Molecular evolution of swine vesicular disease virus.

Zhang, Gang; Haydon, Daniel T.; Knowles, Nick J.; McCauley, John W.

doi:10.1099/0022-1317-80-3-639

Cited by 82 publications

(84 citation statements)

References 48 publications

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“…Swine vesicular disease virus (SVDV) is a picornavirus of the enterovirus genus that causes an emerging disease of pigs (SVD) whose symptoms are similar to those caused by FMDV (Nardelli et al, 1968). The comparison of the complete genome sequences of SVDV and coxsackie B5 viruses (CVB5) reveals a close relationship between these two viruses (Zhang et al, 1999). It has been demonstrated that SVDV is a subspecies of human CVB5 that arose as a result of an adaptation to swine.…”

Section: Introductionmentioning

confidence: 99%

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Heparan sulphate mediates swine vesicular disease virus attachment to the host cell

Escribano-Romero

Jiménez‐Clavero

Gomes

et al. 2004

Journal of General Virology

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Section: Introductionmentioning

confidence: 99%

“…It has been demonstrated that SVDV is a subspecies of human CVB5 that arose as a result of an adaptation to swine. The divergence from a common ancestor has been estimated by phylogenetic studies to have occurred between 1945 and 1965 (Zhang et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Heparan sulphate mediates swine vesicular disease virus attachment to the host cell

Escribano-Romero

Jiménez‐Clavero

Gomes

et al. 2004

Journal of General Virology

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“…2. Published VP1 substitution rates for coxsackievirus B5 (CVB5), echovirus 9 (E9), echovirus 11 (E11), echovirus 30 (E30), HAV, and HPeV were obtained via BEAST analyses similar to those used in this study (15,23,34,(46)(47)(48); those for EV71, FMDV-A, and FMDV-O were obtained via analyses performed in TipDate (58), a precursor to BEAST (29); and the remaining rates were estimated via linear regression (3,4,44,50,66,70,71). These mean rates of enterovirus VP1 evolution range from 3.40 ϫ 10 Ϫ3 to 1.19 ϫ 10 Ϫ2 nucleotide substitutions per site per year (ns/s/y), and mean VP1 rates for nonenteroviruses range from 9.76 ϫ 10 Ϫ4 to 2.79 ϫ 10 Ϫ3 ns/s/y.…”

mentioning

confidence: 99%

Genus-Specific Substitution Rate Variability among Picornaviruses

Hicks

Duffy

2011

J Virol

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Picornaviruses have some of the highest nucleotide substitution rates among viruses, but there have been no comparisons of evolutionary rates within this broad family. We combined our own Bayesian coalescent analyses of VP1 regions from four picornaviruses with 22 published VP1 rates to produce the first within-family meta-analysis of viral evolutionary rates. Similarly, we compared our rate estimates for the RNA polymerase 3D pol gene from five viruses to four published 3D pol rates. Both a structural and a nonstructural gene show that enteroviruses are evolving, on average, a half order of magnitude faster than members of other genera within the Picornaviridae family.Members of the Picornaviridae family are the most common cause of human viral infections in developed countries (28,39). Human picornaviruses produce symptoms ranging from mild respiratory illness to hemorrhagic conjunctivitis, myocarditis, acute flaccid paralysis, and neonatal organ failure (19,27,28,33,40,41). Veterinary picornaviruses, such as foot-and-mouth disease virus (FMDV), encephalomyocarditis virus (EMCV), and porcine teschovirus (PTV), can have devastating effects on livestock (5,8,21).Although picornaviruses such as poliovirus (PV) are known to evolve more rapidly than other viruses with single-stranded RNA (ssRNA) genomes (9, 29), little research has been conducted to investigate how they evolve more rapidly than other viruses with similarly error-prone RNA-dependent RNA polymerases (29, 57) or if certain picornaviruses evolve more rapidly than others. Understanding the evolutionary potentials and constraints of these important pathogens is imperative for the development of durable vaccines and effective treatment plans for individual pathogens (42). As even small, 3-fold differences in RNA virus mutation rates can have dramatic consequences, such as driving a population into lethal mutagenesis (7), similar differences in long-term evolutionary rates could indicate significantly dissimilar evolutionary potentials.While viral evolutionary rates were previously calculated only by linear regression, modern simulation software such as BEAST (11) allows for the estimation of more complex models of viral evolution. These Bayesian coalescent programs can produce both estimated mean rates of evolution and 95% credibility intervals (CIs) that provide a measure of the variability around mean rates. Instead of comparing single-point estimates, now nonoverlapping CIs provide the strongest evidence that genes or organisms are evolving at different rates (11). Many substitution rate estimates have been published for picornaviruses, especially for the antigenically significant VP1 gene, which encodes the most external of the picornavirus structural proteins and interacts with cellular receptors (37,49). Based on sequence availability in GenBank, four novel analyses were conducted, measuring the rate of evolution of the VP1 gene for two enteroviruses and producing the first rate estimates for the type species of the genera Cardiovirus and Teschoviru...

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“…It is spread by direct and indirect contact, as well as through infected feeds and contaminated environments. SVD is caused by the swine vesicular disease virus (SVDV) of the genus Enterovirus within the family Picornaviridae (15), antigenically closely related to Coxsackie B5 virus, a human enterovirus (33,34). It has been assumed that SVD may have arisen from the introduction of Coxsackie B5 into the pig population, but another mechanism for the antigenic similarity cannot be excluded, because sequence differences between Coxsackie B5 virus and SVDV are more extensive in the non-structural region compared to the structural part of the genome (33).…”

Section: Artykuł Przeglądowy Reviewmentioning

confidence: 99%

Occurrence and diagnosis of swine vesicular disease: past and present status

Niedbalski

Fitzner

2017

Medycyna Weterynaryjna

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The clinical resemblance of SVD to FMD highlights the need for its reliable identification and discrimination. Differentiation from FMD, though not possible clinically, is feasible if appropriate diagnostic tests are applied. Improvements in diagnostic techniques are making differential diagnosis of vesicular disease increasingly affordable, feasible and easy, and nowadays, portable devices are capable of a rapid and accurate differentiation of SVDV from FMDV infections on site. As these tests become economical and as competent laboratory services become more and more accessible, the restrictions originally imposed on SVD because of its similarity to FMD will no longer be justified. This, together with the fact that in recent years SVD has been predominantly asymptomatic, makes it necessary to rethink the measures currently in place for the control and diagnosis of SVD. Therefore, by the decision of OIE, the SVD chapter was removed from the Terrestrial Code in January 2015. Consequently, the European Commission (EC) informed the Pirbright Institute that the EU Reference Laboratory for SVD would no longer receive financial support. Moreover, the EC position is that notification requirements have ceased in January 2015.

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Molecular evolution of swine vesicular disease virus.

Cited by 82 publications

References 48 publications

Heparan sulphate mediates swine vesicular disease virus attachment to the host cell

Heparan sulphate mediates swine vesicular disease virus attachment to the host cell

Genus-Specific Substitution Rate Variability among Picornaviruses

Occurrence and diagnosis of swine vesicular disease: past and present status

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