ViMRT
}  
 
Home   
< Docs   

 HBV mutation literature information.


  LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B.
 PMID: 33857724       2021       Journal of infection and public health
Abstract: The major purpose of the study was to screen G1986A mutations at a large scale and also to establish ligase chain reaction as a mutation testing tool.


  Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection.
 PMID: 33458253       2020       Wellcome open research
Abstract: Through application of deep whole-genome sequencing we typed the isolate as genotype-D1, and identified several minority variants including G1764A and G1986A substitutions in the pre-core promoter and pre-core regions, which support CHB-AR rather than AHB.


  rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections.
 PMID: 31402915       2019       Frontiers in immunology
Result: In addition, the rate of G1986A preC mutation was significant higher in patients with rt269I (49.61%) than those with rt269L (28.83%, p < 0.01).
Result: These results suggest that the high frequency of G1986A preC mutation is responsible for HBeAg negative infections in patients with genotype C rt269I infections.


  Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India.
 PMID: 30505167       2018       Saudi journal of biological sciences
Abstract: The study was designed to assess the impact of G1986A mutations in patients with different clinical spectra of the liver disease by PCR-LCR.


  G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B.
 PMID: 26587040       2015       Hepatitis monthly
Method: Association of G1986A with few parameters such as HBeAg status, genotype, liver diseases and e-seroconversion rate were statistically determined by chi-square analysis.
Method: The consensus sequences were then analyzed at the basal core promoter (BCP), precore (PC) and core (C) region and particularly observed for presence of G1986A mutation.
Discussion: When G1986A mutation is paired with C1858T, the epsilon structure is more stabilized, thus enhancing viral replication.



Browser Board

 Co-occurred Entities




   Filtrator