Abstract: Southern blot analysis using wild-type HBV (HBVWT)-encoding-plasmid-transfected HepG2 cells revealed that CdFA efficiently suppresses the production of HBVWT (IC50 = 153.7 nM), entecavir (ETV)-resistant HBV carrying L180M/S202G/M204V substitutions (HBVETVR; IC50 = 373.2 nM), and adefovir dipivoxil (ADV)-resistant HBV carrying A181T/N236T substitutions (HBVADVR; IC50=192.6 nM), whereas ETV and ADV were less potent against HBVETVR and HBVADVR (IC50: >1,000 and 4,022.5 nM, respectively).
Method: Plasmids carrying the 1.24-fold HBV genomes of a wild-type genotype Ce strain (HBVWTCe), entecavir-resistant strain carrying L180M/S202G/M204V substitutions (HBVETVR), or adefovir-resistant strain carrying
Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine.
Abstract: Additionally, we experimentally simulated previously reported ETV/3TC resistance for HBV using HIVY115F/F116Y/Q151M with F160M/M184V (L180M/M204V in HBV RT) substituted.
Result: In fact, M184V in HIV-1 (or M204V in HBV) is not reportedly associated with TDF/TAF resistance.
Result: One possible solution to overcome M184V/I (M204V/I in HBV) resistance is to decrease composition for NRTIs that do not rely on the interactions with Met184.
Result: Previous in vitro antiviral assays have demonstrated that 4'-cyano-containing NRTIs, such as CAdA and CdG, show slightly decreased but moderate activity against HBV with M204V in RT.
Result: The corresponding M204V/I mutation
Entecavir resistance mutations rtL180M/T184L/M204V combined with rtA200V lead to tenofovir resistance.
Abstract: CONCLUSION: An rtL180M/T184L/A200V/M204V mutant with moderate resistance to TDF monotherapy was selected during sequential nucleoside analogue (NA) treatment in a stepwise manner.
Abstract: In vitro phenotyping demonstrated that the rtL180M/T184L/A200V/M204V mutant had moderate resistance to TDF treatment, with a 4.52-fold higher half maximal effective concentration than that of wild-type virus.
Abstract: METHODS AND RESULTS: Here, we report viral rebound in a patient with chronic hepatitis B who underwent TDF monotherapy and harboured a quadruple mutant consisting of cla
Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients.
Introduction: Phenotypic studies showed that the LMV resistance arising from rtM204V/I in the YMDD motif, could negate sensitivity to LMV by more than 100-fold decrease compared with wild-type.
Introduction: The classic ETV resistance mutations rtT184G/rtS202I/rtM250V will reduce susceptibility to ETV, only in conjunction with additional LMV resistance mutations, such as rtM204V/I.
Method: Three different mutations, rtM204V, rtL229V and
Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing.
PMID: 31189581
2019
Journal of clinical microbiology
Result: Considering that the low sensitivity of Sanger sequencing limited the detection of NAr mutations with a low rate (<20%), 4 classical drug resistance mutations (S202C/G/I, M204I/V/S, N236T, and M250I/L/V) and 12 putative NAr mutations (V207I, S213T, V214A, Q215P/S, L217R, E218D, L229G/V/W/F, I233V, P237H, N/H238D/S/T, Y245H, and S/C256G)
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.
Introduction: We recently introduced some mutations in the reverse transcriptase (RT) region of Pol related to HCC from genotype C infected patients [rtM80I, rtN139K/T/H, and rtM204I/V].
Frequency of Hepatitis B Virus Resistance Mutations in Women Using Tenofovir Gel as Pre-Exposure Prophylaxis.
Result: No mutations known to cause tenofovir resistance (L180M, A181I/V, A194T, M204V/I, V214A, Q215S, N236T) or lamuvudine (3TC) resistance (L80V/I, I169T, V173L, L180M, A181T, T184S, M204V/I/S, Q215S) were observed.
Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection.
Discussion: By contrast, it is selected more frequently than M204V in genotype D.
Discussion: For L-nucleosides resistance, M204I/V was the most critical mutation site.
Discussion: In both genotypes L180 was practically necessary for M204V.
Discussion: reported that an combined mutation pattern of L80M, L180M, M204V/I, A200V, F221Y, S223A, T184A/L, R153Q, and rtV191I was detected at the time of virological and biochemical breakthrough em
[HBV pol/S gene mutations in chronic hepatitis B patients receiving nucleoside/nucleotide analogues treatment].
Abstract: Primary/secondary drug mutations (rtM204I/V, rtI169S, rtL180M, rtT184L, rtA194V, rtM204I/rtL91I, rtQ149K, rtQ215H/S, rtN238D) were detected in 38 (45.2%) of the patients.
[Determination of reverse transcriptase inhibitor nucleoside analogue resistance profile in pretreatment phase of patients with viral hepatitis B].
Abstract: Primary drug resistance mutations such as rtI169T, rtA181T/V, rtT184A/C/F/G/I/L/M/S, rtA194T, rtS202C/G/I, rtM204I/V/S, rtN236T, rt M250I/L/V and rtV173L were not detected in any of the patient samples.
HBV mutation literature information.
PMID: 
2020
Antiviral research
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