Mutations and methods of analysis of mutations in Hepatitis B virus

Rajput, Manoj Kumar

doi:10.3934/microbiol.2020024

Cited by 15 publications

(11 citation statements)

References 84 publications

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“…Mutations in the polymerase region of viral isolates in this study were compared to those in previous studies. Only one mutation (G961A) which leads to I278V aa substitution was reported in a previous study, which may cause low viral replication and hence could lead to the development of liver disease [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Full-Length Genome Sequencing and Analysis of Hepatitis B Viruses Isolated from Iraqi Patients

Mamoori,

Ahmed,

Mahmood

et al. 2024

International Journal of Microbiology

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Hepatitis B virus (HBV) causes liver diseases (chronic hepatitis, cirrhosis, and hepatocellular carcinoma) and is a leading health problem worldwide. Sequencing of the whole HBV genome provides insight into the virus genotype, subgenotype, serotype, genetic variation, and viral drug resistance. To date, no study has been conducted on the whole genome sequence of HBV obtained from Iraqi patients. Therefore, this is the first study to sequence clinical samples from these patients. Viral genomic DNA was isolated and amplified using five primer sets to amplify five overlapping regions covering the entire HBV genome. The amplicons were sequenced, aligned to a reference sequence, annotated, and submitted to the National Center for Biotechnology Information GenBank database. Sequence analysis showed that the genome size of the tested viral samples was 3,182 bp and belonged to genotype D, subgenotype D1, and serotype ayw2. Missense mutations were found in the four regions (X, PreS1-S, PreC-C, and P) of the tested samples, leading to amino acid substitutions, which were 8.4%, 5.1%, 4.7%, and 4.6%, respectively. These mutations may cause severe liver diseases.

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Section: Discussionmentioning

confidence: 99%

Full-Length Genome Sequencing and Analysis of Hepatitis B Viruses Isolated from Iraqi Patients

Mamoori,

Ahmed,

Mahmood

et al. 2024

International Journal of Microbiology

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“…Precore mutations in the region from 1858 to 1896 increase the HBV DNA levels in serum. Three cases of the 1862G>T mutation, which is a risk factor for FH and acute liver failure (ALF), were identified [ 17 , 18 ]. Nonsense mutations in 1896 result in the loss of HBe antigen production.…”

Section: Discussionmentioning

confidence: 99%

“…Concurrent double mutation at 1762 and 1764 in the core promoter region and the 1896G>A stop codon mutation in the precore region was identified in two cases in genotype C and in one case of genotype B infection. This combination of mutations is associated with an increased risk of HBV-associated liver injury [ 15 , 18 , 44 ]. Concurrent mutation 1753T>V (C, G, A) in the core promoter and the stop codon mutation 1896G>A in the precore region also increases the risk of FH and ALF [ 17 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

Characterization of mutations in hepatitis B virus DNA isolated from Japanese HBsAg-positive blood donors in 2021 and 2022

Sedohara,

Takahashi,

Arai

et al. 2024

Arch Virol

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Missense mutations in certain small envelope proteins diminish the efficacy of antibodies. Consequently, tracking the incidence and types of vaccine-escape mutations (VEMs) was crucial both before and after the introduction of universal hepatitis B vaccination in Japan in 2016. In this study, we isolated hepatitis B virus (HBV) DNA from 58 of 169 hepatitis B surface antigen (HBsAg)-positive blood samples from Japanese blood donors and determined the nucleotide sequence encoding the small envelope protein. DNA from six (10%) of the samples had VEMs, but no missense mutations, such as G145R, were detected. Complete HBV genome sequences were obtained from 29 of the 58 samples; the viral genotype was A1 in one (3%), A2 in three (10%), B1 in nine (31%), B2 in five (17%), B4 in one (3%), and C2 in 10 (34%) samples. Tenofovir-resistance mutations were detected in two (7%) samples. In addition, several core promoter mutations, such as 1762A>T and 1764G>A, and a precore nonsense mutation, 1986G>A, which are risk factors for HBV-related chronic liver disease, were detected. These findings provide a baseline for future research and highlight the importance of ongoing monitoring of VEMs and drug resistance mutations in HBV DNA from HBsAg-positive blood donors without HBV antibodies.

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“…Nucleotide sequencing is the gold standard method for mutation detection. In comparison to the Sanger sequencing, second-generation sequencing has improved sensitivity for detection and quantification of mutations, mixed genotypes, and viral recombination while third-generation sequencing enables the analysis of the whole virus genome ( Lee et al, 2018 ; Rajput, 2020 ; Garcia-Garcia et al, 2021 ).…”

Section: Molecular Mechanisms Of Hbv-related Hcc Progressionmentioning

confidence: 99%

The role of hepatitis B virus genome variations in HBV-related HCC: effects on host signaling pathways

Shoraka,

Hosseinian,

Hasibi

et al. 2023

Front. Microbiol.

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Hepatocellular carcinoma (HCC) is a significant global health issue, with a high prevalence in many regions. There are variations in the etiology of HCC in different regions, but most cases are due to long-term infection with viral hepatitis. Hepatitis B virus (HBV) is responsible for more than 50% of virus-related HCC, which highlights the importance of HBV in pathogenesis of the disease. The development and progression of HBV-related HCC is a complex multistep process that can involve host, viral, and environmental factors. Several studies have suggested that some HBV genome mutations as well as HBV proteins can dysregulate cell signaling pathways involved in the development of HCC. Furthermore, it seems that the pathogenicity, progression of liver diseases, response to treatment and also viral replication are different among HBV mutants. Understanding the relationship between HBV genome variations and host signaling pathway alteration will improve our understanding of the molecular pathogenesis of HBV-related HCC. Furthermore, investigating commonly dysregulated pathways in HBV-related HCC is necessary to discover more specific therapeutic targets and develop more effective strategies for HCC treatment. The objective of this review is to address the role of HBV in the HCC progression and primarily focus on the impacts of HBV genome variations on HCC-related signaling pathways.

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Mutations and methods of analysis of mutations in Hepatitis B virus

Cited by 15 publications

References 84 publications

Full-Length Genome Sequencing and Analysis of Hepatitis B Viruses Isolated from Iraqi Patients

Full-Length Genome Sequencing and Analysis of Hepatitis B Viruses Isolated from Iraqi Patients

Characterization of mutations in hepatitis B virus DNA isolated from Japanese HBsAg-positive blood donors in 2021 and 2022

The role of hepatitis B virus genome variations in HBV-related HCC: effects on host signaling pathways

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