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HBV serum RNA kinetics during nucleic acid polymers based therapy predict functional cure.
Antiviral Res
December 2024
Program for Experimental & Theoretical Modeling, Division of Hepatology, Department of Medicine, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA. Electronic address:
Article Synopsis
- Serum HBV-RNA (seRNA) is being explored as a marker for measuring the activity of HBV replication in liver cells, and the study investigates its behavior under a specific treatment regimen.
- The trial involved 40 individuals with chronic HBV who received a combination of tenofovir, pegylated interferon, and a nucleic-acid polymer (NAP) over 48 weeks, revealing unique seRNA patterns in response to the treatments.
- Results showed that having a lower seRNA half-life was linked to achieving a partial or functional cure, suggesting that faster inactivation of cccDNA – the genetic material driving the virus – might lead to better treatment outcomes.
DNA Sensor ABCF1 Phase Separates With cccDNA to Inhibit Hepatitis B Virus Replication.
Adv Sci (Weinh)
December 2024
Key Laboratory for Experimental Teratology of Ministry of Education and Department of Immunology, School of Basic Medical Sciences, Cheeloo Medical College, Shandong University, Jinan, Shandong, 250012, China.
Hepatitis B virus (HBV) covalently closed circular DNA (cccDNA) contributes to viral persistence and recurrence, however, how the host innate immune system responds to cccDNA is still less known. Here, based on cccDNA-hepatic proteins interaction profiling, DNA sensor ATP-binding cassette subfamily F member 1 (ABCF1) is identified as a novel cccDNA-binding protein and host restriction factor for HBV replication. Mechanistically, ABCF1 recognizes cccDNA by KKx4 motif and forms phase-separated condensates by the poly-glutamine (PolyQ) region of the N-terminal intrinsically disordered low-complexity domain (LCD).
View Article and Find Full Text PDFPreclinical and clinical antiviral characterization of AB-836, a potent capsid assembly modulator against hepatitis B virus.
Antiviral Res
November 2024
Arbutus Biopharma Inc., Warminster, PA, USA.
HBV capsid assembly modulators (CAMs) target the core protein and inhibit pregenomic RNA encapsidation and viral replication. HBV CAMs also interfere with cccDNA formation during de novo infection, which in turn suppresses transcription and production of HBV antigens. In this report, we describe the antiviral activities of AB-836, a potent and highly selective HBV CAM.
View Article and Find Full Text PDFRational Design, Synthesis, and Structure-Activity Relationship of a Novel Isoquinolinone-Based Series of HBV Capsid Assembly Modulators Leading to the Identification of Clinical Candidate AB-836.
J Med Chem
September 2024
Arbutus Biopharma, Inc., 701 Veterans Circle, Warminster, Pennsylvania 18974, United States.
Inhibition of Hepatitis B Virus (HBV) replication by small molecules that modulate capsid assembly and the encapsidation of pgRNA and viral polymerase by HBV core protein is a clinically validated approach toward the development of new antivirals. Through definition of a minimal pharmacophore, a series of isoquinolinone-based capsid assembly modulators (CAMs) was identified. Structural biology analysis revealed that lead molecules possess a unique binding mode, exploiting electrostatic interactions with accessible phenylalanine and tyrosine residues.
View Article and Find Full Text PDFAssociation of Hepatitis B Surface Antigen Levels With Long-Term Complications in Chronic Hepatitis B Virus Infection: A Systematic Literature Review.
J Viral Hepat
November 2024
Research and Development, GSK, Brentford, Middlesex, UK.
Chronic hepatitis B virus (HBV) infection is a global issue and can lead to cirrhosis and hepatocellular carcinoma (HCC). Hepatitis B surface antigen (HBsAg) is an important marker of HBV infection and HBsAg quantification could be a useful tool in clinical practice. This systematic literature review aimed to explore the association between HBsAg titres and long-term disease outcomes and evaluate the relationship between HBsAg titres, or changes in HBsAg titres, and clinical and treatment characteristics in patients with chronic HBV infection.
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