Poliovirus: Questions

a. The pattern is characteristic: enteroviruses (including poliovirus) are shed abundantly in stool but only rarely reach the cerebrospinal fluid, so a positive stool with a negative CSF PCR is the expected finding and does not weaken the diagnosis. It does not, on its own, prove causation, because enteroviruses are commonly carried in the gut, but combined with acute flaccid paralysis and anterior-horn signal on MRI it strongly suggests a poliovirus-like (anterior-horn) process that must be treated as possible polio until excluded.

b. Investigate as an acute flaccid paralysis (AFP) case: notify immediately, and collect two stool specimens 24 to 48 hours apart, both within 14 days of onset, sent under reverse cold chain to the National Institute for Communicable Diseases for poliovirus isolation and intratypic differentiation (to distinguish wild, Sabin-like and vaccine-derived virus). Record the vaccination history and arrange the 60-day follow-up for residual paralysis.

c. Poliovirus and other enteroviruses spread faecal-orally, so apply enteric (contact) precautions with strict hand hygiene and safe disposal of stool, and manage the case as a potential public-health emergency pending virology.

The picture is residual paralytic poliomyelitis: asymmetric lower-motor-neuron paralysis in infancy leaving a wasted, shortened limb with preserved sensation.

• Salk (inactivated poliovirus vaccine, IPV). A formalin-inactivated preparation given by injection. It raises serum neutralising antibody that protects the individual from paralysis but induces little gut mucosal immunity, cannot cause polio, and is safe in immunocompromised people.
• Sabin (oral poliovirus vaccine, OPV). A live attenuated vaccine given by mouth. Because it replicates in the gut it induces both serum antibody and strong mucosal immunity, interrupting transmission, and it is cheap and needle-free. Its drawback is that the live virus can revert to neurovirulence, rarely causing vaccine-associated paralysis and, on spread, vaccine-derived poliovirus; it is contraindicated in immunocompromise.

Because it replicates in the gut, oral vaccine induces strong intestinal mucosal immunity (secretory IgA) that blocks faecal-oral transmission, which the injected inactivated vaccine does not efficiently provide.

The trade-off runs the other way for the rest: inactivated vaccine is the one that is safe in immunocompromised hosts and carries no risk of vaccine-associated paralysis, and neither vaccine protects against non-polio enteroviruses.

Guillain-Barre syndrome is typically symmetric and ascending with sensory involvement and albuminocytological dissociation in the cerebrospinal fluid, and is usually afebrile.

Poliomyelitis is the opposite: asymmetric, purely motor, with fever at onset. Both can progress quickly, so progression rate does not discriminate.

Over 90% of infections are asymptomatic, and on average only about 1 in 200 infections in a susceptible population results in paralytic disease. Most of the remainder are a minor febrile illness or a non-paralytic aseptic meningitis.

The low ratio of paralytic cases to infections is why surveillance must detect every case, and why environmental sampling can reveal circulation that no clinical case would show.

Poliovirus is a picornavirus (genus Enterovirus, species Enterovirus coxsackiepol) with three serotypes, 1, 2 and 3. The serotypes do not cross-protect, so immunity is needed against all three.

It is a small non-enveloped RNA virus, unrelated to the enveloped Flaviviridae, Togaviridae or Paramyxoviridae, and its genome is not segmented like the Reoviridae.

Poliovirus spreads faecal-orally, and humans are its only reservoir; the virus is shed in stool for weeks, which both sustains transmission and underpins environmental (sewage) surveillance.

There is no arthropod vector or bloodborne cycle; limited pharyngeal replication allows some oral-oral spread, but the faecal-oral route dominates.

The viral 2A protease cleaves eIF4G, disabling cap-dependent translation of host messenger RNA within about two hours, while the virus’s own cap-independent internal ribosome entry site keeps working, diverting ribosomes to viral synthesis.

The virus does not degrade all ribosomes, block nuclear transcription, methylate host RNA or depend on apoptosis for shut-off.

Decades after the acute illness, the enlarged motor units that took over from the neurons lost to polio degenerate under the long-term strain, giving new progressive weakness, pain and wasting in previously affected muscles.

Poliovirus does not establish latency and does not reactivate, and the syndrome is neither a fresh infection nor a demyelinating or motor-neurone disease.

Poliovirus binds CD155 (the poliovirus receptor), an immunoglobulin-superfamily adhesion molecule, which inserts into the capsid canyon and triggers uncoating and delivery of the RNA into the cytoplasm.

CD4 with a coreceptor is used by HIV, the acetylcholine receptor by rabies virus, and complement receptor CD21 by Epstein-Barr virus.

Poliomyelitis causes asymmetric, flaccid, lower-motor-neuron weakness, proximal more than distal and legs more than arms, with reflexes lost and sensation preserved.

Spasticity and a sensory level suggest a cord compression or transverse myelitis; symmetric ascending weakness with numbness suggests Guillain-Barre syndrome; polio is never purely sensory.

Poliovirus destroys the large lower motor neurons of the spinal cord anterior horn, producing a lower-motor-neuron pattern of flaccid, asymmetric weakness with lost reflexes and wasting but preserved sensation.

The sensory pathways and peripheral myelin are spared (unlike Guillain-Barre syndrome), and the lesion is in the neuron cell bodies, not the neuromuscular junction.

The genome is a single positive-sense RNA of about 7.4 kb that is directly translated, with a VPg peptide at its 5’ end and an internal ribosome entry site allowing cap-independent translation of one polyprotein.

It carries no DNA stage, needs no packaged polymerase (unlike negative-sense viruses), and is neither segmented nor reverse-transcribed.

In most hosts the type I interferon response confines poliovirus to the gut and blood, and paralysis follows only when replication in extraneural tissue is not held in check, letting the virus reach the cord. This helps explain why roughly only 1 in 200 infections paralyses.

Poliovirus replicates well in the gut and, in susceptible hosts, in neurons; the receptor is present, and maternal antibody wanes.