Polio Pathogenesis

Poliovirus enters a susceptible host in contaminated drinking water or through contact with contaminated surfaces, such as unwashed hands. After passing through the stomach, the virus reaches the intestine, where it establishes itself in the cells of the intestinal lining (the "gut mucosa"). There, it infects cells and replicates. In most cases, this results in a transient, self-limiting diarrhea, or it may be completely asymptomatic. Unfortunately, the virus is not always so benign.

In approximately 1% of infections, the virus spreads from the intestine into the bloodstream and nervous system, eventually reaching motor neurons and causing paralysis or, in extreme cases, death. The exact mechanism of the virus's spread through the body is still not known, though many models have been proposed. Certain clusters of cells in the intestine, known as Peyer's Patches, appear to support the initial infection. Since the Peyer's Patches are closely associated with the body's immune system, it has been suggested that the virus migrates from there into the bloodstream. Once in the blood, it gains access to the nervous system, where the destruction of motor neurons (those which control muscle movement) results in paralysis.

In an interesting twist, some researchers have found that the virus may be transported directly through nerves rather than blood. When a genetically engineered mouse which is susceptible to polio is injected with the virus in one limb, the virus migrates to the spinal cord and replicates, and the first limb paralyzed is the one which was injected. If the nerves connecting the injected limb to the body are severed before injection, the virus fails to spread to the spinal cord, even though blood still circulates between the limb and the body. This suggests that the virus actually travels along the nerves to reach the spinal cord. It remains to be determined whether or not this mechanism is at work in a normal infection.

Widespread vaccination against polio has effectively eliminated the natural occurrence of the disease in the Western hemisphere. There are two types of vaccines: a killed virus, which is injected (the Salk vaccine, or IPV), and a live attenuated strain of the virus, which is administered orally (the Sabin vaccine, or OPV). Because the Sabin vaccine is inexpensive and easy to administer, it has been used extensively in the campaign to eradicate the virus.

This convenience and effectiveness comes at a price, though. The live virus mutates readily: in every case studied, vaccination with OPV results in the release of a wide variety of live mutant viruses in the feces. Many of the mutations enable the virus to regain virulence. Interestingly, paralysis from the vaccine occurs only in about one case out of one million, despite the fact that the virus seems to mutate the same way in all patients. While the reason for this is not known, many scientists have suggested that some other pathogen, present in some patients at the time of vaccination, suppresses the immune system enough to allow the mutant viruses to enter the nervous system. If we could find the pathogen responsible for this, we could screen patients for it before vaccinating with OPV. A more straightforward solution, recently adopted by the Centers for Disease Control and Prevention , is to use IPV for the first two inoculations, as this vaccine is unable to cause paralysis.


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