Hepatitis B genotyping: The utility for the clinicians

Fletcher, Gnanadurai John; Eapen, C E; Abraham, Priya

doi:10.1007/s12664-019-00995-y

Cited by 12 publications

(11 citation statements)

References 68 publications

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“…Previous studies 14 – 16 showed that singly spliced HBV SP1 RNA generated the expression of HBSP, which was linked to an increased risk of the development of HCC by promoting viral replication, protein production and liver fibrosis. Speculatively, because of the constant production of SP1 variants and thus HBSP regardless of the levels of replication, genotypes B and C will likely cause more severe cellular damage than A, D or E, thus resulting in increased risk of HCC development consistent with previous reports that B and C were associated with more severe disease 23 , 24 and were more oncogenic 20 , 25 – 28 . It has been demonstrated 10 that the spHBV/wtHBV ratio was significantly elevated in serum samples obtained from patients with severe liver fibrosis or necrosis, thus suggesting a direct link between the spHBV/wtHBV ratio and the severity of liver disease.…”

Section: Discussionsupporting

confidence: 83%

“…The regulatory mechanism by which different HBV genotypes generate different splicing patterns and levels is still unclear. It has been reported that different HBV genotypes exhibit distinct preferences in the usage of splice donor/acceptor sites and thus generate different splicing patterns and levels 28 . Based on the results in this study, it is conceivable that genotypes B and C appear to have more efficient splicing mechanism than A, D or E even when viral replication is low (low viral loads) generating more detectable SP1 spliced variants.…”

Section: Discussionmentioning

confidence: 99%

“…Infection with genotype B has been found to be associated with the development of HCC and relapse of HCC in younger age, whereas infection with genotype C has been frequently linked to an increased risk of HCC in the older age (> 40 years) 22 . Genotypes B and C cause more severe cellular damage than A and D 23 , 24 and are more oncogenic 20 , 25 – 28 . While the mechanism of pathogenicity of different HBV genotypes is still not fully understood, it has been reported 6 , 29 that different HBV genotypes produce different levels of HBV splice variants, which are predictive of liver cancer 12 , 30 .…”

Section: Introductionmentioning

confidence: 99%

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More DNA and RNA of HBV SP1 splice variants are detected in genotypes B and C at low viral replication

Luk

Gersch

Harris

et al. 2021

Sci Rep

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HBV produces unspliced and spliced RNAs during replication. Encapsidated spliced RNA is converted into DNA generating defective virions that are detected in plasma and associated with HCC development. Herein we describe a quantitative real-time PCR detection of splice variant SP1 DNA/RNA in HBV plasma. Three PCR primers/probe sets were designed detecting the SP1 variants, unspliced core, or X gene. Plasmids carrying the three regions were constructed for the nine HBV genotypes to evaluate the three sets, which were also tested on DNA/RNA extracted from 193 HBV plasma with unknown HCC status. The assay had an LOD of 80 copies/ml and was equally efficient for detecting all nine genotypes and three targets. In testing 84 specimens for both SP1 DNA (77.4%) and RNA (82.1%), higher viral loads resulted in increased SP1 levels. Most samples yielded < 1% of SP1 DNA, while the average SP1 RNA was 3.29%. At viral load of ≤ 5 log copies/ml, the detectable SP1 DNA varied by genotype, with 70% for B, 33.3% for C, 10.5% for E, 4% for D and 0% for A, suggesting higher levels of splicing in B and C during low replication. At > 5 log, all samples regardless of genotype had detectable SP1 DNA.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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More DNA and RNA of HBV SP1 splice variants are detected in genotypes B and C at low viral replication

Luk

Gersch

Harris

et al. 2021

Sci Rep

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“…Individuals who are core-antibody positive and HB surfaceantibody negative are chronically infected and show a decreased risk of HBV reactivation. There is also no clinical benefit of vaccination for the group of individuals who are positive only for core antibodies due to exposure to HBV or people who are positive for anti-HBc and anti-HBs due to immune control (Cholongitas et al 2018;Ganczak et al 2019).…”

Section: Hbv Serological Markersmentioning

confidence: 99%

“…There are many genotyping systems, including reverse hybridization, restriction fragment polymorphism (RFLP), multiplex nested PCR or real-time PCR, oligonucleotide microarray chips, reverse dot blot, restriction fragment mass polymorphism (RFMP), and invader assay ( Fletcher et al 2019 ). Molecular identification of HBV genotypes could also be done by sequencing the whole HBV genome, followed by phylogenetic analysis.…”

Section: Molecular Assaysmentioning

confidence: 99%

Hepatitis B Virus: From Diagnosis to Treatment

Güvenir

Arıkan

2020

Polish Journal of Microbiology

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Hepatitis B infection is still a global concern progressing as acute-chronic hepatitis, severe liver failure, and death. The infection is most widely transmitted from the infected mother to a child, with infected blood and body fluids. Pregnant women, adolescents, and all adults at high risk of chronic infection are recommended to be screened for hepatitis B infection. The initial analysis includes serological tests that allow differentiation of acute and chronic hepatitis. Molecular assays performed provide detection and quantification of viral DNA, genotyping, drug resistance, and precore/core mutation analysis to confirm infection and monitor disease progression in chronic hepatitis B patients. All patients with chronic hepatitis B should be treated with antiviral medications and regularly monitored for efficient treatment. The current treatment is based on nucleos(t)ide analogs and pegylated interferons that save lives by decreasing liver cancer death, liver transplant, slow or reverse the progression of liver disease as well as the virus infectivity.

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