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Epstein-Barr Virus and Multiple Sclerosis
Arch Neurol. 2006;63:810-811.
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Although the cause of multiple sclerosis (MS) is unknown, clinical and pathologic evidence strongly suggest a link between an infectious agent and an autoimmune response directed against myelin.1-3 Epidemiologic studies also have implicated an environmental factor, most likely an infectious agent, as a necessary element in the development of MS.2 One possibility is that antigens from infectious pathogens may activate autoreactive T cells, causing them to expand and leading to clinical autoimmune disease.4-5 However, molecular mimicry (as this process is termed) has found limited empirical support as a general mechanism to explain the origin and course of a broad range of autoimmune diseases. Another possibility is that rather than there being a specific pathogen causing MS, infections in and of themselves may be able to aggravate autoimmune processes. For example, infectious processes such as Chlamydia pneumoniae can activate antigen-presenting cells and consequently activate autoreactive T cells that do not cross-react . . . [Full Text of this Article]AUTHOR INFORMATION
Amy E. Lovett-Racke, PhD;
Michael K. Racke, MD
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Epstein-Barr Virus and Multiple Sclerosis: Evidence of Association From a Prospective Study With Long-term Follow-up
Gerald N. DeLorenze, Kassandra L. Munger, Evelyn T. Lennette, Norman Orentreich, Joseph H. Vogelman, and Alberto Ascherio
Arch Neurol. 2006;63(6):839-844.
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