Abstract: BACKGROUND AND AIMS: Entecavir (ETV) resistance of hepatitis B virus (HBV) conventionally requires rt184, 202, or 250 mutations plus lamivudine-resistance mutation (rtM204V/I +- L180M).
Introduction: Signature or cla
Result: The patterns of LAMr, in the composition of ETV-resistance mutations, included rtM204V+L180M (82.91%), rtM204I +-L180M (15.25%), and rtM204V /I+L180M (1.84%) (Table 1).
Table: M204I
Table: M204V/I
Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan.
Discussion: M204I/V mutations are frequently accompanied by compensatory mutations in other domains such as 59 rtV173L, rtL180M, rtT184S/G, 58 rtI169T, rt Discussion: For example, dual rtL180M and M204V/I mutants were frequently found in patients in Italy, with three patients having triple mutation of rtV173L, rtL180M and M204V.
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
Abstra
Introduction: It has been indicated that LAM resistance is mostly associated with the rtM204I/V mutation in the tyrosine-methionine-aspartate-aspartate (YMDD) motif of the C domain of the polymerase gene.
Discussion: Similar to previous studies, the present study suggested that truncation mutations (rtA181T/sW172*, rtM204I/sW196* and rtV191I/sW182*) occurred at the highest frequency.
[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.
Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection.
Abstract: Notably, 11 mutations at position 169, 202, 250, 173, 180, 200, 207, 214, 237, 242 and 245 coexisted with M204I or V.
Introduction: These two categories are known as classical mutations, which include: (i) M204I/V mutation, which associates with LAM or LDT resistance; (ii) N236T or A181T/V mutations, which associate with ADV resistance; (iii) M204V + L180M and either T184A/G/I/L/S or S202G or M250V to develop resistance to ETV.
Discussion: In current study, mutation of L229 was not a single mutation site: 75% mutations of this site associated to M204I or V.
Discussion: When takin
Hepatitis B virus reverse transcriptase polymorphisms between treated and treatment-naive chronically infected patients.
Abstract: Drug resistance conferring substitutions (DRCSs) were rtL180M (22/98), rtA194V (11/98), rtM204V (1/98), and rtM204I (11/98).
Complementation of Wild-Type and Drug-Resistant Hepatitis B Virus Genomes to Maintain Viral Replication and Rescue Virion Production under Nucleos(t)ide Analogs.
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.
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.
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].