/G1764A (23.0%) and G1764T/C1766G (26.0%). None of the strains with A1762T/G1764A mutation carried the G1764T/C1766G mutant.
Conclusions:
Our results showed common mutations within HBsAg, occurring in immune epitopes, a high rate of G1896A mutations in the PC region, and a negative correlation between the emergence of A1762T/G1764A mutation and the G1764T/C1766G mutant in the BCP region.
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