Poliovirus: Structure, Replication, Pathogenesis, Clinical Features, and Prevention

Introduction to Poliovirus:

According to Baltimore’s viral categorization system, picornaviruses are categorized as group IV viruses since their genomes are single-stranded and positive sense RNA. Picornaviruses are small, non-enveloped, icosahedral viruses, which contain a single-stranded, non-segmented RNA genome. The viral particle is around 27–30 nm in diameter. The Picornaviridae family includes medically important genera like Enterovirus, Rhinovirus, Hepatovirus.

Individuals are infected with enteroviruses by ingestion of contaminated food or water. Enteroviruses are stable at the low pH of the stomach, replicate in the gastrointestinal (GI) tract, and are excreted in the stool. Enterovirus after replicating in the oropharynx and intestinal tract lymphoid tissue can enter the bloodstream and, thereby, spread to the central nervous system [CNS]).

Morphology of Poliovirus:

Poliovirus particles are typical enteroviruses. The viruses are round, around 27 nm-diameter particles. The virion is composed of 60 subunits, consisting of 4 viral proteins (VP1-VP4). The viral genome is single stranded positive sense RNA which can be directly translated by host ribosomes to form a polyprotein, which is divided into 11 different proteins.

 Morphology of Poliovirus

 Fig: Morphology of Poliovirus

Replication Cycle of Poliovirus:

Attachment and Entry

  • The poliovirus replication cycle occurs in the cytoplasm of cells
  • First, the virion attaches to a specific receptor in the plasma membrane.
  • The receptors for poliovirus are CD155 (cluster of differentiation 155).

Translation and Polyprotein Processing

  • Receptor binding triggers a conformational change in the virion which results in release of the viral RNA into the cell cytosol.
  • The infecting viral RNA is translated into a polyprotein that contains both coat proteins and essential replication proteins.
  • This polyprotein is rapidly cleaved into fragments by proteinases encoded in the polyprotein.

RNA Synthesis and Viral Assembly

  • Synthesis of new viral RNA cannot begin until the virus-coded replication proteins, including an RNA-dependent RNA polymerase, are produced.
  • The infecting viral RNA strand is copied, and that complementary strand serves as template for the synthesis of new plus strands.
  • Many plus strands are generated from each minus-strand template.
  • Some new plus strands are recycled as templates to amplify the pool of progeny RNA; many plus strands get packaged into virions.
Replication of Poliovirus

 Fig: Replication of Poliovirus

Pathogenesis of Poliovirus:

Route of Entry and Spread

  • The virus enters the body through the mouth, and it primarily multiplies in the gut or oropharynx.
  • Before symptoms appear, the virus is frequently found in the throat and feces.
  • One week after infection there is little virus in the throat, but virus continues to be excreted in the stools for several weeks even though high antibody levels are present in the blood.
  • Blood from patients with non-paralytic poliomyelitis during the pre-paralytic stage of the illness may contain the virus.
  • Early in the illness, generally before paralysis sets in, antibodies to the virus start to show up.
  • It is believed that the virus first multiplies in the tonsils, the lymph nodes of the neck, Peyer’s patches, and the small intestine.

Mechanism of Central Nervous System Invasion

  • The central nervous system may then be invaded by way of the circulating blood.
  • Poliovirus can spread along axons of peripheral nerves to the central nervous system, where it continues to progress along the fibers of the lower motor neurons to increasingly involve the spinal cord or the brain.

Cellular Damage and Neurological Manifestations

  • Poliovirus invades certain types of nerve cells, and in the process of its intracellular multiplication it may damage or completely destroy these cells.
  • Myocarditis, lymphatic hyperplasia, and ulceration of Peyer’s patches may be present in addition to pathologic alterations in the neurological system; these alterations in voluntary muscles and peripheral nerves are due to the death of nerve cells.

Incubation period:

  • The incubation period is usually 7–14 days, but it may range from 3 days to 35 days.

Clinical Findings:

Mild Disease

This is the most common form of disease. The patient is merely suffering from a mild illness, which includes fever, malaise, headache, nausea, vomiting, constipation, and sore throat in different combinations. Recovery occurs in a few days.

Non-paralytic poliomyelitis

In addition to the symptoms and indicators, patients with non-paralytic poliomyelitis (aseptic meningitis) also have neck and back pain and stiffness. The illness lasts between two and ten days, and recovery is quick and thorough.

Paralytic poliomyelitis

Many viruses can cause aseptic meningitis, including poliovirus. In a tiny number of instances, the illness progresses to paralysis. The most common complaint of paralytic poliomyelitis is flaccid paralysis, which is caused by damage to lower motor neurons and manifests as weakness or paralysis and decreased muscle tone. The degree of damage varies widely. While residual paralysis lasts considerably longer, maximum recovery often happens after six months.

Prevention and Control of Poliovirus:

  • Poliovirus infection can provide lifelong immunity against the disease, but this protection is limited to the serotype involved. Infection with one type does not protect an individual against infection with the other two types.
  • Two different kinds of vaccine are available, an inactivated (killed) polio vaccine (IPV) and a live attenuated oral polio vaccine (OPV).
  • Killed-virus vaccine are injectable vaccines that induces humoral antibodies but does not induce local intestinal immunity so that virus is still able to multiply in the gut.
  • Oral vaccines contain live attenuated virus. The vaccine produces not only IgM and IgG antibodies in the blood but also secretory IgA antibodies in the intestine. Although additional doses (seven or more) may be necessary in some places to prevent paralytic illness, three or more spaced doses of OPV typically produce a protective immune response against recurrent infections.

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