Poliovirus

Dr Retno Budiarti,dr.,M.Kes
Microbiology Department
Medical faculty of Hang Tuah University
 Picornavirus family

 Proteins: Four major polypeptides. Surface capsid proteins

VP1 and VP3 are major antibody-binding sites. VP4 is an
internal protein.
 Envelope: None 
 Replication: Cytoplasm
 Outstanding characteristics: Family is made up of many
enterovirus and rhinovirus types that infect humans and
lower animals, causing various illnesses ranging from
poliomyelitis to aseptic meningitis to the common cold. 
Properties of poliovirus
 Inactivated at 55 °C for 30’,
 inactivated by a chlorine concentration of 0.1 ppm,
 very restricted host range. Most strains will infect monkeys
when inoculated directly into the brain or spinal cord. can
also be infected by the oral route;
 Requires a primate-specific membrane receptor for infection
 three antigenic types
Poliomyelitis
 is an acute infectious disease that in its serious form affects the
CNS. The destruction of motor neurons in the spinal cord results in
flaccid paralysis (most are subclinical)
Pathogenesis
 Portal entry of the virus : mouth oropharynx or
intestine multiplication circulating
blood spread along axons of
peripheral nerves to the central nervous system
fibers of the lower motor neurons
invades nerves cells (anterior horn
cells of the spinal cord) intracellular
multiplication destroy & damage these cells
changes in peripheral nerves & voluntary
muscles
 Virus doesn’t multiply in muscles, some cells that lose their
function may recover completely
Clinical findings
1. Abortive poliomyelitis
2. Nonparalytic poliomyelitis (aseptic meningitis)
3. Paralytic poliomyelitis
4. Progressive postpoliomyelitis muscle atrophy
Abortive poliomyelitis
 Minor illness, fever, malaise, drowsiness, headache, nausea,
vomiting, constipation, sore throat.
 Recovers in a few days
 Nonparalytic poliomyelitis (aseptic
meningitis)

 Stiffness and pain in back and neck about 2-10 days,

 Recovers is rapid and complete
Paralytic poliomyelitis
 Flaccid paralysis resulting from lower motor neuron damage
 Incoordination secondary to brain stem invasion and painful
spasms of nonparalysed muscles may also occurs
 Recovery within 6 months with residual paralysis lasting
Progressive postpoliomyelitis muscle
atrophy
 Paralysis and muscles wasting has been repeatedly in
individuals decades after their experience with paralytic
poliomyelitis.
 It is not a consequence of persistent infection but a result of
physiologic and aging changes by loss of neuromuscular
functions
Laboratory diagnosis
 Culture of human or monkey cells inoculated, incubated and
observed. Cytopathogenic effects appear in 3-6 days.
 Specific antiserum by neutralization tes
immunity
 Passive immunity during 6 months of life
 Passively administered Ab lasts only 3-5 weeks
 Virus neutralizing Ab forms soon after exposure to the virus,
persists for life
prevention
 Killed virus vaccine
induces humoral Ab, but not induce local
intestinal immunity so that virus is still able to
multiply in the gut
 Oral vaccines contain live attenuated virus grown
in primary monkey or human diploid cell cultures
produces not only IgM and IgG in the blood but
also secretory IgA in the intestine, which become
resistant to reinfection
TERIMA KASIH.......