We have demonstrated a progressive centrifugal migration of poliomyelitis virus from the CNS into various peripheral ganglia and into peripheral nerves, including their distal portions. This phenomenon appears to be a regular occurrence in experimental animals, and is similar to that found in two other neurotropic infections, rabies and Borna disease.
Viremia appears to be secondary to primary neural infection.
The presence of virus in the lumen of the alimentary tract appears to be secondary to primary neural infection and not to viremia, and to be associated with the centrifugal spread of virus in peripheral nerves.
The presence of virus in "extraneural" tissues is not per se referable to infection of their constituent cells but rather to infection of their supplying nerves or, in some instances, to their content of virus-bearing blood.
The finding of virus in the vagus nerve may throw light on some of the electrocardiographic changes noted in certain cases of human poliomyelitis.
The presence of virus in peripheral nerves may throw light on the etiology of the most frequent clinical manifestations of human poliomyelitis, localized pain and tenderness.