UC Irvine discovery could help researchers determine cause of diseaseand lead to development of treatments
Irvine, Calif., Jan. 10, 2000 — A research team at UC Irvine's College of Medicine and in Lyon, France, has discovered a virus in the spinal cords of victims of amyotrophic lateral sclerosis (ALS), a devastating nervous system disorder also known as Lou Gehrig's disease.
The finding provides the best evidence to date of a possible viral cause of the disease and could eventually result in treatments for the disorder, which currently has no known cause or cure. The findings appear in the January issue of Neurology.
Martina Berger, a researcher in the Department of Medicine at UCI, and a team of researchers at the Rockefeller University in Lyon, France, found that 15 of 17 victims of ALS showed evidence of a virus in the motor nerve cells of their spinal cords, while the virus was found in only one of 29 people who died of other causes. The virus was similar to Echovirus-7, an infectious agent known to cause meningitis and rare cases of encephalitis.
"Many researchers have suspected a viral link to ALS, but in this study we were able to identify a virus known for nerve damage in the exact areas of the nervous system that are affected by this disease," said Berger, who conducted the study in France before coming to UCI. "We think this knowledge will help us finally uncover what causes this disease and may someday lead us to developing a treatment."
The researchers used a highly sensitive technique called a reverse-transcriptase polymerase chain reaction, which can detect the presence of viruses using trace amounts of their genetic material. ALS was discovered in 1869. It became known as Lou Gehrig's disease after the legendary baseball player died from the disorder in 1941. The disease affects the motor nerve cells in the spinal cord, gradually weakening muscles in the body and eventually leading to paralysis. The disease does not severely affect the brain, so memory, language and other central nervous system functions are left intact while muscle and nerve cells are gradually impaired.
Nearly all victims of ALS die eventually from respiratory paralysis, usually about five years after diagnosis. About 4,600 people are diagnosed with the disease each year in the United States, according to the National Institutes of Health. Current treatments cannot reverse the course of the disorder but are used to relieve its symptoms.
Berger is continuing her research to determine whether the virus can be confirmed as the cause of the disease or whether it's a byproduct of a still-hidden cause of ALS.
"We need to identify the ways this virus causes damage to nerve cells in order to determine how it may play a role in the development of ALS," Berger said. "If this research is successful, we may be able to design new classes of drugs that could be effective against this tragic disease."
Berger's colleagues in the study include Dr. Nicolas Kopp, of the Hopital Pierre Wertheimer, Lyon, France; Dr. Claude Vital, of the Universite de Bordeaux II, Bordeaux, France; Bernhard Redl, of the Institut fur Medizinische Mikrobiologie, Innsbruck, Austria, and Dr. Michelle Aymard and Dr. Bruno Lina, of the Centre National de Reference pour les Enterovirus, Lyon, France.
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