Subtypes, Genotypes and Molecular Epidemiology of the Hepatitis B Virus as Reflected by Sequence Variability of the S-Gene

Intervirology ◽  
1995 ◽  
Vol 38 (1-2) ◽  
pp. 24-34 ◽  
Author(s):  
Lars O. Magnius ◽  
Helene Norder
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Molecular Epidemiology ◽  
Sequence Variability ◽  
S Gene ◽  
B Virus

scholarly journals Sequence Variability of Hepatitis B Virus (HBV) Surface Antigen Gene (S Gene) Among the Non-responders of Antiviral Therapy

2021 ◽  
Author(s):  
Naveed Alam ◽  
Zubaida Daudzai
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Antiviral Therapy ◽  
Chronic Hepatitis B ◽  
Surface Antigen ◽  
Sequence Variability ◽  
Serum Samples ◽  
S Gene ◽  
B Virus

Abstract BackgroundHepatitis B Virus (HBV), has been among the wide spread lethal causative agent of mortality in the population of Pakistan. Prolonged administration of antiviral therapy for chronic hepatitis B may result in the development of hepatitis B viral mutants. ObjectivesTo gain insight into the mechanism involved in the sequence variability of Hepatitis B Virus (HBV) surface antigen gene (S gene) among responders and non-responders to antiviral therapy, baseline characteristics of the patients and sequences within the S region were investigated in pre-treatment serum samples of responders and post-treatment serum samples of non-responders. Data collection and methodologyThe data was collected from 15 individuals with chronic hepatitis B from Khyber Pakhtunkhwa (KPK) province, Pakistan. The antiviral response was independent of viral genotypes, and nonresponse to antiviral therapy was associated with a complex variability of the viral mutants as determined by PCR. ResultsThe sequence analysis of the S gene among responders and non-responders patients of pre and post-treatment with antiviral therapy showed variability in DNA sequence marked as Pakistani isolates make a distinct cluster in the phylogenetic tree. The S gene of HBV isolates from KPK province shows some similarities with isolates of other countries. No significant variations of nucleotides in the S gene of HBV was found among the responders and non-responders receiving antiviral therapy indicating that S gene may not be important with respect to treatment outcome. ConclusionIt illustrates that antigenicity of other various HBV proteins can be targeted in order to design more effective vaccines against the local strains.

scholarly journals Molecular Epidemiology of Hepatitis B Virus in Central America Reflected in the Genetic Variability of the Small S Gene

1997 ◽  
Vol 176 (4) ◽  
pp. 851-858 ◽  
Author(s):  
Patricia Arauz‐Ruiz ◽  
Heléne Norder ◽  
Kirsten A. Visoná ◽  
Lars O. Magnius
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Genetic Variability ◽  
Molecular Epidemiology ◽  
Central America ◽  
S Gene ◽  
B Virus

scholarly journals Hepatitis B Virus Pre-S Gene Deletions and Pre-S Deleted Proteins: Clinical and Molecular Implications in Hepatocellular Carcinoma

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 862
Author(s):  
Yueh-Te Lin ◽  
Long-Bin Jeng ◽  
Wen-Ling Chan ◽  
Ih-Jen Su ◽  
Chiao-Fang Teng
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Molecular Mechanisms ◽  
Incidence Rates ◽  
Gene Deletions ◽  
S Gene ◽  
B Virus ◽  
Potential Applications ◽  
Prevention And Therapy

Hepatocellular carcinoma (HCC) is one of the most frequent and fatal human cancers worldwide and its development and prognosis are intimately associated with chronic infection with hepatitis B virus (HBV). The identification of genetic mutations and molecular mechanisms that mediate HBV-induced tumorigenesis therefore holds promise for the development of potential biomarkers and targets for HCC prevention and therapy. The presence of HBV pre-S gene deletions in the blood and the expression of pre-S deleted proteins in the liver tissues of patients with chronic hepatitis B and HBV-related HCC have emerged as valuable biomarkers for higher incidence rates of HCC development and a higher risk of HCC recurrence after curative surgical resection, respectively. Moreover, pre-S deleted proteins are regarded as important oncoproteins that activate multiple signaling pathways to induce DNA damage and promote growth and proliferation in hepatocytes, leading to HCC development. The signaling molecules dysregulated by pre-S deleted proteins have also been validated as potential targets for the prevention of HCC development. In this review, we summarize the clinical and molecular implications of HBV pre-S gene deletions and pre-S deleted proteins in HCC development and recurrence and highlight their potential applications in HCC prevention and therapy.

scholarly journals Antiviral effects of hepatitis B virus S gene-specific anti-gene locked nucleic acid in transgenic mice

2018 ◽  
Vol 6 (8) ◽  
pp. 183-191
Author(s):  
Shu-Rong Xiao ◽  
Gui-Dan Xu ◽  
Wu-Jun Wei ◽  
Bin Peng ◽  
Yi-Bin Deng
Keyword(s):  
Hepatitis B Virus ◽  
Nucleic Acid ◽  
Hepatitis B ◽  
Transgenic Mice ◽  
Locked Nucleic Acid ◽  
S Gene ◽  
Antiviral Effects ◽  
B Virus

The possible role of S gene mutations of hepatitis B virus in intrauterine transmission

2020 ◽  
Author(s):  
Jiaxin Wu ◽  
Yongliang Feng ◽  
Zhiqing Yang ◽  
Ruijun Zhang ◽  
Dandan Wang ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hepatitis B Surface Antigen ◽  
Gene Mutations ◽  
Hbv Dna ◽  
Mutation Rates ◽  
Control Group ◽  
Intrauterine Transmission ◽  
S Gene ◽  
B Virus

Abstract Background: Many hepatitis B virus (HBV) substances could inevitably enter fetuses and occurred neonatal intrauterine transmission. HBV often occurs mutation, especially S gene, and may lead to different outcomes on intrauterine transmission. We explored the associations between HBV S gene mutations of hepatitis B surface antigen positive (HBsAg-positive) mothers and intrauterine transmission. Methods: A total of 399 HBsAg-positive mothers and neonates were recruited and their general demographic information was collected between June 2011 and July 2013. The mothers with HBV DNA levels ≥ 106 IU/ml were selected, 22 mothers whose neonates occurred HBV intrauterine transmission were in the HBV intrauterine transmission group (GT) and 22 mothers were randomly selected from the remaining controls were in the control group (GC). Maternal whole-genome HBV DNA was extracted, amplified, cloned, and sequenced. Obtained sequences were adjusted, genotyped, and analyzed for mutation rates. A case-control study was designed to analyze the relationship between mutations in the S gene of HBV and intrauterine transmission. Results: Fifty-five neonates were found to have experienced intrauterine transmission (13.78%). Genotype B (4.55%), genotype C (88.64%) and inter-genotype B/C (6.81%) were found in the 44 HBsAg-positive mothers. The mutation rates of the S gene, in both genotypes B (0.58% vs 1.41%, P = 0.040) and C (7.56% vs 14.71%, P＜0.001), were lower in group T than in group C. Missense substitutions such as L84I, P47S, K10Q, A41P, M133L, A60V, and I42T only existed in group C. The mutation rates of G73S, I126T, and I126S in group C were higher (P < 0.001, P < 0.001, P = 0.010). Deletions occurred in the S gene. The occurrence of intrauterine transmission with maternal mutation A90V was higher (P < 0.001). This may have increased the risk of neonatal HBsAg expression (P = 0.022). Conclusions: The HBV S gene mutations of HBsAg-positive mothers may reduce the occurrence of HBV intrauterine transmission. It is possible for HBsAg-positive mothers infected with A90V to develop HBV chronic infection and transmit it to the fetus during pregnancy, resulting in neonatal HBV infection.

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