Multiple Measle viruses

For the pathogenesis of multiple sklerosis, autoimmune T-lymphocy tes play a predominant role, which are directed against components of the neural myelin sheath. T-lymphocy tes by secreting cytokines such as interferon y maintain the chronic inflammation which destructs the myelin sheath. Also cytotoxic T-lymphocytes may participate directly. The cause of multiple sklerosis is unknown. Significantly increased antibody titers against several vitusses, mostly the measles virus, point to a (latent) virus infection initiating the disease. 

Slow viruses are becoming increasingly suspect in the instances of much more common diseases, particularly the autoimmune diseases. An autoimmune disease may be defined as a disease wheiein the immune system of the body does not direct its attack on an invading foreign substance, but instead at the body s own tissue. Many authorities consider rheumatoid arthritis and multiple sclerosis as autoimmune diseases. The precise causes of these diseases have remained obscure. Multiple sclerosis is a demyelinating disease and has variously been described as an autoimmune disease, a viral disease, or an autoimmune disease provoked by a virus. Epidemiological studies indicate that from 3 to 23 years may elapse between the time of exposure to the virus and the onset of symptoms. Further evidence points to involvement of a myxovirus. Measles virus is of this kind. 

I have been especially interested in that aspect of biological specificity that is involved in the mechanism of protection of the body against disease. When we first become infected with the measles virus, we become ill. After a few days, however, the protective mechanism of the body has come into operation, and we recover from the disease—the symptoms of the disease were the result of the multiplication of the molecules of measles virus within our body, and the recovery is the result of the development of a police force that stops this multiplication. This police force consists of special molecules, formed in the cells of the body, and circulating in the blood stream. These molecules are antibodies, anti-measles antibodies, with the specific property of being able to combine with the measles virus and to prevent its reduplication. Other diseases also lead to the development of special antibodies to counteract them, and even foreign proteins generally, whether they are harmful or not, cause this process of production of special antibodies to become operative. 

Measles, mumps and rubella (German measles) are infectious diseases, with respiratory routes of transmission and infection, caused by members of the paramyxovirus group. Each virus is immunologically distinct and has only one serotype. Whilst the primary multiplication sites of these viruses is within the respiratory tract, the diseases are associated with viral multiplication elsewhere in the host. 

Measles is a severe, highly contagious, acute infection that frequently occurs in epidemic form. After multiplication within the respiratory tract the virus is transported throughout the body, particularly to the skin where a characteristic maculopapular rash develops. Complications ofthe disease can occur, particularly in malnourished children, the most serious being measles encephalitis which can cause permanent neurological injury and death. 

Polyspecific Response Associated with CNS Autoimmune Diseases. The oligoclonal, intrathecally synthesized IgG contains numerous specific antibodies and autoantibodies. Antibodies are frequently found with specificities against measles, the rubella virus and the varicella-zoster virus, but seldom against the herpes simplex virus. The occurrence of one, two, or three of these antibodies is referred to as the MRZ reaction. The corresponding antigens are not present in these cases. The MRZ reaction is typical of multiple sclerosis as well as cerebral lupus erythematosus and is a chronically evolving immune process (F5, KIO, S16). 

Multiple sclerosis Herpes virus type 6, measles, rubella, paramyxovirus, coronavirus, varicella zoster virus, mumps, retrovirus... 

Pyrazomycin. Pyrazomycin (11), 3-(l-p-D-ribofuranosyl)-4-hydroxypyrazole 5-carboxamide, is isolated from S. Candidas (1—4,9,10). The incorporation of [2-13C]acetate and [1- and U-14C]glutamate into the four contiguous carbons of pyrazomycin has been reported (11,12). Pyrazomycin 5 -phosphate inhibits orotidylic acid decarboxylase. Pyrazomycin inhibits adenosine phosphorylation and decreases the incorporation of deoxyuridine into DNA of Novikoff hepatoma cells in culture. It also inhibits the growth of tumor cells and the cytopathic effects of vaccinia, herpes simplex, vesicular stomatitis, Newcasde disease, measles, Sindbis, polio, hepatitis A, and coxsackie viruses (13,14). The inhibitory action of (11) on viral multiplication is reversed by uridine. 

---