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Objective: The ideal endpoint of antiviral therapy in chronic hepatitis B (CHB) patients is to clear hepatitis B surface antigen (HBsAg). This study aimed to evaluate whether the expression of functional molecules on plasmacytoid dendritic cells (pDCs) is associated with HBsAg loss in HBeAg-positive patients during peginterferon alpha-2a (PEG IFN α-2a) therapy.
Methods: A single-center prospective cohort study was performed in HBeAg-positive CHB patients who were treated with PEG-IFN α-2a and followed up for 4 years. HBsAg clearance, HBeAg loss and undetectable HBV DNA achieved by PEG-IFN α-2a therapy was considered as functional cure. The frequencies of pDC and CD86 pDC in peripheral blood, and the mean fluorescence intensity of CD86 (CD86MFI) on the surface of pDC were measured at starting therapy, after 12 and 24 weeks of therapy.
Results: Of 63 patients enrolled, 17 patients achieved HBsAg loss. The baseline HBV DNA load in Non-functional-cure group was significantly higher than that in Functional cure group, and the CD86 pDC% was significantly lower in patients without functional cure. HBV DNA load (OR=0.146, = 0.002) and CD86 pDC% (OR=1.183, = 0.025) were independent factors associated with functional cure confirmed by binary logistic regression analysis. In the Functional cure group, HBsAg, HBeAg, and HBV DNA loads decreased remarkably after 12 weeks and 24 weeks of treatment compared to baseline. In Non-functional-cure group, CD86 pDC% and CD86MFI increased significantly from baseline after 12 weeks of treatment. In the Functional cure group, compared with baseline, pDC% increased significantly at 24 weeks, while CD86MFI increased significantly after 24 weeks of treatment.
Conclusion: The lower the baseline HBV DNA load and the more the baseline CD86 pDC%, the easier it is for patients to obtain functional cure.
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http://dx.doi.org/10.3389/fimmu.2022.891424 | DOI Listing |
J Neurotrauma
September 2025
Institute of Cardiovascular Disease, Gladstone Institutes, San Francisco, California, USA.
Spinal cord injury (SCI) results in an array of debilitating, sometimes permanent-and at times life-threatening-motor, sensory, and autonomic deficits. A broad range of therapies have been tested pre-clinically, and there has been a significant acceleration in recent years of clinical translation of potential treatments. However, it is widely appreciated among scientists and clinical professionals alike that there likely is no "silver bullet" (single treatment) that will result in complete functional restoration after SCI.
View Article and Find Full Text PDFNat Aging
September 2025
Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway.
Beyond their classical functions as redox cofactors, recent fundamental and clinical research has expanded our understanding of the diverse roles of nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) in signaling pathways, epigenetic regulation and energy homeostasis. Moreover, NAD and NADP influence numerous diseases as well as the processes of aging, and are emerging as targets for clinical intervention. Here, we summarize safety, bioavailability and efficacy data from NAD-related clinical trials, focusing on aging and neurodegenerative diseases.
View Article and Find Full Text PDFEMBO Mol Med
September 2025
Department of Neurology, Columbia University, New York, NY, 10032, USA.
Spinal muscular atrophy (SMA) is a neurodegenerative disease caused by ubiquitous deficiency in the SMN protein. The identification of disease modifiers is key to understanding pathogenic mechanisms and broadening the range of targets for developing SMA therapies that complement SMN upregulation. Here, we report a cell-based screen that identified inhibitors of p38 mitogen-activated protein kinase (p38 MAPK) as suppressors of proliferation defects induced by SMN deficiency in mouse fibroblasts.
View Article and Find Full Text PDFJ Viral Hepat
October 2025
Medical Practice Evaluation Center, Massachusetts General Hospital, Boston, Massachusetts, USA.
Discontinuing antivirals in chronic hepatitis B virus (HBV) 'e' antigen negative infection can enhance HBV surface antigen (HBsAg) loss but risks complications. We modelled the clinical impact of discontinuing antivirals in chronic HBV. We developed a Markov state model with Monte Carlo simulation of chronic HBV to compare continuation of antiviral therapy with 3 strategies of cessation and reinitiation for: (1) virologic relapse, (2) clinical relapse, or (3) hepatitis flare.
View Article and Find Full Text PDFAllergol Immunopathol (Madr)
September 2025
Department of Allergy and Immunology, University of Health Sciences, Süreyyapaşa Training and Research Hospital, Istanbul, Turkey.
Background: Antituberculosis drugs can cause hypersensitivity reactions that interrupt treatment and increase morbidity. Early identification and management are essential to prevent complications and drug resistance.
Objective: To evaluate the clinical characteristics, risk factors, and outcomes of antituberculosis drug-induced hypersensitivity reactions over a 10-year period in a tertiary referral center.