Signal-On Electrochemical Detection for Drug-Resistant Hepatitis B Virus Mutants through Three-Way Junction Transduction and Exonuclease III-Assisted Catalyzed Hairpin Assembly.
Abstract: The rtN236T mutation, an error encoded by codon 236 of the reverse transcriptase region of HBV DNA, was employed as the model gene target.
Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro.
Discussion: As such, a vaccine containing both wild-type and the G145R mutant HBsAg can also confer immunity to both types of the virus.
Discussion: At the same time, the inability of HBsAg with the G145R mutation to enhance the expression of CD86 on B cells may indicate a lack of a compensatory mechanism in this escape mutant.
Discussion: Comparative studies of sera from people who were vaccinated with monovalent vaccines and those recovered from HBV infection have demonstrated that only sera of the recovered patients contained highly active antibodies against both the G145R mutant HBsAg and wild-type HBsAg.
Discussion: Evaluation of cytokine production by PBMC from healthy donors in re
Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient.
Abstract: An HIV-coinfected patient presented the rtM204V/I-rtL180M double resistance mutation in serum and DBS.
Discussion: As demonstrated by Mello et al., Y100C alone may not affect HBsAg production, secretion or HBsAg affinity by commercial serological assays, as for our samples.
Discussion: In addition, L109R/V mutations were present in 2/10 samples and have been related to HBV vaccine escape and virus evasion to the host immune system.
Discussion: Overall, Y100C was the most frequent substitution, being present in 6/10 sequenced samples.
Discussion: Regarding resistance mutations, the double rt
Establishment of monoclonal antibodies broadly neutralize infection of hepatitis B virus.
Abstract: In addition, the antibodies neutralized the infection of hepatitis D virus possessing a Gly145 mutation to Arg in S protein, which is a well-known escape mutation against HBIG treatment.
Hepatitis B virus genetic multiplicity and the associated HBV lamivudine resistance mutations in HBV/HIV co-infection in Western Kenya: A review article.
PMID: 34954390
2022
Infection, genetics and evolution
Abstract: HBV polymerase rtV173L, rtL180M, and rtM204V major substitutional mutations were identified.
Combining the HBcrAg decline and HBV mutations predicts spontaneous HBeAg seroconversion in chronic hepatitis B patients during the immune clearance phase.
Abstract: Baseline A1574T, G1862A, G1896A, and C1913G mutations and HBcrAg levels with a sharp decrease at Week 28 were associated with spontaneous HBeAg seroconversion.
Abstract: The mutation frequencies of A1574T (51.11% vs. 18.18%, p = 0.001), G1862A (30.00% vs. 13.03%, p = 0.001), G1896A (27.22% vs. 5.45%, p = 0.001), and C1913G (32.78% vs. 12.73%, p = 0.001) in Group A were significantly higher than Group B.
Preclinical characterization of AB-506, an inhibitor of HBV replication targeting the viral core protein.
Abstract: Evaluation of AB-506 against a panel of core variants showed that T33N/Q substitutions results in >200-fold increase in EC50 values, while L30F, L37Q, and I105T substitutions showed an 8 to 20-fold increase in EC50 values in comparison to the wild-type.
Multiple epitopes of hepatitis B virus surface antigen targeted by human plasma-derived immunoglobulins coincide with clinically observed escape mutations.
Abstract: We then tested in binding assays HBsAg peptides containing clinically relevant mutations previously reported within these sites, such as Y134S, P142S, and G145R, and observed a significant reduction in anti-HBs binding activity to the mutated sites, suggesting a mechanism the virus may use to avoid HBIG-mediated neutralization.
Regulatory function of interferon-inducible 44-like for hepatitis B virus covalently closed circular DNA in primary human hepatocytes.
Abstract: METHODS: Primary human hepatocytes were infected with HBV using genomic plasmids carrying the basic core promoter mutation A1762T/G1764A and/or the precore mutation G1896A and treated with IFN-gamma and IFN-alpha.
HBV mutation literature information.
PMID: 
2022
Analytical chemistry
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