page_title: Picornavirus
section_title: Life cycle
hierarchical_section_title: Picornavirus / Virology / Replication / Life cycle
caption_attribution_description: English: Picornavirus life cycle. (A, B) Picornavirus uses different receptors to enter the cell, some implicated in the signaling internalization (A), meanwhile others can act as carriers that transport the viral particle to meet the primary receptor (B). (C, D) This infection event can be impeded by the action of specific neutralizing antibodies that can destabilize the viral particle (C) or opsonize or stabilize the particle to impair receptor binding or conformational changes required for infection (D). (E) Once the virus enters the cell, the viral RNA delivery mechanism is triggered, and the viral genome (black wavy line) is released into the cytoplasm. (F) Upon removal of VPg (magenta oval), the genome starts the IRES-driven translation leading to the production of the viral polyprotein. (G) The proteolytic cascade produces all viral proteins, structural and non-structural. (H) Some proteins act by hijacking the host cellular systems such as the nuclear pore, the cell translation machinery, and the apoptotic systems and initiate the remodeling of the internal cell membranes. (I) The structural proteins assemble into the capsid intermediates, the protomer and the pentamer, and also procapsids (L). (J) The formed replication complex assembled from non-structural proteins and modified internal membranes firing the picornaviral genome replication by the 3D polymerase via RNA complementary (red wavy lines) and using VPg as a primer. (K) The new progeny genomes including eventual mutations (yellow stars). (M) Mature virions assemble from pentamers that surround and package the new viral genomes. Viral particles escape from the cell by cell lysis or budding within membranes that can protect the viral progeny (P). (N) Some progeny virus with mutations in their capsids (yellow star) may escape from to the action of specific NAbs. (O) Empty capsids can act as molecular decoys for Abs to protect the infecting particles from neutralization.
context_page_description: Picornaviruses are a group of related RNA viruses which infect vertebrates including mammals and birds. They are nonenveloped viruses that represent a large family of small, positive-sense, single-stranded RNA viruses with a 30-nm icosahedral capsid. The viruses in this family can cause a range of diseases including paralysis, meningitis, hepatitis, and poliomyelitis.
  Picornaviruses constitute the family Picornaviridae, order Picornavirales, and realm Riboviria. There are currently 110 species in this family, divided among 47 genera. Notable examples are genera Enterovirus, Aphthovirus, Cardiovirus, and Hepatovirus.
context_section_description: The viral particle binds to cell surface receptors. Cell surface receptors are characterized for each serotype of picornaviruses. For example, poliovirus receptor is glycoprotein CD155 which is special receptor for human and some other primate species. For this reason, poliovirus could not be made in many laboratories until transgenic mice having a CD155 receptor on their cell surface were developed in the 1990s. These animals can be infected and used for studies of replication and pathogenesis. Binding causes a conformational change in the viral capsid proteins, and myristic acid are released. These acids form a pore in the cell membrane through which RNA is injected .
  Once inside the cell, the RNA un-coats and the (+) strand RNA genome is replicated through a double-stranded RNA intermediate that is formed using viral RDRP (RNA-Dependent RNA polymerase). Translation by host cell ribosomes is not initiated by a 5' G cap as usual, but rather is initiated by an IRES (Internal Ribosome Entry Site). The viral life cycle is very rapid with the whole process of replication being completed on average within 8 hours. However, as little as 30 minutes after initial infection, cell protein synthesis declines to almost zero output – essentially the macromolecular synthesis of cell proteins is shut off. Over the next 1–2 hours there is a loss of margination of chromatin and homogeneity in the nucleus, before the viral proteins start to be synthesized and a vacuole appears in the cytoplasm close to the nucleus that gradually starts to spread as the time after infection reaches around 3 hours. After this time the cell plasma membrane becomes permeable, at 4–6 hours the virus particles assemble, and can sometimes be seen in the cytoplasm. At around 8 hours the cell is effectively dead and lyses to release the viral particles.
  Experimental data from single step growth-curve-like experiments have allowed scientists to look at the replication of the picornaviruses in great detail. The whole of replication occurs within the host cell cytoplasm and infection can even happen in cells that do not contain a nucleus (known as enucleated cells) and those treated with actinomycin D (this antibiotic would inhibit viral replication if this occurred in the nucleus.)
  Translation takes place by -1 ribosomal frameshifting, viral initiation, and ribosomal skipping. The virus exits the host cell by lysis, and viroporins. Vertebrates serve as the natural host. Transmission routes are fecal-oral, contact, ingestion, and air borne particles.
caption: Picornavirus life cycle
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