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).


  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
Result: After scrutinizing the frequency of mutations within these sites, only two NA-r mutations, ntG700A (rtV191I, P = 0.01
Result: Putative resistance mutations were observed at 8 AA sites among the panel of treatment-naive patients; they were rtV191I, rtS213T, rtV214A, rtE218D, rtL229V, rtI233V, rtN238S, rtS/C256G.


  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<
Table: V191I


  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


  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.


  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
Discussion: Other mutations, including rtV84M, rtN118H/D/T, rtI169T, rtT184A/L/S,
Discussion: Similar to previous studies, the present study suggested that truncation mutations (rtA181T/sW172*, rtM204I/sW196* and rtV191I/sW182*) occurred at the highest frequency.


  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.


  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
Discussion: Among 435 patients, non-classical mutations were detected at nine sites (V191I, V207I/M, S213T, E218D, F221Y, I224V, L229V, N/H238 and R242D) with virological breakthrough and without classical mutations (Table 4).
Discussion: Interestingly, in vitro test, the V191I mutant remained sensitive to ADV.
Discussion: reported that V191I was observed after 6 months of treatment with ADV, similar with that in present study (Table 4).


  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
Introduction: Virological breakthrough on TDF therapy has been reported in two patients harbouring rtS78T/sC69 mutations, and in another patient with multi-site polymerase mutations; rtL80M, rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A, rtT184A/L, rtR153Q, and


  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.



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