literature

HBV mutation literature information.

Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot.

PMID: 31880889 2019 Polish journal of microbiology

Abstract: The most common NA resistance mutation was rtQ215H/P/S (16.67%), however, for S gene the misdiagnosis mutations were observed most frequently (9.25%).

Result: The most prevalent pol gene mutation was rtQ215H/P/S and it falls in the compensatory mutation category.

A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action.

PMID: 30080852 2018 PLoS neglected tropical diseases

Result: rtQ215S identified in genotype D (4/69, 5.8%).

Table: Q215S

Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression.

PMID: 29713126 2018 World journal of gastroenterology

Method: A total of 26 types of RT mutations, including rtS53N, rtT54N, rtL82M, rtV84M, rtS85A, rtI91L, rtY126C, rtT128I/N, rtN139D, rtW153Q, rtF166L, rt

Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia.

PMID: 29408943 2018 PloS one

Table: Q215S

Discussion: Other than YMDD RT motif resistance gene mutations, the observation of co-prevalence of PC mutations and ADV resistance mutants (rtI233V, rtQ215S/Q and rtV214A) in particular in the HBeAg negative cases was in line with earlier similar reports.

Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B.

PMID: 27504160 2016 Electronic physician

Abstract: T54N, L80I/V, I91L/V, L180M, M204I/V, Q215P/S, and F221Y/S showed the highest number of mutations in all groups with different frequencies.

Result: Q215P/S was found in all groups except group II with frequencies of 6.25 to 25%.

Mutation profiling of the hepatitis B virus strains circulating in North Indian population.

PMID: 24637457 2014 PloS one

Table: Q215S

Discussion: rtN236T a primary mutation in the D domain, rtA181T/V at the B domain and rtQ215S at the C-D inter-domain have been associated with Adefovir and Lamivudine resistance were also observed in 8 cases.

Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan.

PMID: 23865777 2013 BMC infectious diseases

Discussion: When mutations rtA194T, rtV207M rtS213T rtV214A and rtQ215S were tested in our sensitive and reliable in vitro resistance test system, the mutants showed no resistance to lamivudine (LMV), entecavir (ETV), adenofovir (ADF) and tenofovir (TDF).

Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients.

PMID: 23596461 2013 Hepatitis monthly

Result: RT sequence changes implicated in adefovir-resistance were detected, including

Table: Q215S

Discussion: In addition, a number of other mutations have been detected in our study and were clustered into three distinct regions of the RT: the D and A domains (rtP237H, rtN238T/D, rtV84M, and rtS85A) and the C-D interdomain (rtS213T/N, rtV214A, and rtQ215S).

Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population.

PMID: 23409946 2013 Virology journal

Table: Q215S

Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies.

PMID: 22224083 2011 Hepatitis monthly

Result: Single compensatory mutations were not detected in the switch therapy group; however, rtQ215H/P/S +- rtV214A/P mutations were found in 12 out of 88 patients (14%) in the add-on therapy group, and this difference was significant (P < 0.01).

Discussion: Accordingly, in our previously published report, we found that rtQ215A/H/P/S substitutions could be detected as naturally occurring mutations in treatment-naive patients with CHB.

Discussion: Further, rtQ215S and rtV214A mutations were compensatory mutations arising from ADV treatment.|mg

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