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These epidemiologic data point to both a genetic succeptibility and some environmental factor that is encountered in childhood and, after years of latency, evokes the disease In recent years, speculation has grown that this factor is an infection, most often viral A body of indirect evidence has been marshaled in support of this idea, based largely on alterations in humoral and cell-mediated immunity to viral agents (see reviews of R T Johnson, Lampert, K P Johnson et al, McFarlin and McFarland) However, to this day no virus (including all known members of the human retrovirus family) has been seen in or isolated from the tissues of patients with MS despite innumerable attempts to do so Moreover, no satisfactory viral model of MS has been produced experimentally Recently, the bacterial agents Chlamydia pneumoniae and Borrelia burgorferi (the agent of Lyme disease) and herpesvirus type 6 have been similarly implicated by the nding of their genomic material in MS plaques, but the evidence for their direct participation in the disease is, at the moment, not compelling If indeed some obscure infection is the initial event in the genesis of MS, then a secondary factor must be operative in later life to reactivate the neurologic disease and cause exacerbations One popular view is that this secondary mechanism is an autoimmune reaction, attacking some component of myelin and, in its most intense form, destroying all tissue elements, including axons Several lines of argument have been advanced in support of this view One is inclined to draw an analogy between the lesions of MS and those of acute disseminated encephalomyelitis, which is almost certainly an autoimmune disease of delayed hypersensitivity type (see further on) In support of this possibility is the nding of antibodies to speci c myelin proteins eg, myelin basic protein (MBP) in both the serum and cerebrospinal uid (CSF) of MS patients, and these antibodies, along with T cells that are reactive to MBP and to other myelin proteolipids, increase with disease activity; moreover, MBP cross-reacts to some extent with measles virus antibodies The arguments that a chronic viral infection reactivates and perpetuates the disease are, however, less convincing than those proposing a role for viruses in the initiation of the process in susceptible individuals A possible way in which viral infections and autoimmune reactions in the nervous system might be linked to the abnormal expression of autoantigens on CNS cells has been suggested by R T Johnson He found that several different viruses (rubeola, rubella, varicella) could cause the sensitization of T lymphocytes against myelin basic protein This implies that the T lymphocyte recognizes an identical structure in both the virus and the myelin sheath The hypothesis continues with the notion that once the autoimmune process is initiated by a virus in childhood, it can later be reactivated by any of the common viral infections to which the.

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individual is exposed, particularly in the far higher northern and southern latitudes This phenomenon of molecular mimicry (a shared antigen between the virus and CNS myelin, the oligodendrocyte, or cerebral vessels) has been invoked as a mechanism in several diseases, notably in rheumatic fever, certain paraneoplastic diseases, and Guillain-Barre syndrome, but remains speculative in MS The role of humoral and cellular factors in the production of MS plaques is not fully understood The deposition of immunoglobulin in the plaques of patients with acute and relapsing-remitting disease, but not those with progressive MS, has been alluded to earlier That the humoral immune system is involved is evident from the presence in the CSF of most patients of oligoclonal immune protein antibodies, which are produced by B lymphocytes within the CNS Sera from patients with MS (and some normal controls), when added to cultures of nervous system tissue from newborn mice in the presence of complement, can damage myelin, inhibit remyelination, and block axonal conduction Antibodies to oligodendrocytes are present in the serum of up to 90 percent of patients in some studies but far less frequently in others Of note also are the ndings of Berger and colleagues that show a relationship between the clinical progression of early and monosymptomatic MS and the presence of serum autoantibodies against oligodendrocyte glycoprotein and myelin basic protein They have reported that the absence of antibodies, a nding in 38 percent of their patients, identi ed a group with more benign disease, at least for several years Whether this further indicates, as they suggest, that humoral immune mechanisms are essential to the production of MS is uncertain Autoantibodies have been found that are directed against myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP) It has also been demonstrated that subsets of T cells (CD41 Th2 cells) are activated by MBP and MOG to activate B cells, the production of oligoclonal bands and membrane attack complexes, and the release of cytokines [tumor necrosis factor alpha (TNF- ), interleukins, interferon gamma (IFN- )] The in ammatory process erodes the blood-brain barrier and ultimately destroys both oligodendroglia and axons The eventual functional outcome re ects both the activity of this in ammatory cascade and the degree of axonal damage In other cases, there may be a compromise of oligodendroglial function and axonal degeneration in the absence of prominent in ammation (see reviews by French-Constant and Hemmer) Nevertheless, most immunologists currently subscribe to the notion that MS is mediated by a T-cell sensitization to myelin This idea is supported by numerous lines of evidence including the observation that T cells initiate the lesions of experimental allergic encephalomyelitis (EAE), which is assumed to be an animal model of MS, as suggested by Adams Although the entry of autoreactive T cells into the CNS results in a perivascular in ammatory reaction, its relationship to MS is unclear Conceivably, intense T-cell stimulation is in itself suf cient to induce demyelination, but it is also possible that the primary target of the immune reaction is the myelin sheath or some component thereof and that the T-cell in ltration is the result of the demyelination Other investigators believe that an additional insult is required, as illustrated by the EAE animal model, in which myelin alone is not a suf cient factor but always requires an adjuvant immune stimulus EAE is clearly an imperfect model; it is not a naturally occurring disease but one in which a demyelination of the CNS is induced in susceptible animals in a single episode by autologous myelin antigens The.