Evolution of viral load and changes of polymerase and precore/core promoter sequences in lamivudine-resistant hepatitis B virus during adefovir therapy

2007 ◽  
Vol 79 (7) ◽  
pp. 902-910 ◽  
Author(s):  
U Im Chang ◽  
Young Chun Lee ◽  
Seong Heon Wie ◽  
Jeong Won Jang ◽  
Si Hyun Bae ◽  
...  
Keyword(s):  
Viral Load ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Promoter Sequences ◽  
B Virus

scholarly journals Genotyping Hepatitis B virus from whole- and sub-genomic fragments using position-specific scoring matrices in hbv star

2006 ◽  
Vol 87 (6) ◽  
pp. 1459-1464 ◽  
Author(s):  
Richard Myers ◽  
Caroline Clark ◽  
Arshad Khan ◽  
Paul Kellam ◽  
Richard Tedder
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Full Length ◽  
Basal Core Promoter ◽  
Hbv Genotype ◽  
Promoter Sequences ◽  
Hbv Genotypes ◽  
Scoring Matrices ◽  
B Virus

Hepatitis B virus (HBV) genomes have been classified into eight genotypes based on phylogenetic analysis of sequence variation. Identifying and tracking the movement of HBV genotypes is important in terms of both monitoring infection rates and predicting disease and treatment. An HBV genotyping tool has been developed that compares query sequences with position-specific scoring matrices representing the eight HBV genotypes. This tool (hbv star) is rapid, robust and accurate and assigns genotype based on a statistically defined scoring model. hbv star confidently assigned 90 % of 590 full-length HBV genomes to an HBV genotype (Z score >2.0). Thirty-two of the residual 48 sequences were identified as non-human primate viruses and 16 sequences were identified as recombinant or putative recombinants. Receiver-Operated Characteristic (ROC) analysis was used to compare the accuracy of genotype prediction using basal core promoter sequences and surface and core genes with the accuracy achieved by using full-length sequences. A web interface to hbv star is available at http://www.vgb.ucl.ac.uk/starn.shtml.

scholarly journals Retrospective Study Investigating the Prevalence and Clinical Significance of Hepatitis B Virus Precore and Basal Core Promoter Variants

2015 ◽  
Vol 29 (8) ◽  
pp. e1-e6
Author(s):  
Meaghan O’Brien ◽  
Adara Casselman ◽  
Gerry Smart ◽  
Ainsley Gretchen ◽  
Kelly Kaita ◽  
...  
Keyword(s):  
Viral Load ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Clinical Significance ◽  
Core Promoter ◽  
Hepatitis B Surface Antigen ◽  
Basal Core Promoter ◽  
Hbv Genotype ◽  
B Virus ◽  
Index Ratio

BACKGROUND: Hepatitis B virus (HBV) precore (PC) and basal core promoter (BCP) variants are well known; however, their prevalence in North America is unclear, especially among hepatitis B e antigen-negative patients.OBJECTIVE: To investigate the prevalence of PC/BCP mutations and their clinical significance.METHODS: One hundred twenty-eight patients positive for both hepatitis B surface antigen and hepatitis B e antibody were selected, and PC/BCP mutations were identified using a line probe assay. The subjects’ charts were reviewed for race/ethnicity, HBV genotype, HBV viral load, sex, liver enzyme levels, imaging and biopsy results up to 10 years before the study.RESULTS: The prevalence of PC and BCP variants were 47.6% and 62.5%, respectively. Older age was associated with aspartate aminotransferase-to-platelet index ratio (APRI) ≥0.7 (P=0.011) and abnormal imaging/biopsy results (P=0.0008). Although the presence of BCP variant(s) was associated with APRI ≥0.7 (P=0.029), it was not associated with abnormal imaging/biopsy results. The combination of age ≥50 years and the presence of BCP variant(s) was associated with abnormal imaging/biopsy results, suggestive of either cirrhosis or hepatocellular carcinoma (not observed with PC mutation). Neither sex or genotype, or median HBV viral load showed significant influence on any of these outcomes.CONCLUSIONS: The present study suggests that the prevalence of PC and BCP mutations are higher than what has been previously reported. One potential explanation would be increased immigration in the past decade. Considering the potential public health and clinical implications of these variants, long-term multicentre and prospective studies could further unravel the uncertainty around these variants.

Detection of Hepatitis B Genotypes in HBsAg & HBeAg Carriers

2018 ◽  
Vol 7 (5) ◽  
Author(s):  
Salman Khan ◽  
Molly Madan
Keyword(s):  
Chronic Hepatitis ◽  
Viral Load ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Central Research ◽  
Elisa Kit ◽  
B Virus ◽  
Negative Chronic Hepatitis ◽  
Genotype A

Objective:- Hepatitis B is noteworthy medical issues that may include the late continuation of liver cirrhosis and hepatocellular carcinoma. The present study aimed for the detection and diffrentiation of Hepatitis B virus HBsAg inactive non-replicative carriers, HBeAg-positive inactive replicative carriers, active carriers & HBeAg-negative chronic hepatitis B by Real Time PCR and their genotyping Methods: This research conducted on 245 positive for HBsAg, 118 (48.16 %) were male and 127 (51.84%) were female patients, which was performed in central research station labortory of Microbiology at netaji subhash Chandra Bose subharti Medical College and Hospital, Meerut Between march 2016 to November 2017 The sera were separated and screened for HBsAg by ELISA kit. Positive samples for HBsAg were tested for HBeAg ELISA kit and DNA Viral load then sequenced for genotying Results:. Of the 245 HBsAg Positive case 55 (1.12%) were HBeAg positive. In 16 PCR positive and HBV genotyping, In HBsAg inactive Non-Replicative 37.5% (n=6) genotype-B and 6.25% (n=1) genotype-A, In HBeAg inactive Replicative 12.5% (n=2) genotype-B and 12.5% (n=2) genotype-A and In HBeAg Active Chronic Hepatitis B 18.75% (n=3) genotype-B and 12.5% (n=2) genotype-A were detected Conclusions: Management strategy, using HBsAg, HBeAg and HBV DNA viral load, seems adequate for the confirmation and diffrentiation of Hepatitis B virus inactive, active carriers & HBeAg-negative chronic hepatitis B patients and genotype B was more prevalent in comparission to genotype A. Distribution of carriers & genotypes, help physicians to prescribe proper antiviral/interferon therapy according to current genotyping pattern in this region Keywords: Hepatitis B virus, Carrier State, HBsAg, HBeAg, RT-PCR

Precore/Core Promoter Mutant Hepatitis B Virus Produces More Severe Histologic Liver Disease than Wild Type Hepatitis B Virus

2007 ◽  
Vol 1 (1) ◽  
pp. 41-46 ◽  
Author(s):  
Mamun-Al-Mahtab ◽  
Salimur Rahman ◽  
Mobin Khan ◽  
Ayub Mamun ◽  
Kamal
Keyword(s):  
Liver Disease ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Wild Type ◽  
B Virus ◽  
Promoter Mutant

scholarly journals Hepatitis B virus (HBV) viral load, liver and renal function in adults treated with tenofovir disoproxil fumarate (TDF) vs. untreated: a retrospective longitudinal UK cohort study

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tingyan Wang ◽  
David A. Smith ◽  
Cori Campbell ◽  
Jolynne Mokaya ◽  
Oliver Freeman ◽  
...  
Keyword(s):  
Viral Load ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Renal Impairment ◽  
Clinical Guidelines ◽  
Untreated Group ◽  
Liver Inflammation ◽  
B Virus ◽  
The Impact

Abstract Background Current clinical guidelines recommend treating chronic hepatitis B virus (HBV) infection in a minority of cases, but there are relatively scarce data on evolution or progression of liver inflammation and fibrosis in cases of chronic HBV (CHB) that do not meet treatment criteria. We aimed to assess the impact of TDF on liver disease, and the risk of renal impairment in treated CHB patients in comparison to untreated patients. Methods We studied a longitudinal ethnically diverse CHB cohort in the UK attending out-patient clinics between 2005 and 2018. We examined TDF treatment (vs. untreated) as the main exposure, with HBV DNA viral load (VL), ALT, elastography scores and eGFR as the main outcomes, using paired tests and mixed effects model for longitudinal measurements. Additionally, decline of eGFR during follow-up was quantified within individuals by thresholds based on clinical guidelines. Baseline was defined as treatment initiation for TDF group and the beginning of clinical follow-up for untreated group respectively. Results We included 206 adults (60 on TDF, 146 untreated), with a median ± IQR follow-up duration of 3.3 ± 2.8 years. The TDF group was significantly older (median age 39 vs. 35 years, p = 0.004) and more likely to be male (63% vs. 47%, p = 0.04) compared to the untreated group. Baseline difference between TDF and untreated groups reflected treatment eligibility criteria. As expected, VL and ALT declined significantly over time in TDF-treated patients. Elastography scores normalised during treatment in the TDF group reflecting regression of inflammation and/or fibrosis. However, 6/81 (7.4%) of untreated patients had a progression of fibrosis stage from F0-F1 to F2 or F3. There was no evidence of difference in rates or incidence of renal impairment during follow-up in the TDF vs. untreated group. Conclusions Risk of liver inflammation and fibrosis may be raised in untreated patients compared to those receiving TDF, and TDF may benefit a larger percentage of the CHB population.

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