Poliomyelitis, commonly known as polio, is a highly infectious disease caused by the poliovirus. Understanding how this virus operates within the human body is important, especially as global efforts continue towards its eradication. This knowledge illuminates the mechanisms behind its devastating effects and the importance of continued prevention.
The Poliovirus: The Agent of Disease
The poliovirus is a member of the Enterovirus genus within the Picornaviridae family. It is a small, non-enveloped virus. The virus contains a single-stranded, positive-sense RNA genome encased within an icosahedral protein shell called a capsid. This RNA genome serves directly as messenger RNA upon entry into a host cell, allowing for immediate translation of viral proteins. There are three distinct serotypes of poliovirus (types 1, 2, and 3), each with slightly different capsid proteins.
Entry and Initial Spread in the Body
The poliovirus primarily enters the human body through the oral-fecal route, typically by ingesting contaminated food or water. Once ingested, the virus initially infects and replicates in the cells of the pharynx and gastrointestinal tract. The virus gains entry by binding to a specific receptor on the surface of host cells, known as the poliovirus receptor.
Following initial replication, the poliovirus spreads to nearby lymphatic tissues. From these sites, the virus can then enter the bloodstream, a condition known as viremia. This bloodstream dissemination allows the poliovirus to travel throughout the body, though in most cases, the body’s immune system successfully clears the virus during this stage, preventing further progression of the infection.
Invasion of the Nervous System
In a small percentage of infections, the poliovirus can breach the blood-brain barrier, a protective mechanism that normally prevents harmful substances from entering the central nervous system (CNS). Once inside the CNS, the virus exhibits tropism for motor neurons. Motor neurons are specialized nerve cells responsible for transmitting signals from the brain and spinal cord to muscles, controlling voluntary movement.
The poliovirus binds to receptors on these motor neurons and enters them. Once inside, the virus hijacks the neuron’s cellular machinery to replicate itself extensively. This rapid viral multiplication overwhelms the infected motor neurons, leading to their damage or destruction, a process known as neuronophagia. The destruction of these motor neurons disrupts the transmission of signals from the brain to skeletal muscles, resulting in muscle weakness and the characteristic flaccid paralysis associated with poliomyelitis.
Diverse Outcomes of Poliovirus Infection
The majority of poliovirus infections (estimated 70-95%) are asymptomatic. In these cases, the virus replicates in the gastrointestinal tract and may enter the bloodstream, but it does not progress to cause overt illness or significant neurological damage. Even without symptoms, infected individuals can still shed the virus in their feces for several weeks, contributing to its spread.
A smaller proportion of infections (roughly 25%) result in a minor illness, sometimes called abortive poliomyelitis, characterized by mild, flu-like symptoms such as a sore throat and low fever. In about 1-5% of cases, the virus reaches the CNS but causes non-paralytic aseptic meningitis, an inflammation of the meninges (the membranes surrounding the brain and spinal cord) without leading to paralysis. This form may present with headache, neck stiffness, and muscle pain. The most severe outcome, paralytic poliomyelitis, occurs in less than 1% of infections, leading to muscle weakness and permanent paralysis due to the destruction of motor neurons.