A comment about the relationship of virus infection to autoimmune disease in general is warranted. Infectious mononucleosis occurs only when adolescents or young adults are infected with the EBV. The symptoms of infectious mononucleosis (and other autoimmune phenomena) occur as a result of the immune reaction to the viral infection. Dr. Gertrude Henle, who discovered the relationship between EBV and infectious mononucleosis, studied a possible link between MS and this virus; it was concluded that there was none. Research continues because of consistently high antibody titers to EBV in many patients with MS. HSV-6 and HSV-7 are very closely related families of viruses. Indeed, their structure (EBV, HSV-6, and HSV-7) is two thirds identical, which has made
Brain-derived nerve growth factor a specific nervous system hormone which can stimulate repair of the nervous system.
T-cell growth factor beta-1
Sclerotic a term referring to hardened tissue such as MS plaques in the brain. This hardness or sclerosis is caused by scarring.
Infectious mononucleosis glandular fever. It is a common form of infection with the Epstein-Barr virus (EBV) consisting of fever, fatigue, enlarged lymph nodes, often with rash, splenic enlargement and hepatic enzyme elevation.
progress difficult. An immune reaction to tissue damaged by an immune reaction has been theorized to cause damage to myelin as well as other tissues. There is now good evidence in experimental animals and in humans that this is correct. Another theory is that part of the protein in a virus is similar in some aspect or even identical to a natural protein in myelin or other tissue. As noted previously, an immune reaction to seemingly dissimilar proteins, one being a myelin protein and the other a component of the EBV, has been documented. An immune response to the virus can result in myelin damage. Regulation or control of immune responses may be genetically impaired to a greater or lesser degree in certain patients.
In summary, it is theorized that a virus that children are protected from early in life infects genetically predisposed adolescents. This results in an immune reaction to proteins in the virus that resemble proteins in myelin, thus initiating an attack of the person's own myelin in MS. This immune attack then leads to additional damage to myelin (and other nervous system tissue). The damage to normal tissues is then followed by additional immune reactions and more potential attacks. Immunologists think that part of the problem is an ineffective control of the immune reaction in MS patients that allows additional attacks to occur.
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