The researchers injected a cold virus called Coxsackievirus A21 into mice that were engineered to be susceptible to this particular virus. However, instead of developing a cold, the mice unexpectedly displayed paralytic symptoms characteristic of polio. The researchers determined that administering the virus directly into muscles, instead of the virus's normal home in the nasal cavity, was critical for development of polio.
The findings challenge traditional views as to what defines a poliovirus, said Matthias Gromeier, M.D., a Duke virologist and senior author of the study.
"In principle, Coxsackieviruses could cause polio in humans," said Gromeier. "We are in the process of eradicating polio worldwide, but if we eliminate the poliovirus and cease polio vaccinations, our immune systems wouldn't produce antibodies against polio, and Coxsackievirus could theoretically fill the niche of eradicated polio" he said.
Results of the study will be published in the Sept. 6, 2004, issue of the Proceedings of the National Academy of Sciences.
Until now, it has been widely accepted that Coxsackievirus and poliovirus cause distinct illnesses because they bind to different docking sites, called receptors, on host cell surfaces. The current study turned that belief on its head, said Gromeier. Poliomyelitis has long been regarded as the signature of poliovirus, a virus that recognizes and binds to the CD155 receptor. However, the mice were genetically engineered to have only the Coxsackie A21 receptor, called ICAM-1, and they did not have the poliovirus receptor. Still, when the mice were injected with Coxsackievirus, it initiated infection through the ICAM-1 receptor, and caused symptoms of polio.