Transcript poliovirus grp 8 PCL II

Virology presentation
Group 8
Pcl II
Poliovirus
Poliovirus , a highly contagious
virus that causes the medical
condition polio (poliomyelitis) is a
human enterovirus and member of
the family of Picornaviridae.
Virus classification
 Group: Group IV ((+) ssRNA)
 Order: Picornavirales
 Family: Picornaviridae
 Genus: Enterovirus
 Species: Human enterovirus C
 Scientific name: Poliovirus
There are three serotypes of
poliovirus, PV1, PV2, and PV3; each with a
slightly different capsid protein. Capsid
proteins define cellular receptor specificity
and virus antigenicity. PV1 is the most
common form encountered in nature,
however all three forms are
extremely infectious.
General properties:
Poliovirus particle are typical enterovirus.
They are inactivated when heated at 550c for
30min,by a high chlorine concentration,by
formaldehyde and ultra violet light.
Poliovirus are not affected ether or sodium
deoxycholate
Structure
RNA genome.
protein capsid.
single-stranded positive-sense.
RNA genome that is about
7500 nucleotides long.
The viral particle is about 30 nanometres in
diameter with icosahedral symmetry.
non-enveloped .
Replication cycle
 The virus first multiplies in tonsil, the lymph
nodes of the neck, Peyer’ s paches, and the
small intestine.
 The central nervous system may be invaded
by way of the circulating blood. Large
amounts of anti-body are necessary to prevent
passage of the virus along nerve fiber.
 Poliovirus can spread along axons of
peripheral ner-ves to the central nervous
system, along the fibers of the lower motor
neurons to the spinal cord or the br-ain.
 Virus invades certain types of nerve cell, and
may da-mage or completely destroy these
cells for its intracell-ular multiplication.
Events in replication
• 1. Binding to the cell surface receptor
CD155.
• 2&3.Taken via endocytosis and
decapsulated and then the viral RNA
released.
• 4. Translation of the viral RNA occurs and
polyprotein is cleaved yielding mature viral
proteins.
• 5. Double stranded replicative form RNA is
produced and many positive strands RNA
copies are produced from single negative
strand.
• 6. Newly synthesized positive sense RNA
molecules serve as templates for translation
of more viral proteins or can be enclosed in
a capside (capside assembly)
• 7. Lysis of infected cell results in release of
infections progeny virions (liberation of
virions)
Pathogenesis ﹠ Pathology:
The mouth is the portal of entry of the virus
and primary multiplication takes place in
the oropharynx or intestine.
The virus is regularly present in the throat
and in the stools before the onset of illness.
The virus may be found in the blood of
patients with nonparalytic poliomyelitis. Ab
to the virus appear early in the disease,
usually before paralysis occurs
Transmission
 Fecal – oral route
via hands and objects
via food and water
Clinical findings:
Abortive poliomyelitis
Nonparalytic poliomyelitis
Paralytix poliomyelitis
Progressive postpoliomylitis muscle atrophy
Clinical Manifestations
 Most infections asymptomatic, 95%
 Abortive polio (minor illness), 5%: fever, malaise, sore throat,
myalgia, headache)
 Aseptic meningitis (non paralytic polio), 1%
 Paralytic polio (major illness), 0.1%: asymetric flaccid paralysis /
paresis. Lower, or upper extremities, thoracic, abdominal, bulbar.
Involvement : spinal cord anterior horn cells, motor cortex, dorsal
root ganglia
neurologic sequela (2/3)
 Post-polio syndrome: progressive atrophy years later
 Perhaps the first written
record of a virus
infection consists of a
heiroglyph from
Memphis, drawn in
approximately 1400BC,
which depicts a temple
priest called Siptah
showing typical clinical
signs of paralytic
poliomyelitis
Victims of paralytic polio
Child with polio sequelae
Laboratory diagnosis:
The virus may be recovered from throat swabs,
rectal swabs, or stool samples.
Specimens should be kept frozen during transit
to the laboratory
Cultures of human or monkey cells
Paired serum specimens are required to show
rise in antibody titer during the course of
disease.
Laboratory Diagnosis
 Virus Isolation
 Mainstay of diagnosis of poliovirus infection
 poliovirus can be readily isolated from throat swabs,
faeces, and rectal swabs, but rarely from the CSF
 Can be readily grown and identified in cell culture
 Requires molecular techniques to differentiate
between the wild type and the vaccine type
 Serology
 Very rarely used for diagnosis since cell culture is
efficient. Occasionally used for immune status
screening for immunocompromised individuals
Immunity:
Immunity is permanent to the type causing the infection.
Passive immunity is transferred from
mother to offspring, which gradually
disappear during the first 6 months of
life.
Virus-neutralizing antibody forms soon
after exposure to the virus, often before
the onset of illness.
Epidemiology:
Poliomyelitis occurs worldwide – year-round
in tropics and during summer and fall in temperate zone. Winter outbreaks are rare.
The disease occurs in all age groups ,but children are more susceptible than adult because
of the acquired immunity of the adult population.
Human are the only known reservoir of infection.
Prevention ﹠ control:
Both live-virus and killed-virus vaccines are available . They induce antibody and protect the central
nervous system from subsequent invasion by wild
virus.
A potential limiting factor for oral vaccine is interference, and for vaccine-associated disease, a switch to
the use of only inactivated poliovaccine (four doses)
for children
Immune globulin can provide protection for a few
weeks against the paralytic disease but does not
prevent subclinical infection.
The application of recombinant DNA
Vaccines Available
 Intramuscular Poliovirus Vaccine (IPV)
 consists of formalin inactivated virus of all 3 poliovirus
serotypes (Salk)
 Produces serum antibodies only: does not induce local
immunity and thus will not prevent local infection of the gut
 However, it will prevent paralytic poliomyelitis since viraemia is
essential for the pathogenesis of the disease
 Oral Poliovirus Vaccine (OPV)
 Consists of live attenuated virus of all 3 serotypes (Sabin).
 Produces local immunity through the induction of an IgA
response as well as systemic immunity
 Rarely causes paralytic poliomyelitis, around 1 in 3 million
doses
 Most countries use OPV because of its ability to
induce local immunity and also it is much cheaper to
produce than IPV
 The normal response rate to OPV is close to 100%.
 OPV is used for the WHO poliovirus eradication
campaign
 Because of the slight risk of paralytic poliomyelitis,
some Scandinavian countries have reverted to using
IPV. Because of the lack of local immunity, small
community outbreaks of poliovirus infections have
been reported