Lessons from the foot and mouth disease outbreak in the Netherlands in 2001

Pluimers, F. H.; Akkerman, A M; Wal, P. van der; Dekker, A.; Bianchi, Alessandro

doi:10.20506/rst.21.3.1371

Cited by 72 publications

(42 citation statements)

References 2 publications

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“…On 21 March FMD was confirmed in The Netherlands. The disease was introduced by calves that had become infected in a staging area in France where infected sheep from the United Kingdom were present (366). Soon after, the disease was detected in additional farms, and The Netherlands decided on suppressive ring vaccination, which implied that all of the vaccinated animals would be slaughtered.…”

Section: The 2001 United Kingdom Outbreak and Its Aftermathmentioning

confidence: 99%

“…The United Kingdom inquiries, as well as commissions in France and The Netherlands, indicated the need to coordinate new strategies on a regional basis within the European Union as well as at the international level through the OIE. In addition, public reaction, predominantly within The Netherlands, questioned the need for largescale slaughter of susceptible animals, particularly the slaughter of vaccinated animals that were healthy (366).…”

Section: The 2001 United Kingdom Outbreak and Its Aftermathmentioning

confidence: 99%

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Foot-and-Mouth Disease

2004

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Foot-and-mouth disease (FMD) is a highly contagious disease of cloven-hoofed animals. The disease was initially described in the 16th century and was the first animal pathogen identified as a virus. Recent FMD outbreaks in developed countries and their significant economic impact have increased the concern of governments worldwide. This review describes the reemergence of FMD in developed countries that had been disease free for many years and the effect that this has had on disease control strategies. The etiologic agent, FMD virus (FMDV), a member of the Picornaviridae family, is examined in detail at the genetic, structural, and biochemical levels and in terms of its antigenic diversity. The virus replication cycle, including virus-receptor interactions as well as unique aspects of virus translation and shutoff of host macromolecular synthesis, is discussed. This information has been the basis for the development of improved protocols to rapidly identify disease outbreaks, to differentiate vaccinated from infected animals, and to begin to identify and test novel vaccine candidates. Furthermore, this knowledge, coupled with the ability to manipulate FMDV genomes at the molecular level, has provided the framework for examination of disease pathogenesis and the development of a more complete understanding of the virus and host factors involved

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Section: The 2001 United Kingdom Outbreak and Its Aftermathmentioning

confidence: 99%

Section: The 2001 United Kingdom Outbreak and Its Aftermathmentioning

confidence: 99%

Foot-and-Mouth Disease

2004

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“…FMD is listed by the International Organization of Animal Health (OIE) as a reportable disease, and severe trading restrictions are imposed upon notification of an outbreak (2). Disease outbreaks in previously FMD-free countries are initially controlled by culling of infected and in-contact animals, restriction of susceptible animal movement, disinfection of infected premises, and occasionally vaccination with an inactivated whole-virus antigen preparation (3). In countries where the disease is enzootic, animals are prophylactically vaccinated.…”

Section: Foot-and-mouth Disease (Fmd) Ismentioning

confidence: 99%

Synonymous Deoptimization of Foot-and-Mouth Disease Virus Causes Attenuation In Vivo while Inducing a Strong Neutralizing Antibody Response

Segundo

Medina

Ramírez-Medina

et al. 2016

J Virol

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Codon bias deoptimization has been previously used to successfully attenuate human pathogens, including poliovirus, respiratory syncytial virus, and influenza virus. We have applied a similar technology to deoptimize the capsid-coding region (P1) of foot-andmouth disease virus (FMDV). Despite the introduction of 489 nucleotide changes (19%), synonymous deoptimization of the P1 region rendered a viable FMDV progeny. The resulting strain was stable and reached cell culture titers similar to those obtained for wild-type (WT) virus, but at reduced specific infectivity. Studies in mice showed that 100% of animals inoculated with the FMDV A12 P1 deoptimized mutant (A12-P1 deopt) survived, even when the animals were infected at doses 100 times higher than the dose required to cause death by WT virus. All mice inoculated with the A12-P1 deopt mutant developed a strong antibody response and were protected against subsequent lethal challenge with WT virus at 21 days postinoculation. Remarkably, the vaccine safety margin was at least 1,000-fold higher for A12-P1 deopt than for WT virus. Similar patterns of attenuation were observed in swine, in which animals inoculated with A12-P1 deopt virus did not develop clinical disease until doses reached 1,000 to 10,000 times the dose required to cause severe disease in 2 days with WT A12. Consistently, high levels of antibody titers were induced, even at the lowest dose tested. These results highlight the potential use of synonymous codon pair deoptimization as a strategy to safely attenuate FMDV and further develop live attenuated vaccine candidates to control such a feared livestock disease. Our work demonstrates that newly developed codon pair bias deoptimization technologies can be applied to FMD virus to obtain attenuated strains with potential for further development as novel live attenuated vaccine candidates that may rapidly control disease without reverting to virulence.

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“…Interestingly, the N17D mutation was located close to but not at the interpentamer interfaces. The mutants described here extend the panel of FMDV variants exhibiting different pH sensitivities and illustrate the adaptive flexibility of viral quasispecies to pH variations.Foot-and-mouth disease virus (FMDV) is the causative agent of a highly contagious disease of cloven-hoofed animals (23) that poses important restrictions for international trading (11,45,49,51). FMDV is the type species of the Aphthovirus genus within the family Picornaviridae (20).…”

mentioning

confidence: 99%

“…Foot-and-mouth disease virus (FMDV) is the causative agent of a highly contagious disease of cloven-hoofed animals (23) that poses important restrictions for international trading (11,45,49,51). FMDV is the type species of the Aphthovirus genus within the family Picornaviridae (20).…”

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confidence: 99%

A Single Amino Acid Substitution in the Capsid of Foot-and-Mouth Disease Virus Can Increase Acid Resistance

Martín-Acebes

Vázquez-Calvo

Rincón

et al. 2011

J Virol

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Foot-and-mouth disease virus (FMDV) particles lose infectivity due to their disassembly at pH values slightly below neutrality. This acid-dependent disassembly process is required for viral RNA release inside endosomes. To study the molecular determinants of viral resistance to acid-induced disassembly, six FMDV variants with increased resistance to acid inactivation were isolated. Infection by these mutants was more sensitive to drugs that raise the endosomal pH (NH 4 Cl and concanamycin A) than was infection by the parental C-S8c1 virus, confirming that the increase in acid resistance is related to a lower pH requirement for productive uncoating. Amino acid replacement N17D at the N terminus of VP1 capsid protein was found in all six mutants. This single substitution was shown to be responsible for increased acid resistance when introduced into an infectious FMDV clone. The increased resistance of this mutant against acid-induced inactivation was shown to be due to its increased resistance against capsid dissociation into pentameric subunits. Interestingly, the N17D mutation was located close to but not at the interpentamer interfaces. The mutants described here extend the panel of FMDV variants exhibiting different pH sensitivities and illustrate the adaptive flexibility of viral quasispecies to pH variations.Foot-and-mouth disease virus (FMDV) is the causative agent of a highly contagious disease of cloven-hoofed animals (23) that poses important restrictions for international trading (11,45,49,51). FMDV is the type species of the Aphthovirus genus within the family Picornaviridae (20). Its genome is composed of a single RNA molecule of positive polarity and about 8.5 kb in length. Like other RNA viruses, FMDV populations consist of complex and dynamic distributions of variants termed quasispecies (17) and exhibit a high potential for variation and adaptation, reflected in seven serotypes and multiple antigenic variants (18,50). FMDV RNA is protected by a capsid that comprises 60 copies of each of the four structural proteins (VP1 to VP4) arranged in an icosahedral lattice of 12 pentameric subunits, which constitute intermediates of capsid assembly and disassembly (56). After attachment to the host cell using a variety of receptors, such as different ␣ v ␤ integrins, heparan sulfate glycosaminoglycans (for some tissue culture-adapted variants), or other not-well-characterized molecules (2, 3, 5, 25-28, 46), FMDV particles are internalized by endocytosis mediated by clathrin (for viruses using integrin receptor) or caveolae (in the case of variants using heparan sulfate). In both cases, FMDV particles are delivered to early endosomes for capsid disassembly and viral genome release (7,29,33,43,44).FMDV particles display extreme acid lability, being inactivated at pH values slightly below neutrality (12,35,41,55). The pH sensitivity of FMDV is required for capsid disassembly triggered by acidification inside endosomes, allowing release of the RNA genome within infected cells (4, 9, 10). An acid-labile capsid is...

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Lessons from the foot and mouth disease outbreak in the Netherlands in 2001

Cited by 72 publications

References 2 publications

Foot-and-Mouth Disease

Foot-and-Mouth Disease

Synonymous Deoptimization of Foot-and-Mouth Disease Virus Causes Attenuation In Vivo while Inducing a Strong Neutralizing Antibody Response

A Single Amino Acid Substitution in the Capsid of Foot-and-Mouth Disease Virus Can Increase Acid Resistance

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