Poliovirus is transmitted by the fecal oral route on ingestion of contaminated water. The viral particles initially multiply in the nasopharynx and the gastrointestinal mucosa. The virions are resistant to acidity of stomach and to lytic activi-ties of the protease and other enzymes of the intestinal tract and bile.
On entering the body, the virus infects and multiplies in the tonsils and Peyer’s patch of the ileum. It then spreads to regional lymph nodes and enters the blood, causing a primary viremia. On continued infection and multiplication of virus in the reticuloendothelial cells, it invades the blood stream again and causes secondary viremia. During this period of viremia, the poliovirus crosses the blood–brain barrier or gains access to the brain by infecting skeletal muscle and traveling up on the nerves to the brain as in rabies virus.
Poliovirus shows tissue tropism by specifically combining with neural cells. It recognizes a receptor present on the anterior horn cells of (a) the spinal cord, (b) dorsal root ganglia, and (c) motor neurons. On combination at these sites, the poliovirus causes destruction of the motor neurons, anterior horn, and brain stem. The destruction of motor neurons leads to paralysis of the muscles innervated by those neurons. Paralysis is not caused by the virus infect-ing the muscles. The poliovirus also infects the brain stem, causing bulbar poliomyelitis associated with respiratory paralysis.
Poliovirus causing the pathological changes in the central nervous system (CNS) is usually responsible for causing symp-toms of poliomyelitis. Immune mechanisms do not play any role in pathogenesis of the disease.
Host immunity in poliomyelitis is mostly dependent on the humoral antibodies. Both the serum and secretory antibod-ies play an important role in conferring protection against poliomyelitis.
· Serum IgM antibodies appear within a week of infection andpersist for nearly 6 months. IgG antibodies, which develop subsequently, persist lifelong. The neutralizing antibodies in the blood protect against disease by the same serotype of poliovirus. These antibodies, however, do not prevent infection of the intestinal neuron and excretion of virus in the feces.
· Secretary IgA antibodies provide mucosal immunity againstthe virus (a) by preventing intestinal infections and (b) by preventing shedding of virus. The IgA antibody in the breast milk protects the infants from infection. Therefore, the poliomyelitis tends to be more severe and shedding of virus is more prolonged in the infected human host with altered humoral immune response.
Cell-mediated immunity plays little or very insignificant role in the immunity against poliovirus. Host immunity is type specific. However, there is a significant amount of cross-protection between type 1 and 2 and type 2 and 3 poliovi-ruses. There is little or no cross-protection between type 1 and 3 strains.