Genetics, Pathogenesis and Evolution of Picornaviruses

Gromeier, Matthias; Wimmer, Eckard; Gorbalenya, Alexander E.

doi:10.1016/b978-012220360-2/50013-1

Cited by 66 publications

(68 citation statements)

References 235 publications

(321 reference statements)

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“…We have proposed that ancestral PV may have originated from C-CAVs (13). To analyze the relationships among these viruses in greater detail, we have performed a phylogenetic analysis of the HEV-Cs using Bayesian posterior probability trees (14) (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…In case of global PV eradication, worldwide cessation of OPV vaccination has been proposed (9) as a radical measure to target OPV as a new genetic base of PV evolution. However, if the vaccination is terminated, the world is destined to become free of anti-PV antibodies, and contemporary C-CAVs may provide a fertile ground for PV (re)emergence by mutation (13).…”

Section: Parent-specific Asymmetry Of Genetic Compatibility Is Evidenmentioning

confidence: 99%

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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: Resultsmentioning

confidence: 99%

Section: Parent-specific Asymmetry Of Genetic Compatibility Is Evidenmentioning

confidence: 99%

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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“…Mutations that confer resistance to guanidine, an inhibitor of viral RNA replication, are located in 2C [219] and a helicase domain is present in this polypeptide [181]. In poliovirus, 2B and 2C are involved in viral RNA synthesis (reviewed in [109,250]). The polypeptide 2C and its precursor 2BC are associated and induce cell membrane vesicle proliferation [29].…”

Section: Genomic Organisationmentioning

confidence: 99%

Foot-and-mouth disease virus: a long known virus, but a current threat

et al. 2001

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-Foot-and-mouth disease virus (FMDV) was the first animal virus identified. Since then, FMDV has become a model system in animal virology and a considerable amount of information on its structure, biology and vaccinology has been obtained. However, the disease that this virus produces (FMD) still constitutes one of the main animal health concerns. In this review, we have attempted to summarise the state of the knowledge in different basic and applied areas of FMDV research, with emphasis on those aspects relevant to the control of the disease. FMDV / structure / immunity / vaccine / variability / diagnosisRésumé -Le virus de la fièvre aphteuse : un virus connu de longue date, qui demeure une menace. Le virus de la fièvre aphteuse a été le premier virus animal identifié. Depuis lors, il est devenu un système modèle en virologie animale, et une quantité importante d'informations sur sa structure, sa biologie et sa vaccinologie a été obtenue. Cependant la maladie provoquée par ce virus constitue encore une inquiétude majeure en santé animale. Dans cette revue, nous avons tenté de résumer l'état des connaissances dans différents domaines de recherche, à la fois fondamentaux et appliqués, sur le virus de la fièvre aphteuse, en mettant l'accent sur les aspects relatifs au contrôle de la maladie. virus de la fièvre aphteuse / immunité / vaccin / variabilité / diagnostic

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“…If PV, a member of the genus Enterovirus of Picornaviridae, is an evolutionary descendant of C-cluster Coxsackie viruses (C-CAVs) (12), the evolution of PV nucleotide sequences was constrained as it adhered to the basic architecture of C-CAVs, its evolutionary parents (13). A second well-known restriction of sequence variability in ORFs is "codon bias" (14), the unequal use of synonymous codons.…”

mentioning

confidence: 99%

Limits of variation, specific infectivity, and genome packaging of massively recoded poliovirus genomes

Song¹,

Gorbatsevych²,

Liu³

et al. 2017

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

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Computer design and chemical synthesis generated viable variants of poliovirus type 1 (PV1), whose ORF (6,189 nucleotides) carried up to 1,297 "Max" mutations (excess of overrepresented synonymous codon pairs) or up to 2,104 "SD" mutations (randomly scrambled synonymous codons). "Min" variants (excess of underrepresented synonymous codon pairs) are nonviable except for P2 Min , a variant temperature-sensitive at 33 and 39.5 • C. Compared with WT PV1, P2 Min displayed a vastly reduced specific infectivity (si) (WT, 1 PFU/118 particles vs. P2 Min , 1 PFU/35,000 particles), a phenotype that will be discussed broadly. Si of haploid PV presents cellular infectivity of a single genotype. We performed a comprehensive analysis of sequence and structures of the PV genome to determine if evolutionary conserved cis-acting packaging signal(s) were preserved after recoding. We showed that conserved synonymous sites and/or local secondary structures that might play a role in determining packaging specificity do not survive codon pair recoding. This makes it unlikely that numerous "cryptic, poliovirus | genome recoding | packaging signal | specific infectivity T he capsid precursor P1 (881 amino acids) of type 1 poliovirus (PV), mapping to the N terminus of the polyprotein (PP) (Fig. 1A), can be encoded in 10 442 ways (1) due to the degenerate genetic code. The tiniest fraction of these possible sequences defines PV, the cause of poliomyelitis. PV occurs in three serotypes, of which the most neurovirulent type 1 Mahoney [PV1(M)], the main viral species analyzed in this study, was isolated in 1941 from pooled feces of three healthy children (2).Genome sequence (3, 4) and gene organization (3) of PV1(M) revealed highly complex structures in its 5'-terminal nontranslated region (5'-NTR), followed by a single ORF encoding the PP, followed by a complex 3'-heteropolymeric region and poly(A) tail (Fig. 1A) (5, 6). The PP (7) is an active molecule that cleaves itself into ∼29 polypeptides by two viral proteinases (2A pro and 3C pro /3CD pro ) and an enzyme-independent maturation cleavage (Fig. 1A) (5,6,8).Capsid domain P1 controls the identity of PV by determining virion structure (9), serotype identity (10), and interaction with the cellular receptor CD155 (10). Since PV replicates as quasispecies at an error rate of ∼10 −4 (11), the following questions arise: How conserved is its synonymous sequence given the astronomical number of alternative possibilities? What encoding could have coevolved that would be optimal to specify 881 capsid residues?If PV, a member of the genus Enterovirus of Picornaviridae, is an evolutionary descendant of C-cluster Coxsackie viruses (C-CAVs) (12), the evolution of PV nucleotide sequences was constrained as it adhered to the basic architecture of C-CAVs, its evolutionary parents (13). A second well-known restriction of sequence variability in ORFs is "codon bias" (14), the unequal use of synonymous codons. Encoding the PV1 P1 domain with an excess of "rarely used" (human) synonymous codons results in a ...

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Genetics, Pathogenesis and Evolution of Picornaviruses

Cited by 66 publications

References 235 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

Foot-and-mouth disease virus: a long known virus, but a current threat

Limits of variation, specific infectivity, and genome packaging of massively recoded poliovirus genomes

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