HBV mutation literature information.


  Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient.
 PMID: 35203489       2022       Biomedicines
Result: Clone 1-2 harbored 7 mutations (AIHILAT: rtT38A (A), rtV191I (I), rtN226H (H), rtV266I (I), rtQ267L (L), rtS317A (A) and rtA329T (T)) (Figure 2a).


  Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues.
 PMID: 32765014       2020       Infection and drug resistance
Table: V191I


  Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia.
 PMID: 32915862       2020       PloS one
Result: Amino acid changes including rtL80I, rtV173L, rtL180M, rtV191I and rtM204I/V in the reverse transcriptase (RT) region of the pol gene, and sE164D, sW182*, sI195M and sW196LS in the overlapping small HBsAg (SHB) region wer


  Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients.
 PMID: 33124952       2020       Emerging microbes & infections
Abstract: rtV191I and rtA181T/V were the only resistance mutations identified as genotype-specific mutation.
Result: After scrutinizing the frequency of mutations within these sites, only two NA-r mutations, ntG700A (rtV191I, P = 0.014) and ntC671T (rtA181T/V, P = 0.048) from treatment-naive and post-treatment samples, respectively, were identified as genotype-specific mutations (Figure 3(C-D)).
Result: Putative resistance mutations were observed at 8 AA sites among the panel of treatment-naive patients; they were rtV191I,


  Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy.
 PMID: 30906435       2019       Experimental and therapeutic medicine
Result: Common and frequent mutations identified in the cohort of the present study included rtL80V/I, rtV84M, rtL91I, rtN118H/D/T, rtT128A, rtL180M, rtT184L/S/A, rtV191I, rtS202G, rtV207I/M, rtS213T


  Association of HBsAg mutation patterns with hepatitis B infection outcome: Asymptomatic carriers versus HCC/cirrhotic patients.
 PMID: 31105017       2019       Annals of hepatology
Abstract: In RT, some potentially resistant substitutions such as Q215S, V191I and V214A, were revealed.


  Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection.
 PMID: 31147594       2019       Scientific reports
Result: In this study, non-classical mutations were observed in 29 patients who suffering from virological breakthrough and without classical mutations (Table 4) at 9 sites (V191I, V207I/M, S213T, E218D, F221Y, I224V, L229V, N/H238 and R242D).
Result: These sites could be classified into the following groups: V191I and V207I/M were detected in cases experienced ADV treated; F221Y were found in cases experienced LAM treated; S213T, I224V and H/N238 seemed to be the sharing mutation sites of LAM, ADV and ETV.
Table: <


  Complementation of Wild-Type and Drug-Resistant Hepatitis B Virus Genomes to Maintain Viral Replication and Rescue Virion Production under Nucleos(t)ide Analogs.
 PMID: 31218588       2019       Virologica Sinica
Abstract: In the present study, HBV genomes with frequently detected reverse transcriptase (RT)/surface truncation MTs, rtA181T/sW172*, rtV191I/sW182* and rtM204I/sW196*, were phenotypically characterized alone or together with their WT counterparts in different ratios by transient transfection in the absence or presence of NAs.


  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: V191I


  The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway.
 PMID: 29609638       2018       Virology journal
Discussion: Lee et al.found that the percentage of S-phase cells increased in the presence of HBV rtV191I/sW182* as compared to that in the presence of wide-type HBV, and the possible mechanism may be associated with the down-regulation of p53 and p21 and up-regulation of Cyclin A and CDK4 gene expressions, which also could promote cells from G1 phase to S phase thus accelerating cell proliferation.
Discussion: has been reported that the presence of HBV rtV191I/sW182* mutant may induce cell canceration via inhibiting TGFBI expression and increasing CyclinD1expression.



Browser Board

 Co-occurred Entities




   Filtrator