Abstract: A unique D3 presented the G1896A substitution at the preC (HBeAg negative phenotype).
Abstract: The double substitution G1764A/A1762T at the BCP (reduced HBeAg expression) was found in 20% F1b, 2% A2, 2% D1, and 2% D3 samples.
Synthesis of an Anti-hepatitis B Agent, 2'-Fluoro-6'-methylene-carbocyclic Adenosine (FMCA) and Its Phosphoramidate (FMCAP).
PMID: 30589264
2019
The Journal of organic chemistry
Abstract: 2'-Fluoro-6'-methylene-carbocyclic adenosine (FMCA, 12) and its phosphoramidate prodrug (FMCAP, 14) have been proven as a potential anti-HBV agent against both adefovir-resistant as well as lamivudine-resistant double (rtL180M/rtM204V) mutants.
Abstract: Furthermore, in vitro, these agents have demonstrated significant activity against lamivudine/entecavir triple mutants (L180M + S202G + M204V).
Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients.
Abstract: G120A mutation resulted in an increased HBV DNA level in vitro, consistent with the serological results in patients.
Abstract: G82A, A115C and G120A mutants boosted the intracellular HBV total RNA level.
Abstract: In vitro experiments in HepG2 cells showed that G82A, A115C and G120A mutants increased the hepatitis B surface antigen (HBsAg) levels, while C18T had an opposite effect.
Abstract: Luciferase assay revealed distinct promoter activities among SPII mutants; especially SPII of G120A mu
CMCdG, a Novel Nucleoside Analog with Favorable Safety Features, Exerts Potent Activity against Wild-Type and Entecavir-Resistant Hepatitis B Virus.
PMID: 30670420
2019
Antimicrobial agents and chemotherapy
Abstract: CMCdG also reduced the level of HBVETV-R L180M/S202G/M204V viremia by ~1 log in HBVETV-R L180M/S202G/M204V-infected human liver-chimeric mice, while ETV (1 mg/kg/day q.d.) completely failed to reduce the viremia.
Abstract: CMCdG potently inhibited HBV production in HepG2.2.15 cells (50% inhibitory concentration [IC50], ~30 nM) and HBVWT Ce plasmid-transfected Huh7 cells (IC50, 206 nM) and efficiently suppressed ETV-resistant HBVETV-R L180M/S202G/M204V (IC50, 2,657 nM), while it showed no or little cytotoxicity (50% cytotoxic concentration, >500 muM in most hepatocytic cells examined).
Abstract: CMCdG's in vitro activity was determined using quantitative PCR a
HBV T1719G mutation reduced HBV replication through mutant Enh II and HBx protein in vitro.
Abstract: And such reduction caused by T1719G mutation could be rescued by HBx protein.
Abstract: In this study, we aimed to evaluate the function and mechanisms of the T1719G mutation on viral replication capacity.
Abstract: It was repeatedly reported that the hepatitis B virus (HBV) T1719G mutation was very common and related to progression and malignancy of liver disease.
Abstract: Our results show that the T1719G mutation decreases HBV viral replication capacity possibly by mutant HBx protein and altered Enh II activity.
Abstract: Our results showed that the T1719G mutation impaired viral replication efficacy compared with the wild type both by reducing
Diverse immune responses to HBV surface epitope variants after vaccine booster in adolescents immunized in infancy.
PMID: 30771531
2019
Clinical microbiology and infection
Abstract: Antibody affinity to sG145R and the IFN-gamma-secreting cell response to some epitope 16-33 variants were still impaired even after booster administration.
Abstract: IFN-gamma-secreting T cells to epitope 16-33 containing R24K and the antibody affinity to sG145R were still significantly lower than to the wild type.
Identification of a quadruple mutation that confers tenofovir resistance in chronic hepatitis B patients.
Abstract: RESULTS: Five mutations (rtS106C [C], rtH126Y [Y], rtD134E [E], rtM204I/V, and rtL269I [I]) were commonly found in viral isolates from 2 patients.
Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients.
Abstract: By contrast, the emergence of rtI163V was not related to ETV treatment.
Abstract: Classical ETV-resistance mutations rtT184/S202/M250substitution+rtM204V/I+-L180M (LAM-r), rtA186T, and rtI163V were detected in 1252 (5.69%), 14 (0.06%), and 230 (1.05%) of the 22,009 patients, respectively.
Abstract: Compared to wild-type strain, two patient-derived mutants' rtL180M+A186T+M204V and rtL180M+
Pre-S/Surface and Core Promoter/Precore Mutations in Chronic Hepatitis B Patients with Severe Acute Exacerbation.
PMID: 30835025
2019
Digestive diseases and sciences
Abstract: Cox regression analysis showed that independent predictors for mortality at week 24 of treatment in SAE patients were higher international normalized ratio, the presence of ascites, and T1753C/A/G mutations.
Abstract: Multivariate analysis showed that the independent factors for SAE were V14G/A and L21S in surface genes, codons 109-119 deletions in pre-S1 genes, M1V/T/I in pre-S2 genes, and C1766T/T1768A and C1913A/G mutations in BCP/PC genes.
Abstract: The S
Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice.
Abstract: Artificial elimination of rtA181C largely restored the rtL180M+A181C+M204V mutant's sensitivity to ETV.
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).
Abstract: CONCLUSIONS: Both clinical and experimental data support rtL180M+A181C+M204V as a novel non-classical ETV-resistance mutation pattern.