|(About Measles)||3||About Measles|
|4||Mild Or Benign MS||19_-_22
|8||Research On MS||43_-_47
In a paper concerned with Genetic factors in MS, several diseases were discussed; but only in Multiple Sclerosis was a strong association of Lymphocyte determinants observed.
The authors reported that in patients with MS an increased frequency of HL-A3 and HL-A7 types were observed, confirming findings that had previously been observed in several other laboratories.
The influence of the Genetic factors on the clinical course of the disease had been analyzed, and only among patients who carry the HL-A7 or the LD-7 Genetic determinants, were rapidly developing disease observed.
These investigators found an association between the occurrence of high Measles' AntiBodies in MS patients who carry HL-A3, 7 and/or W18. Suggesting that Genetic factors contribute to the control of AntiBody production.
No conclusion was reached as little is known about the components of the Measles Virus involved in this activity.
These authors did state that the Leukocyte migration test (MIF) was the rationale behind the treatment of MS patients with Transfer Factor (TR), the substance which normalizes the reactivity.
Finally, it was evident from their studies that the LD-7A is a Genetic determinant which occurs in 60% to 70% of patients with MS, and this when compared to 16% in normal individuals provides some insight into Genetic factors in Multiple Sclerosis.
The second group of investigators reported Immunologic factors as they relate to the Genetics of DeMyelinating disease.
The authors agreed with previously outlined report that HL-A3 and HL-A7 types are over-represented in MS, when compared to control populations and they also agreed that LD-7A is strikingly over-represented in Multiple Sclerosis.
Measles AntiBodies tend to be higher in MS patients than in controls but persons who bear HL-A3 have higher Measles AntiBody titers than those who do not, whether or not they have MS. Measles AntiBody titers were higher in the Serum of patients with MS than in those individuals with LD-7A, and also higher in brothers and sisters.
A third report analyzed HL-A in nine families in which at least two individuals had MS. Although inconclusive, it suggested that differences in exposure to enviromental factors such as Measles Virus may explain why not all individuals with the Genetic susceptibility develope the disease.
It is possible that immune deficiency is why some individuals are more susceptible than others to common childhood illnesses. Also the occurrence of Measles late in childhood might increase the likelihood of acquiring Multiple Sclerosis.
The difficulties of evaluating any form of treatment were emphasized. A theoretical basis for attacking the Genetic relationship in MS was cited since HL-A studies have shown a dominance of the 7A type and its correlation with progression of disease.
Another study found a selective cellular suppression to Measles Virus was present in patients with Multiple Sclerosis. It was this selective suppression which prompted the investigation of TR and the ability of cells in the body and in the test tube to react to Measles Virus.
The authors selected individuals who exhibited a high degree of reactivity to Measles Virus and these individuals provided the TR used in their study.
Fifteen patients were studied and eleven developed significantly higher values to Measles Virus following the use of TR. The majority of these patients exhibited an increased response to Measles Virus. Increased migration values continued for six weeks following the injection of TR.
The last paper in this series was a further study of immunity in patients with MS. Serum from patients with MS inhibited the immune release in Lymphocytes from patients with Measles-infected cells. This data suggests the Lymphocyte killer function in patients with Multiple Sclerosis.
A recently published report on visna, a chronic inflammatory DeMyelinating in the CNS of sheep, throws further light on the problem of how a Virus is able to persist in the host and become a "slow Virus".
This Virus produces a severe crippling DeMyelinating disease in sheep; however there is no evidence that it has any counterpart disease in human beings.
Another recent report showed mouse tissue culture cells were markedly inhibted in their growth when exposed to Brain and spleen tissues from patients with MS.
First these researchers tested samples from ten cases of MS and found a reduction in the total cells in their cultures treated with Brain material from seventy-one MS patients and samples from forty-five non MS patients.
These cultures showed a reduction in the yield from the MS material when compared to control material.
The presence of the agent responsible for the decrease was not limited to the Brain and Spleen tissue from the patients but also found in the Serum and CerebroSpinal Fluid and in Kidney tissue and in Lymph Nodes from MS patients.
It was concluded that the cause of the reduction in the cell yields was high in the mice treated with MS material, but no response was observed in samples from the non-MS patients.
The Virus-like agent found in association with MS patients is small and similar in size to the Scrapie agent. An important difference is that the effect produced by this agent can be neutralozed by Sera from MS patients; while no such neutralization has been detected in Scrapie.
This research represents an important milestone in MS and offers hope in the search for answers.
A report on the relationship between Measles Virus AntiBodies and OligoClonal Immune globulin (IgG) in CerebroSpinal fluid (CSF) in patients with MS shows: Measles Virus AntiBody occurred in the Serum and CSF of 80% of patients with MS.
Several methods to study Measles AntiBodies in the Serum and Spinal fluid were used to compare patients with MS and with SSPE. These authors concluded that in the patients with SSPE the IgG represents an OligoClonal IgG response to a high level of AntiBody against the Measles Virus.
Studies with the electron microscope were presented with pictures of tissue culture cells infected with the SSPE Virus and Measles Virus. Brain material from patients dying with MS were studied and changes similar to those initally reported in 1972 by John Prineas.
The structural changes were much like those found previously in association with cells proved to be infected with the Measles Virus. The intertwined Measles Virus tubules fill the nucleus of all cells.