Polio Virus

Poliovirus

Poliovirus causes poliomyelitis

Serotypes: types 1, 2 & 3

Morphology

Typical enterovirus

Spherical, 28 nm

capsid shell of 60 capsomeres

Capsomere: made of one molecule of each of the four viral proteins (VP1-VP4) arranged in icosahedral symmetry

VP1 faces outside

Resistance

stable at

pH 3.0

In faeces: at 4^OC for months and at -20^OC for yrs

at room temp.:1 day-several days (depends on temp., moisture, pH and quantity of virus)

Heat: 55^OC for 30 mins

Resistant to :

ether, chloroform, proteolytic enzymes of intestinal contents and bile

Chlorination:

0.1 ppm inactivates but much higher concentration to destroy the virus in sewage containing organic matter

Antigenic structure

3 antigenic types: 1,2 &3

Type 1: most epidemics

Type 2: usually endemic infections

Type 3: epidemics (but lesser extent)

2 antigens:

C (capsid) and D (dense)

D antigen:

native or N antigen, associated with the whole virus and is type specific

C antigen:

cross reactive among types,

heated or H antigen associated with the empty noninfectious virion

at 56^OC, D antigen is converted into C antigen

Anti-D antibody is protective

Animal susceptibility and cultivation

Very restricted host range

Natural infection:

occurs only in humans

experimentally into monkeys

requires a primate-specific membrane receptor for infection

pathogenesis

Infection

by  contaminated food or water

also  by droplet infection during the first week of illness

replicate in mucosa of intestine, the mucosa and lymphoid tissue of the tonsils and pharynx

later infects submucous lymphoid cells of payer's patches

spreads to the regional lymph nodes

minor primary viraemic phase ensues

spread and replicate in the reticuloendothelial cells of lymph nodes, spleen and liver

results in major or secondary viraemia

then to the spinal cord and brain

Can also spreads directly from muscle to CNS along axons of peripheral nerves

causes symptoms

poliovirus is cytolytic for the motor neurons of the anterior horn and brain stem

multiplies in the neurons of the central nervous system

destroys anterior horn cells of the spinal cord, as well as nerve cells in the spinal cord or the brain causing flaccid paralysis

Children are most susceptible to poliomyelitis

may also cause myocarditis, lymphatic hyperplasia and ulceration of Payer's patches

Clinical disease

Earliest features

fever, malaise, headache, drowsiness, constipation, and sore throat and lasts for 1-5 days

I.P.- 4 days to 4 wks (10 days)

Most infections

subclinical

Only 1%: clinical illness

Inapparent infection without symptom:

90%, recovery in a few days

Abortive infections or minor illness:

4-8% , nonspecific symptoms

fever, headache, malaise and sore throat within 3-4 days of exposure

Nonparalytic poliomyelitis (aseptic meningitis):

approximately 1%

stiffness and pain in back and neck

lasts for 2-10 days

recovers rapidly and is complete

Paralytic poliomyelitis:

in 0.1-2%

major illness

3-4 days after the minor illness subsided

Flaccid paralysis  due to damage of lower motor neurons.

Muscle involvement is most frequent

Maximal recovery takes place within 6 months but residual paralysis lasts much longer

Encephalitis:

as a complication of poliomyelitis

rare but when occurs, carries a grave prognosis

Post-polio syndrome:

a sequelae of poliomyelitis

20-30% of the original victims

much later in life (25-30 yrs)

deterioration of the originally affected muscles

believed to result from loss of neurons affected in the original episode

Laboratory diagnosis

Isolation of virus:

pharyngeal aspirations (3-5 days) and faeces (up to 5 wks)

Specimen: should be kept frozen during transit

Cultivation:

primary monkey kidney cells, HeLa and Hep-2.

Cytopathic effect

in 2-3 days

Identification of virus

by neutralisation test with pooled and specific antisera

Direct demonstration of virus:

electron microscopy as well as by immune electron microscopy

PCR:

from CSF, serum, urine, throat swabs and tissues

highly sensitive (95%) and specific(80%)

Serological test:

done frequently.

Neutralising antibody

forms soon after exposure  even before the onset of illness

apparently persists throughout life.

Paired serum specimens

immunity

3 antigenic types,

2 type specific antigens- C and D

C antigen of all types are cross-reactive and D antigens are specific

One attack

gives permanent immunity only against the same type only

 Humoral and secretory immunity

CMI response does not have a significant role

prophylaxis

Both live and killed polio vaccines

Killed vaccine

only humoral antibodies but no intestinal immunity

Live vaccine

humoral antibodies (IgM and IgG) and  local secretory and circulating IgA antibodies

Salk’s killed polio vaccine (IPV)

Inactivated polio vaccine

Contains

formalized strains of poliovirus types 1,2 and 3

by subcutaneous or intradermal injection,

1^st dose after the age of 6 months

3 doses are at intervals of 4-6 wks

A booster dose: 6 months after  third dose

only a systemic immune response no secretory IgA in the intestine

Immunity can be sustained by booster doses every 3-5 years thereafter

IPV:  in most developed countries 

OPV: in most developing countries

Live attenuated oral polio vaccine(OPV) (sabin vaccine)

Contains live strains of polio virus types 1,2 and 3

Attenuated  virus:

 can multiply in the oropharynx and intestinal tract but cannot infect neuronal cells

shelf-life : one year at 4^OC, 2 years at -20^OC and for weeks at a room temp.

given orally  ( oral polio vaccine)

for  all infants at 2 months of age-simultaneously with the first DPT injection

second and third doses are administered 2-month intervals

fourth dose is administered at 1.5 years of age

produces serum antibodies and local gut immunity (secretory IgA antibodies) in the intestine

Live vaccine multiplies, infects the intestine and the progeny viruses are disseminated in the community through faecal-oral route, and thus, it protects the individual and the community

Occasional cases of poliomyelitis in vaccinated child and their close contacts

By reversion of OPV-derived viruses

particularly by types 2 and 3.

1-2 cases per million

not used in immunocompromised patients

Advantages and disadvantages  of live and killed polio vaccines
Property	Sabin’s vaccine	Salk’s vaccine
Immunising agent	Live, attenuated	Killed virus
Route of administration	Oral	Parenteral
Immunity	Mucosal (IgA) and humoral (IgG,IgM)	Only humoral
Induction of herd immunity	Yes	No
Reversion to virulent form (vaccine associated poliomyelitis)	Possible, but very rare	No
Duration of protections	Lifelong immunity	Booster vaccine needed for life long immunity