Cerebrospinal fluid virological analysis in multiple sclerosis

Journal of autoimmune diseases, 2006

Epidemiological data suggest the notion that in Multiple Sclerosis (MS) is an acquired autoimmune disease and the cause may be an environmental factor(s), probably infectious, in genetically susceptible individuals. Several cases of viral induced demyelinatimg encephalomyelitis in human beings and in experimental models as well as the presence of IgG oligoclonal bands in the cerebrospinal fluid indicate that the infectious factor may be viral. However, the absence of a specific virus identification in MS central nervous system may hardly support this notion. On the other hand, the partial response of patients with MS to immunosuppressive and immunomodulatory therapy support the evidence of an autoimmune etiology for MS. However, the autoimmune hypothesis shares the same criticism with the infectious one in that no autoantigen(s) specific to and causative for MS has ever been identified. Nevertheless, the absence of identifiable infectious agent, especially viral does not rule out its presence at a certain time -point and the concomitant long term triggering of an autoimmune cascade of events thereafter. Several concepts have emerged in an attempt to explain the autoimmune mechanisms and ongoing neurodegeneration in MS on the basis of the infectious -viral hypothesis.

The Lancet Neurology, 2005

Journal of Neuroimmunology, 1999

In the century and a half since multiple sclerosis MS was first recognized, the pathology of the condition has been defined with increasing detail. From the recognition and definition of MS as a clinical phenomenon, studies of the diseased brain tissue have progressed in a manner dependent on the science of the time. Through multiple generations, the increasingly detailed analysis of the MS lesion itself has lead to an increasingly sophisticated understanding of a complex, apparently diverse, immunopathological process. During this evolution, many hypotheses concerning the pathogenesis of MS have been overturned, and the interpretation of some clearly delineated gross and histological findings have been reversed. This review plots the progress and highlights current theories and emerging concepts regarding one of the most enigmatic of neurological diseases.

Reviews in Medical Virology, 2000

Multiple sclerosis (MS) is a chronic, demyelinating disease of the CNS in which autoimmunity to myelin plays a role in pathogenesis. The epidemiology of MS indicates that it may be triggered by a virus infection before the age of adolescence, but attempts to associate a speci®c virus with MS have produced equivocal results. Many studies of the aetiology of MS have postulated that a persistent virus infection is involved, but transient virus infection may provide a plausible alternative mechanism that could explain many of the inconsistencies in MS research. The most studied animal model of MS is chronic relapsing experimental autoimmune encephalomyelitis (CREAE), which is induced in susceptible animals following injection of myelin components. While CREAE cannot provide information on the initiating factor for MS, it may mimic disease processes occurring after an initial trigger that may involve transient virus infection. The disease process may comprise separate triggering and relapse phases. The triggering phase may involve sensitisation to myelin antigens as a result of damage to oligodendrocytes or molecular mimicry. The relapse phase could be similar to CREAE, or alternatively relapses may be induced by further transient virus infections which may not involve infection of the CNS, but which may involve the recrudescence of anti-myelin autoimmunity. Although current vaccines have a high degree of biosafety, it is suggested that the measles-mumps-rubella vaccine in particular could be modi®ed to obviate any possibility of triggering anti-myelin autoimmunity.

Current Microbiology

Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS). Compared to other types of self-limiting myelin disorders, MS compartmentalizes and maintains chronic inflammation in the CNS. Even though the exact cause of MS is unclear, it is assumed that genetic and environmental factors play an important role in susceptibility to this disease. The progression of MS is triggered by certain environmental factors, such as viral infections. The most important viruses that affect MS are Epstein-Barr virus (EBV), human herpes virus 6 (HHV-6), human endogenous retrovirus (HERV), cytomegalovirus (CMV), and varicella zoster virus (VZV). These viruses all have latent stages that allow them to escape immune detection and reactivate after exposure to various stimuli. Furthermore, their tropism for CNS and immune system cells explains their possible deleterious function in neuroinflammation. In this study, the effect of viral infections on MS disease focuses on the details of viruses that can change the risk of the disease. Paying attention to the most recent articles on the role of SARS-CoV-2 in MS disease, laboratory indicators show the interaction of the immune system with the virus. Also, strategies to prevent viruses that play a role in triggering MS are discussed, such as EBV, which is one of the most important.

Acta Neurologica Belgica, 2007

Financial support: 'Nationaal fonds voor wetenschappelijk onderzoek Vlaanderen (FWO)'

Infection and immunity, 1974

The occurrence of a local production in the central nervous system (CNS) of antibodies against different selected viruses was analyzed by comparison of titers in serum and cerebrospinal fluid samples from groups of 50 patients with multiple sclerosis from Finland, Norway, and Sweden. Measles antibodies were determined in hemagglutination inhibition, hemolysis inhibition, and nucleocapsid complement fixation tests; mumps, parainfluenza virus type 1, and rubella virus antibodies were determined in hemagglutination inhibition tests; and herpes simplex virus type 1 antibodies were determined in passive hemagglutination tests. For reference purposes tests were also made for adenovirus antibodies in penton hemagglutination enhancement tests and poliovirus antibodies in neutralization enhancement tests. Among the 150 multiple sclerosis patients, a local production of antibodies against measles virus was found in the CNS in 57%, against rubella virus in 19%, mumps virus in 15%, herpes simpl...

Current neurology and neuroscience reports, 2003

Viruses have been major players in the search for the cause of multiple sclerosis (MS). In support of the viral theory is the predominance of CD8+ T cells and class-I major histocompatibility complex in lesions, the powerful therapeutic effects of beta interferons, the ease of inducing demyelination in experimental models following virus challenge, and the documented examples of several human demyelinating diseases conclusively demonstrated to be of viral origin. We propose two hypotheses of how viruses may cause MS. In the "Hit-Hit" hypothesis, the virus persists or may be reactivated in the central nervous system (CNS). Injury is the result of direct viral damage and by an attempt of the immune response to clear the infectious agent. In the "Hit-Run" hypothesis, virus infects the periphery but never enters the CNS. The virus sets up an abnormal immunologic milieu for subsequent autoimmunity. In both scenarios, knowing the inciting virus would be expected to eli...

Neurology, 2001

Clinical Case Reports and Reviews, 2016