Comparison Between Clinical and MRI Multiple Sclerosis Activity and Expression of Human Endogenous Retrovirus Type W and Herpesvirus in Peripheral Blood of Patients

Background/Rationale:

Multiple Sclerosis (MS) is an inflammatory demyelinating disease that affects the spinal cord (especially in posterior cords). The clinical heterogeneity of MS is well described, but currently it is known that lesions of MS and mechanisms underlying involved in the pathological destruction of the central nervous system (CNS) are also heterogeneous. It is a multifactorial disease in which one immunopathogenic mechanism is suggested as responsible for the destruction of the sheath myelin.

However, the pathology of inflammatory joint lesions of MS suggests that specific autoimmune responses against components of CNS myelin may have a crucial role in the destruction of myelin. This concept is supported by the high level of oligoclonal immunoglobulin G (IgG) in cerebrospinal fluid by linkage with the locus of the major histocompatibility complex (MHC), expansion of B and T cells reactive to myelin in MS lesions and the fact that immunization with myelin proteins induces an MS-like disease in animals, experimental autoimmune encephalomyelitis (EAE).

The autoreactivity for various myelin proteins, including myelin basic protein, proteolipid protein, and myelin-associated glycoprotein in myelin oligodendrocyte glycoprotein (MOG), has been observed in patients with MS.

It is noted however, that T cells of patients with MS show a predominant activity against MOG in relation to other myelin proteins, and anti-MOG antibodies were identified connected to the myelin's disintegration around axons in acute lesions of MS. In addition, sensitization with MOG reproduces the clinical and demyelinating degenerative pathology of MS in rodent models and primates.