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Equine encephalomyelitis.

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Venezuelan equine encephalomyelitis.

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Le virus de l’encéphalomyélite murine de Theiler (TMEV) fait partie de la famille des Picornaviridae et au genre Cardiovirus. Les souches persistantes du virus, telle que la souche DA persistent dans la substance blanche de la moelle épinière de la souris malgré une réponse immunitaire spécifique et soutenue.La protéine accessoire L* codée par le virus joue un rôle-clé dans l'échappement de cette réponse immunitaire.Cette protéine L* est un exemple unique de protéine, chez les Picornavirus, à être traduite par un cadre ouvert de lecture alternatif .Dans une cellule infectée par le virus de Theiler, L* se localise en partie dans le cytosol et en partie dans la membrane externe de la mitochondrie. La L* participe à l'échappement du virus à la réponse immunitaire en inhibant l'activité RNase L par une interactiondirecte avec celle-ci. La RNase L est l'un des effecteurs les mieux caractérisés de la réponse à l'interféron. Cette enzyme est activée par des oligoadénylates, les 2-5A, synthétisés en réponse à l 'infection virale par une famille d'enzymes appelées oligoadénylates synthétases (OAS). Une fois activée, la RNase L dégrade l'ARN simple brin cellulaire et viral afin de limiter la propagation du virus.À l'heure actuelle, nous ne savons pas quel avantage a la protéine L* à se localiser à la mitochondrie. Le but premier de ce mémoire était de déterminer si la localisation mitochondriale de L* contribue à son activité antagoniste de la RNase L. Un but secondaire consistait à définir les résidus de la protéine L* responsables de l’interaction entre la protéine L* et la RNase L. Pour ce faire, une série de mutants de la protéine L* ont été construits et testés dans des expériences de transfection et d'infection. Nous avons ensuite tenté d' isoler les mutants L* qui perdent leur localisation mitochondriale, mais gardent leur activité inhibitrice de la RNase L vise-versa. Lors ce mémoire, nous avons découvert plusieurs mutants L* intéressants. Premièrement le mutant L* L140P qui montre une association moins prononcée aux mitochondries. Deuxièment, nous avons identifié deux mutants L* qui perdent leur activité anti-RNase-L. Theiler's Murine Encephalomyelitis Virus (TMEV) belongs to the Picornaviridae family and to the Cardiovirus genus. Persistent strains of this virus persist in the white matter of the spinal cord of mice despite a specific and sustained immune response.The L * accessory protein encoded by the virus allows the initiation of a persistent infection by counteracting the innate immune response.This L* protein is a unique example of a Picornavirus protein to be translated by an alternative open reading frame. In Theiler's virus infected cell, L * is partially located in the cytosol and partially anchored in the mitochondrial outer membrane. In our laboratory, F. Sorgeloos showed that L * inhibits RNase L activity through a direct binding to the enzyme.RNase L is one of the best-characterized effectors of the interferon response. This enzyme is activated by 2', 5'-linked oligoadenylate (2-5A) synthesized in response to viral infection, by a family of enzymes called oligoadenylates synthetases (OAS). Once activated, RNase L degrades single-stranded cellular and viral RNA, which limits viral propagation and ultimately leads to apoptosis of infected cells.At present, we do not know the reason for the mitochondrial localization of a fraction of the L* protein. The main objective of this work was to determine whether the mitochondrial localization of L * contributes to its anti-RNase L activity. A secondary aim was to identify residues of the L* protein responsible for interaction between L * and RNase L. In this purpose, a series of L* protein mutants were constructed and tested after transient transfection and after infection. We attempted to identify L* mutants that lost the mitochondrial localization, but kept the anti-RNase L activity and vice-versa .During this master thesis, we identified one L* mutant that lost the mitochondrial localization. Secondly we identified two L* mutants that lost the anti-RNase L activity.

Theilovirus --- L(asterisk) protein, Theiler's encephalomyelitis virus --- Encephalomyelitis

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"Myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS) are serious, debilitating conditions that affect millions of people in the United States and around the world. ME/CFS can cause significant impairment and disability. Despite substantial efforts by researchers to better understand ME/CFS, there is no known cause or effective treatment. Diagnosing the disease remains a challenge, and patients often struggle with their illness for years before an identification is made. Some health care providers have been skeptical about the serious physiological - rather than psychological - nature of the illness. Once diagnosed, patients often complain of receiving hostility from their health care provider as well as being subjected to treatment strategies that exacerbate their symptoms. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome proposes new diagnostic clinical criteria for ME/CFS and a new term for the illness - systemic exertion intolerance disease(SEID). According to this report, the term myalgic encephalomyelitis does not accurately describe this illness, and the term chronic fatigue syndrome can result in trivialization and stigmatization for patients afflicted with this illness. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome stresses that SEID is a medical - not a psychiatric or psychological - illness. This report lists the major symptoms of SEID and recommends a diagnostic process.One of the report's most important conclusions is that a thorough history, physical examination, and targeted work-up are necessary and often sufficient for diagnosis. The new criteria will allow a large percentage of undiagnosed patients to receive an accurate diagnosis and appropriate care. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome will be a valuable resource to promote the prompt diagnosis of patients with this complex, multisystem, and often devastating disorder; enhance public understanding; and provide a firm foundation for future improvements in diagnosis and treatment."--

Myalgic encephalomyelitis --- Chronic fatigue syndrome --- Diagnosis.

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"ME/CFS: Causes, Clinical Features and Diagnosis" addresses the early stages of ME/CFS and underlying predisposing factors. It considers the plight of the individual patient, and also the impact of the illness on society as a whole, which is considerable, in terms of both costs and social disruption. Patients and their families and carers frequently experience discrimination and difficulties accessing care. This volume will be of particular interest to those undertaking scientific research and those providing clinical care for ME/CFS patients, as well as to social policy analysts, policy makers and governments, and specialists in social research and medical education. There is a major focus on shortcomings in terms of medical education, resulting in considerable gaps in knowledge and understanding of the condition among many doctors. International comparisons indicate that these problems are encountered in many countries. This is particularly topical at a time when Long Covid-19 has moved post-viral syndromes to the forefront of the political agenda, and confronted society with new challenges in this area on a hitherto unprecedented scale. The volume addresses the many points of similarity between Long Covid-19 and ME/CFS. Mitigation of the illness is also addressed, through espousal of a more patient-centred approach to care, and through consideration of the scope for prevention. Sixty-nine authors from seventeen European countries, and from Canada and the USA have contributed to this volume, which is a truly international collaboration.

Myalgic encephalomyelitis. --- Chronic fatigue syndrome --- Diagnosis.