The researchers were left wondering how this intramuscular portal of entry could affect the virus's ability to access the types of cells normally infected by polio.
In studying the virus' action within infected mice, they found that the virus traveled from the calf muscle where it was injected to the central nervous system along "motor neuron axons." Such axons extend from the central nervous system to muscles throughout the body and convey commands for muscle movement. The site in the muscle where axons physically attach is called a neuromuscular junction. These junctions likely served as the cold virus' portal of entry into the nervous system.
"We gave the coxsackievirus a distinct advantage by injecting it directly into muscle, where it had direct access to the kinds of nerve cells polio normally attacks," said Gromeier. "The resulting polio symptoms were milder than those caused by the poliovirus, but it was polio nonetheless."
Such a subtle change in entry mode significantly changed the virus' behavior, and therein lies one of the greatest dangers associated with viruses, said Gromeier.
Viruses are extremely adaptable and they can alter themselves dramatically based upon their environment. Coxsackievirus A21 is one of a large group of cold viruses that are genetically very similar to polioviruses.
"Our study reveals how similar these viruses actually are," he said. "It is fascinating that a minor change such as injection site may cause a harmless cold virus to attack the central nervous system."
Gromeier's team is now collaborating with the Centers for Disease Control to test numerous Coxsackievirus sa
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Contact: Becky Levine
Levin005@mc.duke.edu
919-684-4148
Duke University Medical Center
6-Sep-2004