Multiple Sclerosis:
Scars Of Childhood

Discovered in 1957, Interferon has proved to be a defense mechanism in recovery from acute and sometimes chronic infections. It is a most important component of the body's defense against many different kinds of infections and particularly Viral Infections.

As one of the body's first defenses against invading organisms, it acts sooner than the Humoral and Cell Mediated AntiBodies.

In fact, Interferon is the major determinant in recovery from illness by inducing the formation of a substance in body cells which interfere with the multiplication of Viruses.

It not only arrests the multiplication and spread of Viruses but also is active in actual destruction of Viruses and prevention of reinfection. Interferon's importance extends beyond its action against Viruses; in fact, it has been shown to have an antagonistic effect against Bacteria, Rickettsia and Protozoa.

Interferon is not in itself directly AntiViral but induces the formation of a new substance which activates the AntiViral mechanism. There are at least two ways in which Interferon acts with cells to produce the AntiViral effect.

First, it stimulates the production of another substance by cells, which is directly AntiViral. Or, a small amount of Interferon works in combination with cell components to produce an AntiViral state.

AntiBodies on the other hand inhibit Viral Infections by combining with the Virus and making it noninfectious for cells. AntiBodies are usually produced after infection, serving mainly to prevent reinfection and to promote resistance to reinfection.

The effective role of existing AntiBodies is primarily one of prevention and it is questionable whether AntiBody is effective after the Viral infection has become established in the body.

Most of the experimental evidence supports a direct relationship between the Interferon system and recovery from infections.

The control of Virus disease may be approached from several points of view. First, Immunologic control is accomplished by prevention through the development of vaccines. A second method is through certain chemical substances which have AntiViral activity.

A chemical known as IodoDeoxyUridine (IDU) which has been shown to have an AntiViral effect against Herpies Viruses types one and two. The third approach is to heighten resistance of the host exemplified by the Interferon mechanism.

Living cells in the body infected by Viruses produce Interferon, a process independent of AntiBody formation. Interferon's early AntiViral activity has a protective effect evident before the presence of AntiBodies can be demonstrated.

Interferon can be found in body fluids, in the blood and spinal fluid in patients early in the course of their disease. An example is Influenza where it is found in the fluids from the nose, and in Influenza Meningitis in Spinal Fluid.

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In summary, Interferon provides the first line of defense against infection, acting on the cells and preventing further spread of infection. The fate of the individual cell depends on substances other than AntiBody.

Certainly the Interferon mechanism, having a wide spectrum of AntiViral activitym offers some real hope for the control of Viral Infections.

Several factors determine the effective role of Interferon in any particular infection:

1. Cells of the body must be available to respond by forming Interferon

2. The capacity of the infecting Virus to turn off the body's cell which is vital to the production of Interferon and its action

3. The degree of stimulation exerted by the Virus in provoking the Interferon response

4. The sensitivity of the Virus to the action of Interferon

The Interferon mechanism appears to be very complicated; the end result depends not only on the production of Interferon, but also on the Virus, and the ability of the cells to produce Interferon.

Interferon has been demonstrated in acute Viral Infections in the Serum of the blood and in washings from the nose of patients with the common cold and in the saliva of patients with Mumps. Interferon when injected into the Veins lasts but a few minutes.

In the research laboratory mice previously infected with Tuberculosis produced Interferon after intravenous injection with Tuberculin whereas the injection of Tuberculin in noninfected mice failed to cause an Interferon response.

Immune systems of the body are interrelated and the substances that interfere with AntiBodies may also interfere with the production of Interferon. X-ray radiation, Steroids, and other toxic agents may also interfere with the production of Interferon.

A substance known as BCG has been found to promote the production of AntiBody and Interferon. Certain drugs known to suppress the Immune Response may not affect Interferon production.

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Effective AntiViral treatment is greatly needed to control diseases such as Hepatitis, various forms of Encephalitis and other crippling illnesses.

A major problem is the production of sufficient quantities of effective Interferon for the treatment of patients. Intensive study is being carried out to develop methods of producing sufficient quantities of human Interferon.

It appears that Multiple Sclerosis is exactly what the name implies: a disease of many scars causally related to common Virus infections occurring most often in childhood. MS is complex because the Brain is very complex, made up of many essential and vital organs.

Common childhood diseases are caused by different Viruses, many of which may cause inflammation of the Brain and Spinal Cord as a complication or after effect. This complicating disease is called Acute EncephaloMyelitis.

The term might be applied to the acute form of MS. When remissions and exacerbations occur the disease is diagnosed as MS. The Viruses of common childhood diseases in particular are known to cause Acute EncephaloMyelitis.

The changes in the Brain cells are similar to those found in the chronic form of scarred or DeMyelinated areas in the Brain designated as plaques. A final definition of MS could be multiple scars from previous Acute EncephaloMyelitis.

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The symptoms and signs often begin with inflammation of the Optic Nerve or portions of the body involving half of the limbs, one arm or one leg or all four limbs. When the Optic Nerve is inflamed and the Spinal Cord also becomes inflamed the disease is designated NeuroMyelitis Optica.

This is a form of Acute EncephaloMyelitis which is very acute and severe with a high mortality. It occurs in its most acute form in children and complete survival rarely occurs or the process leads to death within a few months or a year.

The diagnosis of Acute EncephaloMyelitis is based on scattered signs of involvement of the Nervous System very similar to those seen in the chronic form of MS.

EncephaloMyelitis rarely follows a vaccination with live Virus; it may follow infectious diseases such as Chicken Pox, Rubella or the common Herpes Virus infection often referred to as a cold sore or fever blister proved to be caused by the Herpes Virus.

Other common childhood diseases such as colds or Mumps on occasion cause Encephalitis but don't cause serious DeMyelination as is known to be associated with Rubella or Measles Virus.

The latter cause inflammation of the Brain, years after childhood Measles is diagnosed Subacute Sclerosing PanEncephalitis (SSPE). The chronic form of Measles Encephalitis is occasionally referred to as Disseminating or Multiple Sclerosis.

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Measles is worldwide and like MS and Poliomyelitis is recognized as involving the Nervous System more commonly in the colder regions of the world. Measles Encephalitis, the most serious form of the disease, is rare in Africa and tropical climates.

The Measles and Polio Viruses are grouped together by Virologists. They are both found in the nose and throat and in the bowels of humans. The changes caused by these Viruses are very distinct and different.

Paralysis in PolioMyelitis is mainly of the Motor Nerves to the legs and arms. Weakness and paralysis in Measles Encephalitis is manifest by involvement of the Brain and Spinal Cord.

Optic Neuritis is common in association with Measles Encephalitis and many patients with Optic Neuritis eventually develop the signs of MS. In the northern hemisphere, high risk regions sre found in Europe or in places colonized by the Europeans.

Recent research in Multiple Sclerosis has been concerned with Genetic factors, and certain HL-A antigens are found increased in patients with MS.

Patients with high Measles AntiBodies carry HLA-3,7 and/or 18, suggesting that Genetic factors contribute to the control of AntiBody production.

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Geneticists find that LD7A is a Genetic determinant which occurs in 60 - 70% of patients with Multiple Sclerosis. It is known that Measles AntiBodies tend to be higher in MS patients than in controls.

But persons who beaar HLA-3 have higher Measles AntiBodies Titers than those who do not, whether they have MS or not. It has been suggested by some investigators, that the occurrence of Measles late in childhood might increase the likelihood of acquiring MS.

Immunologists have been studying the results of Transfer Factor in patients with MS. A selective suppression of Measles Virus was present in some patients with MS.

And it was this selective depression which prompted the investigation of transfer and the ability of cells in the body to react to the Measles Virus. Sixteen patients inoculated with Transfer Factor at weekly intervals exhibited an increase in their response to Measles Virus.

The relationship between Measles AntiBodies and OligoClonal Immune Globulin in Spinal Fluid of patients with MS recorded that Measles Virus AntiBodies occurred in the Serum and Spinal Fluid of more than 80% of patients with MS.

In patients with SSPE the Immune Globulin represents an Oligoclonal response to a high level of AntiBody against the Measles Virus. Brain material from patients with Multiple Sclerosis has been studied and are similar to those occurring in cells proved to be infected by Measles Virus.

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Finally, what are some of the answers on the horizon for Multiple Sclerosis? Prospectives for earlier diagnostic procedures are bright, making possible earlier treatment and stabilization of the scarring process in MS.