Poliovirus infection – pathogenesis, clinical findings and immunity in poliomyelitis
Structural properties of polioviruses are typical for enteroviruses. Polioviruses don’t contain hemagglutinin. Poliomyelitis is an infectious disease that is manifested as severe central nervous system disorder that may result in flaccid paralysis.
Poliomyelitis affects solely humans, which are the only known reservoir of infection (anthroponotic disease).
Infection is transmitted via fecal-oral mechanism (waterborne and alimentary routes).
Incubation period ranges 1-2 weeks.
Primary viral replication is performed within tonsils, and then in Peyer’s patches and intestine epithelial cells. The virus is excreted with stools prior to the disease onset.
After propagation in the lymphoid and epithelial tissues it undergoes blood dissemination and reaches CNS along axons of peripheral nerves.
Infection of CNS by polioviruses can result in deep destruction of spinal cord neurons (predominantly, motor neurons of anterior horns) and brain neurons with subsequent irreversible paralysis. Polioviruses don’t multiply in muscles in vivo. The impairment of innervation of striated muscles is secondary to the destruction of neurons.
Despite active CNS involvement, most poliomyelitis cases are subclinical (inapparent) or mild.
Clinical forms of poliomyelitis infection are the follows:
– abortive poliomyelitis is the most common manifestation of the disease; the patient has only fever, malaise, headache, nausea, and recovers in a few days;
– nonparalytic poliomyelitis that may result in aseptic viral meningitis; it is characterized by stiffness, back and neck pain and meningeal symptoms together with above manifestations;
– paralytic poliomyelitis arises in about 1% of total disease cases; it results in flaccid paralysis due to motor neuron damage; maximal recovery may occur within 6 months after the infection, but residual paralysis lasts much longer.
Nowadays the cases of poliovirus infection are predominantly registered as vaccine-associated poliomyelitis (VAP) after the immunization with live poliovaccine.
Virus-neutralizing antibodies elevate soon after the exposure to infection. However, polioviruses located in brain and spinal cord are not influenced by high titers of blood antibodies.
Post-infectious immunity is high-grade and long-lasting, but only type-specific. Passive immunity is transferred from mother to newborn; nevertheless, the levels of maternal antibodies gradually decline during first 5-6 months after birth