Interferon β1a treatment does not influence serum Epstein-Barr virus antibodies in patients with multiple sclerosis
Ingrid Anne LieBrit Ellen RødSilje Stokke KvistadTrygve HolmøyKjell‐Morten MyhrØivind TorkildsenStig Wergeland
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Pathogenesis
Multiple sclerosis is a multifactorial and heterogeneous neurological disease; hence, several experimental animal models had to be developed to mimic the different features of human pathology. Three main classes of animal models have been developed: experimental autoimmune encephalomyelitis (EAE), cuprizone intoxication, and Theiler's murine encephalomyelitis virus (TMEV) infection. The EAE model is the most versatile as it allows the reproduction of different patterns of multiple sclerosis; it is mostly relevant for relapsing-remitting multiple sclerosis and has allowed the development of several first-line, disease-modifying drugs for the treatment of multiple sclerosis. The other two models are less flexible than the EAE model and, to date, have not led to the discovery of any clinically relevant therapies. The cuprizone model mostly mimics the acute and chronic courses of multiple sclerosis, and it may represent a useful tool to develop novel therapies to protect oligodendrocytes and stimulate remyelination. Finally, the TMEV infection is the reference model to specifically study viral-mediated mechanisms of acute and primary progressive multiple sclerosis.
Remyelination
Encephalomyelitis
Demyelinating disease
Animal model
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Background: There is a growing need for biomarkers that can help in early diagnosis of multiple sclerosis (MS) and in recognizing patients with MS activity.Moreover, many studies are recently focusing on biomarkers that may help in diagnosis of the transition from relapsing remitting multiple sclerosis (RRMS) to secondary progressive multiple sclerosis (SPMS).Circulating microRNAs (miRNAs) are now considered promising biomarkers.Objectives: Studying the role of plasma miRNA-145 and miRNA-484 in the diagnosis of MS, disease activity and in diagnosing the transition from RRMS to SPMS.Patients and Methods: Forty-six subjects of both sexes were included, 31 patients with MS )21 with RRMS, 8 with SPMS and Two patients with primary progressive multiple sclerosis (PPMS)) and 15 healthy controls.Expression analysis of plasma miRNAs; miR-145 and miR-484 were assessed by real-time quantitative polymerase chain reaction (PCR) after miRNA extraction.Results: MicroRNAs 145 and 484 could significantly discriminate between MS cases and controls, with best cut-off values > 0.6 and > 1.7 respectively.They could also significantly discriminate between active and inactive MS cases, with best cut-off values > 0.8 and > 2 respectively.Plasma miRNA-145 could discriminate between RRMS and SPMS cases, with best cut-off value ≤1.4.Conclusion: Plasma miRNAs 145 and 484 might be used as promising biomarkers for early diagnosis of MS and in diagnosis of disease activity.Plasma miRNA-145 could be also helpful in diagnosis of the transition from RRMS to SPMS.
Relapsing remitting
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This article is the first in a series on multiple sclerosis. It describes how this neurological disease affects a person's level of abilities. Multiple sclerosis (MS) is a progressive neurological disease. MS is generally diagnosed between the ages of 20 and 50years but can appear later and, in rare cases, children can be affected. The Multiple Sclerosis Society (2007) states ‘MS is the most common disabling neurological condition affecting young adults’. Around 85000 people in the UK have MS.
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Multiple sclerosis is a disorder of the immune system that is caused by a malfunction of our body defenses. In multiple sclerosis, healthy cells of the nervous system are destroyed, and this leads to many health problems, like paralysis. Multiple sclerosis affects a lot of people worldwide. Treatments exist but are still not entirely efficient and do not work for all patients. Many researchers are studying this disease and our group is focusing on specific cells of the immune system that might be playing a role in multiple sclerosis.
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Multiple sclerosis-associated genetic variants indicate that the adaptive immune system plays an important role in the risk of developing multiple sclerosis. It is currently not well understood how these multiple sclerosis-associated genetic variants contribute to multiple sclerosis risk. CD4+ T cells are suggested to be involved in multiple sclerosis disease processes.We aim to identify CD4+ T cell differential gene expression between multiple sclerosis patients and healthy controls in order to understand better the role of these cells in multiple sclerosis.We applied RNA sequencing on CD4+ T cells from multiple sclerosis patients and healthy controls.We did not identify significantly differentially expressed genes in CD4+ T cells from multiple sclerosis patients. Furthermore, pathway analyses did not identify enrichment for specific pathways in multiple sclerosis. When we investigated genes near multiple sclerosis-associated genetic variants, we did not observe significant enrichment of differentially expressed genes.We conclude that CD4+ T cells from multiple sclerosis patients do not show significant differential gene expression. Therefore, gene expression studies of all circulating CD4+ T cells may not result in viable biomarkers. Gene expression studies of more specific subsets of CD4+ T cells remain justified to understand better which CD4+ T cell subsets contribute to multiple sclerosis pathology.
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Background – Multiple sclerosis (MS) is associated with Epstein–Barr virus (EBV) infection, but the relationship between the virus and the disease is not clear. As many different types of EBV exist, it is possible that MS is caused by one particular type of EBV. Objectives – The aim of this study was to determine whether MS is associated with a particular genotype of EBV. Materials and methods – We collected blood from MS patients and controls, amplified and sequenced the latent membrane protein-1 (LMP-1) gene, and compared the groups. Results – We found a variety of LMP-1 sequences in both MS and controls, with no significant differences between the groups. Conclusion – We conclude that MS is not associated with a particular genotype of EBV.
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Neuroradiology
Clinical neurology
Optic neuritis
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Although many studies have found a kind of a relationship between an Epstein-Barr Virus (EBV) and the development of Multiple Sclerosis (MS), a fundamental aspect of this relationship remains uncertain. What is the cause of Multiple Sclerosis (MS)? In this study, we re-analysed the data as published by Wandinger et al. and were able to establish a new insight: without an Epstein-Barr Virus (EBV) infection no development of Multiple Sclerosis (MS). Furthermore, we determined a highly significant causal relationship between Epstein-Barr Virus (EBV) and multiple sclerosis. Altogether, Epstein-Barr Virus (EBV) is the cause of multiple sclerosis (p-value 0.0004251570).
Epstein–Barr virus infection
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Abstract Eight patients with multiple sclerosis were followed for several months to determine if serum levels of galactosylceramide, a major lipid component of myelin, correlate with the clinical evolution of the disease. In the patients with the chronic progressive form of multiple sclerosis, galactosycleramide remained undetectable. In the patients with relapsing‐remitting multiple sclerosis, there was a good correlation between the elevation of serum galactosylcermide levels and clinical relapses. This serum assay should prove of value in the follow‐up of patients with multiple sclerosis.
Demyelinating disease
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Reports on fatty acids levels in multiple sclerosis remain inconclusive.To determine the erythrocyte membrane fatty acid levels in multiple sclerosis patients and correlate with Kurtzke Expanded Disability Status Scale.Fatty acid composition of 31 multiple sclerosis and 30 control individuals were measured by gas chromatography.The membrane phosphatidylcholine C20:4n - 6 concentration was lower in the multiple sclerosis patients when compared to that of the control group, P = 0.04 and it correlated inversely with the EDSS and FSS.Decrease in C20:4n - 6 in the erythrocyte membrane could be an indication of depleted plasma stores, and a reflection of disease severity.
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