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Description The cellular life cycle of poliovirus. It is initiated by binding of a poliovirion to the cell surface macromolecule CD155, which functions as the receptor (1). Uncoating of the viral RNA is mediated by receptor-dependent destabilization of the virus capsid (2). Cleavage of the viral protein VPg is performed by a cellular phosphodiesterase, and translation of the viral RNA occurs by a cap-independent (IRES-mediated) mechanism (3). Proteolytic processing of the viral polyprotein yields mature structural and non-structural proteins (4). The positive-sense RNA serves as template for complementary negative-strand synthesis, thereby producing a double-stranded RNA (replicative form, RF) (5). Initiation of many positive strands from a single negative strand produces the partially single-stranded replicative intermediate (RI) (6). The newly synthesized positive-sense RNA molecules can serve as templates for translation (7) or associate with capsid precursors to undergo encapsidation and induce the maturation cleavage of VP0 (8), which ultimately generates progeny virions. Lysis of the infected cell results in release of infectious progeny virions (9).
Date
Source De Jesus NH (2007). "Epidemics to eradication: the modern history of poliomyelitis". Virol. J. 4: 70. DOI:10.1186/1743-422X-4-70. PMID 17623069.
Author Nidia H De Jesus (image and caption)
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(Reusing this file)		 This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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current16:29, 26 September 2007Thumbnail for version as of 16:29, 26 September 20071,202 × 975 (276 KB)DO11.10{{Information |Description= The cellular life cycle of poliovirus. It is initiated by binding of a poliovirion to the cell surface macromolecule CD155, which functions as the receptor (1). Uncoating of the viral RNA is mediated by receptor-dependent desta

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