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| __NOTOC__
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| {{Polio}}
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| {{CMG}}
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| ==Overview==
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| Polio is a highly infectious disease caused by Poliovirus that invades the [[nervous system]]. Poliovirus are small (27–30 nm), nonenveloped viruses with [[capsid]]s enclosing a single-stranded, positive-sense [[RNA]] genome about 7,500 nucleotides long. Person-to-person spread of poliovirus via the fecal-oral route is the most important route of transmission, although the oral-oral route may account for some cases.
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| ==Taxonomy==
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| ==Biology==
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| {| style="float: right;"
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| | [[File:Polio EM PHIL 1875 lores.PNG|200px|thumb|none|A Transmission electron microscopy of poliovirus<SMALL> ''Image provided by the CDC [http://phil.cdc.gov/phil/details.asp Centers for Disease Control and Prevention] ''<ref>{{Cite web | title = http://phil.cdc.gov/phil/details.asp | url = http://phil.cdc.gov/phil/details.asp}}</ref></SMALL>]]
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| [[Poliovirus]] is a member of the genus [[enterovirus]], family [[Picornaviridae]]. Enteroviruses are small, nonenveloped, positive stranded RNA viruses. Other members of the family include: [[Rhinovirus]], [[Hepatovirus]], [[Cardiovirus]] and Apthovirus. Poliovirus is a transient inhabitant of the [[gastrointestinal tract]], stable at an acid pH.<ref name=CDC>{{cite web | title = Polyomavirus | url = http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/polio.pdf }}</ref><ref name="pmid15885840">{{cite journal| author=Mueller S, Wimmer E, Cello J| title=Poliovirus and poliomyelitis: a tale of guts, brains, and an accidental event. | journal=Virus Res | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840 }} </ref> [[Enteroviruses]] in general do not cause disease, or are responsible for mild symptoms. Disease syndromes resulting from viral spread to other secondary regions are rare. Despite rare, these syndromes may lead to severe disease complications, seldom with fatal outcomes.
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| There are three poliovirus [[serotype]] (P1, P2, and P3) that replicate efficiently in the gastrointestinal tract. There is minimal heterotypic [[immunity]] between the three [[serotype]]s. That is, immunity to one [[serotype]] does not produce significant immunity to the other serotypes. The poliovirus is rapidly inactivated by heat, formaldehyde, chlorine, and ultraviolet light.<ref name=CDC>{{cite web | title = Polyomavirus | url = http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/polio.pdf }}</ref>
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| The characteristics of [[poliovirus]] make it a good model for [[viral]] study, specifically: high viral titers, stable [[capsid]] and ease of purification, along with a low bio-safety requirement.<ref name="pmid15885840">{{cite journal| author=Mueller S, Wimmer E, Cello J| title=Poliovirus and poliomyelitis: a tale of guts, brains, and an accidental event. | journal=Virus Res | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840 }} </ref>
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| ==Structure==
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| The poliovirus genome consists of a single (+) sense RNA molecule of about 7440 nucleotides (Fig. 1). A relatively long 5′ NTR of 742 nt is followed by a single open reading frame coding for a polyprotein of 2209 amino acids and a 3′ NTR of 70 nt (Dorner et al., 1982; Kitamura et al., 1981; Racaniello and Baltimore, 1981b). The first 88 nucleotides at the 5′ end of the genome form a clover leaf like secondary structure (Andino et al., 1990; Rivera et al., 1988), which has been implicated in the formation of the replication complex during (+) strand RNA synthesis. The 3′ NTR contains two stem loops that may interact to form a tertiary pseudoknot structure (Pilipenko et al., 1992, p. 2557; Jacobson et al., 1993, p. 2558). The very 3′ end of the viral RNA is com- prised of a genetically encoded stretch of poly(A) varying around 60 adenylate residues in length (Yogo and Wimmer, 1972). Unlike most eukaryotic mRNAs the poliovirus ge- nomic RNA does not carry the m7G cap structure essential for translational initiation of normal eukaryotic mRNA. In- stead a small viral protein, VPg, is covalently linked to the 5′ terminus (Lee et al., 1977). Contrary to canonical eukaryotic translational initiation, cap-independent translation of the po- liovirus genome is initiated by binding of the host transla- tional machinery to a highly structured RNA cis-acting ele- ment within the 5′ non-translated region of the genome. This element has been termed internal ribosomal entry site (IRES) for its propensity to initiate translation regardless of its loca- tion within an RNA molecule (Jang et al., 1989, 1988; Molla et al., 1992). First discovered in encephalomyocarditis virus and poliovirus (Jang et al., 1988; Pelletier and Sonenberg, 1988), later in other picornaviruses (Bandyopadhyay et al., 1992; Borman and Jackson, 1992), IRES-dependent transla- tion is now established as a novel mechanism of eukaryotic cap-independent protein synthesis. More and more IRES elements have been discovered not only in viral genomes, but in the 5′ untranslated region of many cellular mRNAs (reviewed in Hellen and Sarnow, 2001)
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| ==Tropism==
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| ==Natural Reservoir==
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| Humans are the only known reservoir of poliovirus, which is transmitted most frequently by persons with inapparent infections. There is no asymptomatic carrier state except in immune deficient persons.
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| Because the poliovirus receptor is only expressed on cells of humans and a few subhuman primate species, there are no known extrahuman reservoirs (7, 8). Following infection, the virus replicates in the gastrointestinal tract and may cause viremia (9, 10). (2)
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| ==References==
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| {{Reflist|2}}
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| [[Category:Needs overview]]
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| [[Category:Disease]]
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| [[Category:Infectious disease]]
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| [[Category:Primary care]]
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| {{WH}}
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| {{WS}}
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