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Viral Genetics: Enteroviruses and Enterovirus Structure

What is an enterovirus? Discover the facts about the life cycle and genetics of this important family of viruses, the second most common in humans, and cause of many serious diseases.

By Robyn Broyles
Desk Science
Reading time 3 min read
Word count 545
Genetics Science Genetic testing
Viral Genetics: Enteroviruses and Enterovirus Structure
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Quick Take

What is an enterovirus? Discover the facts about the life cycle and genetics of this important family of viruses, the second most common in humans, and cause of many serious diseases.

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The Enteroviruses: An RNA Virus Family

The enteroviruses are a family of RNA viruses that cause a number of human diseases, ranging from the common cold to polio (poliomyelitis). They are members of the family Picornaviridae, which are small RNA viruses (“pico-rna-viridae”: small RNA viruses). The name “enterovirus” comes from the fact that they are found in the intestines, although they are not a common cause of “stomach flu” (viral gastroenteritis).

Human enteroviruses include poliovirus, Coxsackie A virus, Coxsackie B virus, echoviruses, and several others. The diseases they cause are not zoonotic (i.e. spread by animals), although some animals are affected by their own enteroviruses.

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Enteroviruses are highly contagious. They are spread through the fecal-oral route and through secretions such as saliva and nasal mucus. They are the second most common viruses infecting humans, after the rhinoviruses.

Structure of the Virion

An enterovirus consists of genetic material surrounded by a protein coat called a capsid. Like the influenza virus , enteroviruses use a single strand of RNA (ssRNA) for their genome. This strand is positive-sense, unlike influenza, which uses negative-sense RNA. Influenza viruses are not considered to be related to enteroviruses because they use opposite sense in their single-stranded genome.

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Enteroviruses are cytolytic, that is, they cause the host cell to burst when they have finished replicating. The new virions (virus particles) are then released to find new cells to infect.

The enterovirus capsid is icosahedral in shape and contains four proteins, called VP1, VP2, VP3, and VP4. After entering the host cell, the genome is released from the capsid and acts as mRNA to create the viral proteins. Some are structural proteins and are assembled into new capsids; others are non-structural and involved with replication or cell lysis. Next, to replicate the genome, the original genome’s complement (negative sense) is synthesized, then used as a template to produce positive-sense ssRNA. These strands become the genomes packed into the newly assembled capsids.

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Genetics

The complete nucleotide sequences for at least 25 enteroviruses are now known, and partial sequences are known for many more. Like all RNA-based viruses, enteroviruses mutate rapidly and contain only the bare minimum amount of genetic material necessary. In these viruses, even a single point mutation can cause a change in phenotype.

When an enterovirus enters a cell, it first translates its entire ssRNA genome into long polypeptide called a polyprotein. This giant protein is then processed by viral proteases, which cleave it at specific sites. The resulting fragments are the structural and nonstructural viral proteins (including more proteases for daughter virions).

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All enteroviruses have the same basic genetic organization. The capsid proteins are coded on the 5’ end of the ssRNA in a section called P1 (precursor 1). The rest of the genome codes for nonstructural proteins, divided into P2 and P3. Changes in the structural protein genes of different enterovirus species reflect phylogentic relationships . On the 3’ end, completely different patterns of gene variation are found; these are thought to result from recombination of the nonstructural protein genes.

References

  • Hellen, Christopher, and Eckerd Wimmer. “Enterovirus Genetics.” Chapter 2 in Human Enterovirus Infections, ed. Henry Robart. 1995; ASM Press. ISBN 9781555810924.
  • Juhana Santti et al. “Molecular epidemiology and evolution of coxsackievirus A9.” Journal of General Virology 2009; 81: pp. 1361–1372.
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