Poliovirus: Characteristics, Pathogenesis and Lab Diagnosis

Poliovirus is the etiologic agent of the paralytic disease known as poliomyelitis. Poliomyelitis is a contagious disease that spreads through person-to-person contact, mainly via the fecal-oral route. The virus affects young children (mainly children under five years of age) and can cause permanent disability.  

Poliovirus has been eradicated from most countries, but two countries, Pakistan and Afghanistan, are still endemic.

Characteristics of Poliovirus

  1. Poliovirus is a member of a family of viruses called Picornaviridae. The Picornaviridae includes many other human pathogens, such as Coxsackieviruses, echoviruses, enteroviruses, hepatitis A virus, and rhinoviruses. Poliovirus is one of the smallest viruses.
  2. Poliovirus is a small and simple virus composed of a shell, or capsid, made of protein. The poliovirus capsid is about 30 nanometers in diameter. 
  3. A single molecule of ribonucleic acid (RNA) is found within the capsid. This RNA carries genetic information to make new virus particles. It has single-stranded RNA of positive polarity. Its genome is infective. The infectious nucleic acid of poliovirus can bypass the host range specificity provided by the viral protein-cell receptor interaction. For example, intact poliovirus can grow only in human or primate cells, but purified poliovirus RNA can also enter and replicate in nonprimate cells.
  4. Polioviruses have three serotypes. Based on the nature of surface antigens, polioviruses have three different antigenic determinants (poliovirus type 1, poliovirus type 2, and poliovirus type 3).
  5. Poliovirus has a narrow range of specificity. It can enter the cells of only humans and other primates.


People acquire poliovirus infection from other humans through contact with virus-containing feces or contaminated water. The virus multiplies in the cells of the gastrointestinal tract and lymphatic tissue (tonsils/payers patches). Newly synthesized virus particles are released into the intestine and shed in the feces.

After multiplying in the gastrointestinal tract, poliovirus spreads to the regional lymph nodes and enters the bloodstream (minor / 20 viremia). It crosses the blood-brain barrier (BBB) and may enter the spinal cord and brain.

Direct neural transmission may also occur, e.g., after tonsillectomy. In the CNS, Virus multiplies selectively in the neurons and destroys the anterior horn cells of the spinal cord.  The destruction of motor neurons by the virus leads to limb paralysis.

The earliest change is degeneration of Nissils bodies. When degeneration becomes irreversible, the necrotic cell lyses or is phagocytosed. Viruses don’t multiply in muscle in vivo. Changes in peripheral nerves and voluntary muscles are secondary to the destruction of nerve cells.

Clinical findings

The incubation period is 7-14 days. The manifestations may range from the asymptomatic stage (>90 % cases) to the most severe paralytic disease (<1%).

  • Inapparent infections: Following infection, the majority (91-96%) of cases are asymptomatic.
  • Abortive infection: About 5% of patients develop minor symptoms such as fever, malaise, sore throat, anorexia, myalgia, and headache.
  • Nonparalytic poliomyelitis is seen in 1% of patients who presented with aseptic meningitis.
  • Paralytic poliomyelitis is the least common form (<1%) among all the stages and is characterized by descending asymmetric acute flaccid paralysis (AFP). Proximal muscles are affected earlier than the distal muscles; paralysis starts at the hip and proceeds towards the extremities, which leads to the characteristic tripod sign (child sits with flexed hip, both arms are extended towards the back for support). Sites involved can be spinal, bulbospinal, and bulbar. Accordingly, the nature of paralysis varies (e.g., respiratory insufficiency or dysphagia are common in bulbar involvement).

Lab diagnosis

Sample: Poliovirus can be detected in specimens from the throat, feces (stool), and occasionally blood or cerebrospinal fluid (CSF).

Virus Isolation and Detection

Virus isolation from stool specimens is the most sensitive method to diagnose poliovirus infection. Collecting at least two stool specimens  24 hours apart from suspected poliomyelitis patients is recommended to increase the probability of isolating poliovirus. Poliovirus may also be isolated from pharyngeal swabs. Isolation is less likely from blood or CSF.  Samples should be collected early during the disease (ideally within 14 days after onset).

Primary monkey kidney cells are the most recommended cell lines. Various methods can identify virus growth.

  • Cytopathic effects appear in 3-6 days; described as crenation and degeneration of the entire cell sheet.
  • Isolated viruses can be identified and serotyped by neutralization with a specific antiserum.
  • Specific gene sequences of the virus can be detected by polymerase chain reaction (PCR) assays.


For the patients who did not receive polio vaccination, the serological test may help support the diagnosis of paralytic poliomyelitis. An acute serum specimen should be obtained early in the course of the disease, and a convalescent specimen should be obtained at least three weeks later.

A four-fold rise in antibody titer in paired sera confirms the diagnosis.  Neutralization and complement fixation tests can be useful to measure the concentration of antibodies.


Vaccination is the best way to protect people and stop the transmission of Poliomyelitis. There are two types of vaccine; inactivated poliovirus vaccine (IPV) and oral poliovirus vaccine (OPV).

References and Further Reading

  1. Menant, J. C., & Gandevia, S. C. (2018). Poliomyelitis. Handbook of clinical neurology, 159, 337–344. https://doi.org/10.1016/B978-0-444-63916-5.00021-5
  2. Skern T. (2010). 100 years poliovirus: from discovery to eradication. A meeting report. Archives of virology, 155(9), 1371–1381. https://doi.org/10.1007/s00705-010-0778-x
  3. Alleman, M. M., Wannemuehler, K. A., Weldon, W. C., Kabuayi, J. P., Ekofo, F., Edidi, S., Mulumba, A., Mbule, A., Ntumbannji, R. N., Coulibaly, T., Abiola, N., Mpingulu, M., Sidibe, K., & Oberste, M. S. (2014). Factors contributing to outbreaks of wild poliovirus type 1 infection involving persons aged ≥15 years in the Democratic Republic of the Congo, 2010-2011, informed by a pre-outbreak poliovirus immunity assessment. The Journal of infectious diseases, 210 Suppl 1, S62–S73. https://doi.org/10.1093/infdis/jiu282
  4. Nathanson, N., & Kew, O. M. (2010). From emergence to eradication: the epidemiology of poliomyelitis deconstructed. American journal of epidemiology, 172(11), 1213–1229. https://doi.org/10.1093/aje/kwq320

Acharya Tankeshwar

Hello, thank you for visiting my blog. I am Tankeshwar Acharya. Blogging is my passion. As an asst. professor, I am teaching microbiology and immunology to medical and nursing students at PAHS, Nepal. I have been working as a microbiologist at Patan hospital for more than 10 years.

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