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Chemical characterization and evaluation of antiviral activity of two fucoidans extracted from Mediterranean brown seaweeds, Padina pavonica and Dictyopteris membranacea.
Lett Appl Microbiol
January 2025
Laboratory for Chemical, Galenic and Pharmacological Development of Drugs (LR12ES09), Faculty of Pharmacy of Monastir, University of Monastir, Tunisia.
Brown seaweeds are known for their bioactive compounds, particularly sulfated polysaccharides such as fucoidans, which have demonstrated antiviral properties. However, limited studies have focused on the antiviral potential of fucoidans extracted from Mediterranean brown seaweeds. In this study, two brown seaweeds Padina pavonica and Dictyopteris membranacea (Fuc-Pad and Fuc-Dic) were collected from monastir coasts, Tunisia, and a specific extraction protocol was employed to obtain fucoidans.
View Article and Find Full Text PDFAdvancing Myocarditis Research: Evaluating Animal Models for Enhanced Pathophysiological Insights.
Curr Cardiol Rep
January 2025
Medical College, Hunan University of Chinese Medicine, Changsha, 410208, Hunan, China.
Purpose Of Review: This review aims to assess the current landscape of animal models used in myocarditis research, with a focus on understanding their utility in uncovering the pathophysiology of the disease. The goal is to evaluate these models' strengths and weaknesses and propose optimizations to make them more relevant and reliable for both mechanistic studies and therapeutic interventions in myocarditis.
Recent Findings: Recent studies have primarily utilized animal models, particularly viral and autoimmune myocarditis models, to study disease mechanisms.
Common Chemical Plasticizer Di(2-Ethhylhexyl) Phthalate Exposure Exacerbates Coxsackievirus B3 Infection.
Viruses
November 2024
Department of Biological Sciences, University of Alabama, Tuscaloosa, AL 35487, USA.
Unlabelled: Di(2-ethhylhexyl) phthalate (DEHP) is a common plastic rubberizer. DEHP leaches from plastic matrices and is under increasing scrutiny as numerous studies have linked it to negative human health manifestations. Coxsackievirus B3 (CVB) is a human pathogen that typically causes subclinical infections but can sometimes cause severe diseases such as pancreatitis, myocarditis, and meningoencephalitis.
View Article and Find Full Text PDFImmunodeficiency-Related Vaccine-Derived Poliovirus (iVDPV) Infections: A Review of Epidemiology and Progress in Detection and Management.
Pathogens
December 2024
World Health Organization Headquarters, Av Appia 10, 1211 Geneva, Switzerland.
Individuals with certain primary immunodeficiency disorders (PID) may be unable to clear poliovirus infection after exposure to oral poliovirus vaccine (OPV). Over time, vaccine-related strains can revert to immunodeficiency-associated vaccine-derived poliovirus (iVDPVs) that can cause paralysis in the patient and potentially spread in communities with low immunity. We reviewed the efforts for detection and management of PID patients with iVDPV infections and the epidemiology through an analysis of 184 cases reported to the World Health Organization (WHO) during 1962-2024 and a review of polio program and literature reports.
View Article and Find Full Text PDFThe N6-methyladenosine RNA epigenetic modification modulates the amplification of coxsackievirus B1 in human pancreatic beta cells.
Front Microbiol
December 2024
ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Article Synopsis
- Type 1 diabetes (T1D) results from an autoimmune attack that destroys insulin-producing beta cells, with its initiation linked to genetic, immunological, and environmental factors, particularly viral infections like Coxsackievirus B (CVB).
- Research reveals that CVB serotype 1 (CVB1) may trigger autoimmune responses in genetically susceptible individuals, but the exact mechanisms of its replication in beta cells are unclear.
- New findings indicate that the N6-methyladenosine (m6A) modification influences CVB1 amplification, where downregulating m6A "writers" increases viral replication, while inhibiting "erasers" like FTO significantly decreases infectious CVB1 production, highlighting m6A's role
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