Poliovirus and poliomyelitis: A tale of guts, brains, and an accidental event

Mueller, Steffen; Wimmer, Eckard; Cello, Jerónimo

doi:10.1016/j.virusres.2005.04.008

Cited by 115 publications

(99 citation statements)

References 171 publications

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“…Picornaviridae, is a human pathogen feared for its ability to cause a neurological disease called poliomyelitis that can lead to irreversible paralysis and death (1). Its genome is a plus-stranded Ϸ7-kb RNA encoding a single polyprotein that is cleaved by virus-encoded proteinases into polypeptides forming the capsid (P1, structural region) and the replication proteins (P2-P3, nonstructural region) (2) (Fig.…”

Section: P Oliovirus (Pv) a Member Of The Genus Enterovirus Of Thementioning

confidence: 99%

“…Although PVs and C-cluster CAVs (C-CAVs) both use the gastrointestinal tract as their primary site of replication (where they may recombine), they cause remarkably different diseases in humans (paralysis and upper respiratory disease, respectively) (1,5). (Hereafter and unless otherwise stated, all CAVs mentioned belong to HEV-C).…”

Section: P Oliovirus (Pv) a Member Of The Genus Enterovirus Of Thementioning

confidence: 99%

“…PV is the subject of an intense eradication campaign conducted by the World Health Organization (WHO), using predominantly the live, oral PV vaccine (OPV) developed by A. Sabin (1). The global eradication effort has been a success, considering the greatly reduced incidence of poliomyelitis.…”

Section: P Oliovirus (Pv) a Member Of The Genus Enterovirus Of Thementioning

confidence: 99%

See 2 more Smart Citations

Evidence for emergence of diverse polioviruses from C-cluster coxsackie A viruses and implications for global poliovirus eradication

Jiang

Faase²,

Toyoda³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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The poliovirus (PV) eradication campaign is conducted on the premise that this virus, because of the lack of a zoonotic reservoir, will not reemerge once eradicated. This report examines the origin of PV using theoretical and experimental approaches. Our rooted phylogenetic analysis suggests a speciation of PV from a C-cluster coxsackie A virus (C-CAV) ancestor through mutation of the capsid that caused a receptor switch from intercellular adhesion molecule-1 to CD155, leading to a change of pathogenicity. This hypothesis is supported experimentally with chimeras generated from three different pairs of PV and C-CAV. Those carrying the PV capsid and the replication proteins of C-CAVs replicated well, whereas their reciprocal counterparts were either debilitated or dead. This phenomenon of asymmetry is observed also in recombinants between PV1 and C-CAV20, selected in tissue culture cells using a previously undescribed protocol. The recombinants are generated at frequencies of 10 ؊6 typical for PV interserotype recombination. Strikingly, they resemble genetically and phenotypically, including neurovirulence in CD155 transgenic mice, the large majority of circulating vaccine-derived PVs that have caused poliomyelitis outbreaks in different parts of the world. These data provide experimental evidence for C-CAVs being partners to PVs in generating diverse PV progeny by homologous recombination. They support speciation of a novel human pathogen (PV) from a pool of different human pathogens (C-CAVs). In a PV-free world without PV neutralizing antibodies, contemporary C-CAV, like their ancestor(s), could be fertile ground for a PV-like agent to emerge by mutation.circulating vaccine-derived poliovirus ͉ genetic recombination ͉ rooted phylogenetic analysis ͉ transgenic mouse neurovirulence ͉ emerging infections

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Section: P Oliovirus (Pv) a Member Of The Genus Enterovirus Of Thementioning

confidence: 99%

Section: P Oliovirus (Pv) a Member Of The Genus Enterovirus Of Thementioning

confidence: 99%

See 1 more Smart Citation

Evidence for emergence of diverse polioviruses from C-cluster coxsackie A viruses and implications for global poliovirus eradication

Jiang

Faase²,

Toyoda³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…Humans are the only natural host of PV, although chimpanzees and Old World monkeys, which express receptors closely related to human CD155, can be experimentally infected (11). Like many other receptor molecules used by picornaviruses, CD155 is a long, highly glycosylated, single-span cell surface molecule belonging to the Ig super family (12).…”

mentioning

confidence: 99%

Crystal structure of CD155 and electron microscopic studies of its complexes with polioviruses

Zhang

Mueller

Morais

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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When poliovirus (PV) recognizes its receptor, CD155, the virus changes from a 160S to a 135S particle before releasing its genome into the cytoplasm. CD155 is a transmembrane protein with 3 Ig-like extracellular domains, D1-D3, where D1 is recognized by the virus. The crystal structure of D1D2 has been determined to 3.5-Å resolution and fitted into Ϸ8.5-Å resolution cryoelectron microscopy reconstructions of the virus-receptor complexes for the 3 PV serotypes. These structures show that, compared with human rhinoviruses, the virus-receptor interactions for PVs have a greater dependence on hydrophobic interactions, as might be required for a virus that can inhabit environments of different pH. The pocket factor was shown to remain in the virus during the first recognition stage. The present structures, when combined with earlier mutational investigations, show that in the subsequent entry stage the receptor moves further into the canyon when at a physiological temperature, thereby expelling the pocket factor and separating the viral subunits to form 135S particles. These results provide a detailed analysis of how a nonenveloped virus can enter its host cell.cell entry ͉ receptor ͉ virus

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“…Poliovirus, a member of the Enterovirus genus in the Picornaviridae family, is best recognized as the causative agent of poliomyelitis (for review, see Mueller et al 2005). Following oral entry, it replicates in the gastrointestinal tract as is characteristic of enteroviruses.…”

mentioning

confidence: 99%

Inhibition of U snRNP assembly by a virus-encoded proteinase

Almstead¹,

Sarnow²

2007

Genes Dev.

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It has been proposed that defects in the assembly of spliceosomal uridine-rich small nuclear ribonucleoprotein (U snRNP) complexes could account for the death of motor neurons in spinal muscular atrophy (SMA). We discovered that infection of cultured cells with poliovirus results in the specific cleavage of the host factor Gemin3 by a virus-encoded proteinase, 2A pro . Gemin3 is a component of the macromolecular SMN complex that mediates assembly of U snRNP complexes by aiding the heptameric oligomerization of Sm proteins onto U snRNAs. Using in vitro Sm core assembly assays, we found that lowering the intracellular amounts of Gemin3 by either poliovirus infection or small interfering RNA (siRNA)-mediated knockdown of Gemin3 resulted in reduced assembly of U snRNPs. Immunofluorescence analyses revealed a specific redistribution of Sm proteins from the nucleoplasm to the cytoplasmic periphery of the nucleus in poliovirus-infected cells. We propose that defects in U snRNP assembly may be shared features of SMA and poliomyelitis.[Keywords: snRNP assembly; picornaviral proteinases; Gemins] Supplemental material is available at http://www.genesdev.org.

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Poliovirus and poliomyelitis: A tale of guts, brains, and an accidental event

Cited by 115 publications

References 171 publications

Evidence for emergence of diverse polioviruses from C-cluster coxsackie A viruses and implications for global poliovirus eradication

Evidence for emergence of diverse polioviruses from C-cluster coxsackie A viruses and implications for global poliovirus eradication

Crystal structure of CD155 and electron microscopic studies of its complexes with polioviruses

Inhibition of U snRNP assembly by a virus-encoded proteinase

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