Theiler disease (serum hepatitis or idiopathic acute hepatic necrosis) has long been suspected to have a viral etiology. Four viruses have been described in association with hepatitis in horses. Further investigation suggests equine pegivirus and Theiler disease-associated virus (a second pegivirus) are neither hepatotropic nor pathogenic. Nonprimate hepacivirus (NPHV) causes subclinical disease in experimental models and has been associated with hepatitis in some clinical cases. Equine parvovirus-hepatitis (EqPV-H) experimentally causes subclinical-to-clinical liver disease and is found in the vast majority of Theiler disease cases. EqPV-H is likely of clinical significance, whereas the significance of NPHV is unknown.
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http://dx.doi.org/10.1016/j.cveq.2019.03.001 | DOI Listing |
Int J Med Microbiol
December 2024
Institute of Medical Microbiology, University Hospital Münster, Münster, Germany; Masanga Medical Research Unit, Masanga Hospital, Masanga, Sierra Leone.
Background: Nasopharyngeal colonization with Staphylococcus aureus is a risk factor for subsequent infection. Isolates from colonization can therefore provide important information on virulence factors and antimicrobial resistance when data from clinical isolates are lacking. The aim of this study was to assess colonization rates, resistance patterns and selected virulence factors of S.
View Article and Find Full Text PDFSci Rep
December 2024
Institute of Pharmacology and Toxicology, School of Veterinary Medicine, Freie Universität Berlin, Koserstraße 20, 14195, Berlin, Germany.
Despite the international effort to improve laboratory animal welfare through the 3R principles (Reduce, Refine, Replace), many scientists still fail to implement and report their assessment of pain and well-being, likely due to concerns regarding the potential effects of analgesics on experimental outcomes. This study aimed to determine whether refining our viral encephalitis model with perioperative analgesia could enhance well-being and recovery after intracerebral virus infection without impacting disease outcomes. We routinely use the Theiler's Murine Encephalomyelitis Virus (TMEV) model to study virus-induced epilepsy.
View Article and Find Full Text PDFJ Clin Endocrinol Metab
December 2024
Department of Medicine III and Technische Universität Dresden, Dresden, Germany.
Context: Sclerostin inhibits canonical Wnt signaling, a pathway promoting bone formation. The effects of vitamin D3, omega-3 fatty acids (omega-3s), and exercise on serum sclerostin levels and bone metabolism are unclear.
Objective: To investigate the effects of 2000 IU/d vitamin D3, 1g/d omega-3s, and a simple home-based strength exercise program (SHEP), alone or in combination, on serum sclerostin and bone turnover marker levels.
Epilepsy Curr
April 2024
Department of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Roughly 80% of the global burden of epilepsy resides in low- and middle-income countries (LMICs; WHO, 2022). Despite numerous new therapies for the treatment of epilepsy, the number of patients who remain resistant to available medications is unchanged. Additionally, no therapy has yet been clinically proven to prevent or attenuate the development of epilepsy in at-risk individuals.
View Article and Find Full Text PDFCurr Neurol Neurosci Rep
November 2024
Neuroscience Department, Meyer Children's Hospital IRCCS, Viale Pieraccini 24, 50139, Florence, Italy.
Purpose Of Review: This review examines the role of different viral infections in epileptogenesis, with a focus on Herpesviruses such as Human Herpesvirus 6 (HHV-6) and Epstein Barr Virus (EBV), Flaviviruses, Picornaviruses, Human Immunodeficiency Virus (HIV), Influenzavirus and Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2).
Recent Findings: A growing literature on animal models, such as the paradigmatic Theiler's murine encephalomyelitis virus (TMEV) model, and clinical investigations in patients with epilepsy have started to elucidate cellular mechanisms implicated in seizure initiation and development of epilepsy following viral infections. A central role of neuroinflammation has emerged, with evidence of activation of the innate and adaptive immunity, dysregulation of microglial and astrocytic activity and production of multiple cytokines and other inflammatory mediators.
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