Multiple Sclerosis (MS) is a progressive and chronic inflammatory disorder of the central nervous system. MS is characterized by a pathological demyelination of axons. Depending on the site of inflammation symptoms vary greatly and include paralysis or numbness of extremities, impaired vision and speech, dizziness, cognitive impairment, and fatigue. An underlying cause for the development of MS has not been identified so far. A widely accepted theory of MS pathology focusses on auto-reactive T-cells acting against axonal myelin. This simplistic view is challenged by a number of clinical observations arguing against a sole autoimmunological process.
First, newly emerging MS lesions are devoid of immune cells and second, MRI imaging suggests alterations in affected areas before the appearance of signs of inflammation. Furthermore, relapses during disease progression do not correlate with the disability patients face in the later stages of MS and standard therapy using immune modulatory and/or immune suppressive drugs has no influence on primary or secondary progredient forms of MS. Consequently, MS consists of 2 arms, 1) an inflammatory part (relapses) and 2) a slowly progressive neurodegenerative part.
The less understood 2nd arm might be correlated with the expression of human endogenous retroviruses (HERVs). HERVs are remnants of an ancient retroviral infection integrating viral DNA into the human genome. A number of HERVs still possess open reading frames, e.g. coding for the former viral envelope protein. These proteins could show superantigenic properties.
Therefore, the project focusses on the immunological properties of HERV-derived viral envelope proteins and the development of humanized monoclonal antibodies as alternative therapy for the treatment of MS.