The Experts below are selected from a list of 282 Experts worldwide ranked by ideXlab platform
T. David K. Brown - One of the best experts on this subject based on the ideXlab platform.
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Alpha2,6-linked sialic acid acts as a receptor for Feline Calicivirus.
The Journal of general virology, 2007Co-Authors: Amanda D. Stuart, T. David K. BrownAbstract:Feline Calicivirus (FCV) is a major causative agent of respiratory disease in cats. It is also one of the few cultivatable members of the family Caliciviridae. It has recently been reported that FCV binding is in part due to interaction with junction adhesion molecule-A. This report describes the characterization of additional receptor components for FCV. Chemical treatment of cells with sodium periodate showed that FCV recognized carbohydrate moieties on the surface of permissive cells. Enzymic treatment with Vibrio cholerae neuraminidase demonstrated that sialic acid was a major determinant of virus binding. Further characterization using linkage-specific lectins from Maackia amurensis and Sambucus nigra revealed that FCV recognized sialic acid with an alpha2,6 linkage. Using various proteases and metabolic inhibitors, it was shown that alpha2,6-linked sialic acid recognized by FCV is present on an N-linked glycoprotein.
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α2,6-Linked sialic acid acts as a receptor for Feline Calicivirus
Journal of General Virology, 2007Co-Authors: Amanda D. Stuart, T. David K. BrownAbstract:Feline Calicivirus (FCV) is a major causative agent of respiratory disease in cats. It is also one of the few cultivatable members of the family Caliciviridae. It has recently been reported that FCV binding is in part due to interaction with junction adhesion molecule-A. This report describes the characterization of additional receptor components for FCV. Chemical treatment of cells with sodium periodate showed that FCV recognized carbohydrate moieties on the surface of permissive cells. Enzymic treatment with Vibrio cholerae neuraminidase demonstrated that sialic acid was a major determinant of virus binding. Further characterization using linkage-specific lectins from Maackia amurensis and Sambucus nigra revealed that FCV recognized sialic acid with an α2,6 linkage. Using various proteases and metabolic inhibitors, it was shown that α2,6-linked sialic acid recognized by FCV is present on an N-linked glycoprotein.
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Entry of Feline Calicivirus is dependent on clathrin-mediated endocytosis and acidification in endosomes
Journal of virology, 2006Co-Authors: Amanda D. Stuart, T. David K. BrownAbstract:Feline Calicivirus is a major causative agent of respiratory disease in cats. It is also one of the few cultivatable members of Caliciviridae. We have examined the entry process of Feline Calicivirus (FCV). An earlier study demonstrated that acidification in endosomes may be required. We have confirmed this observation and expanded upon it, demonstrating, using drugs to inhibit the various endocytic pathways and dominant-negative mutants, that FCV infects cells via clathrin-mediated endocytosis. We have also observed that FCV permeabilizes cell membranes early during infection to allow the co-entry of toxins such as alpha-sarcin. Inhibitors of endosome acidification such as chloroquine and bafilomycin A1 blocked this permeabilization event, demonstrating that acidification is required for uncoating of the genome and access to the cytoplasm.
Sabah Bidawid - One of the best experts on this subject based on the ideXlab platform.
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Survival of Calicivirus in foods and on surfaces: experiments with Feline Calicivirus as a surrogate for norovirus.
Journal of Food Protection, 2007Co-Authors: Kirsten Mattison, Michael Abebe, J.m. Farber, K Karthikeyan, N Malik, Syed A Sattar, Sabah BidawidAbstract:Although there is a large body of evidence incriminating foods as vehicles in the transmission of norovirus, little is known about virus survival in foods and on surfaces. Feline Calicivirus was us...
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Survival of Calicivirus in foods and on surfaces: experiments with Feline Calicivirus as a surrogate for norovirus.
Journal of food protection, 2007Co-Authors: Kirsten Mattison, Michael Abebe, J.m. Farber, K Karthikeyan, N Malik, Syed A Sattar, Sabah BidawidAbstract:Although there is a large body of evidence incriminating foods as vehicles in the transmission of norovirus, little is known about virus survival in foods and on surfaces. Feline Calicivirus was used as a surrogate for norovirus to investigate its survival in representative foods of plant and animal origin and on metal surfaces. Known concentrations of Feline Calicivirus in a natural fecal suspension were deposited onto lettuce, strawberries, ham, or stainless steel and incubated for 7 days at refrigeration or room temperatures. Virus was recovered at 1-day intervals, and the titers of the virus were determined by plaque assay. Infectious virus was recoverable until day 7 from lettuce, ham, and stainless steel. Statistically higher titers of Feline Calicivirus (P < 0.05) were recovered from ham under all conditions than from lettuce, strawberries, or stainless steel. These data provide valuable information for epidemiological and monitoring purposes as well as for the development of food processing practices and appropriate strategies to inactivate norovirus and control its transmission via foods and surfaces.
Alan D Radford - One of the best experts on this subject based on the ideXlab platform.
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european molecular epidemiology and strain diversity of Feline Calicivirus
Veterinary Record, 2016Co-Authors: J Hou, Susan Dawson, Fernando Sanchezvizcaino, David Mcgahie, C Lesbros, Thibaut Almeras, D Howarth, V Ohara, Alan D RadfordAbstract:Feline Calicivirus (FCV) causes a variable syndrome of upper respiratory tract disease, mouth ulcers and lameness. A convenience-based prospective sample of oropharyngeal swabs (n=426) was obtained from five countries (France, Germany, Greece, Portugal and the UK). The prevalence of FCV by virus isolation was 22.2 per cent. Multivariable analysis found that animals presenting with lymphoplasmacytic gingivitis stomatitis complex were more likely to test positive for FCV infection. Furthermore, vaccinated cats up to 48 months of age were significantly less likely to be infected with FCV than unvaccinated animals of similar ages. Phylogenetic analysis based on consensus sequences for the immunodominant region of the capsid gene from 72 FCV isolates identified 46 strains. Thirteen of the 14 strains with more than one sequence were restricted to individual regions or sites in individual countries; the exception was a strain present in two sites close to each other in France. Four strains were present in more than one household. Five colonies, four of which were rescue shelters, had multiple strains within them. Polymerase sequence suggested possible rare recombination events. These locally, nationally and internationally diverse FCV populations maintain a continuous challenge to the control of FCV infection and disease.
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Feline Calicivirus infection. ABCD guidelines on prevention and management.
Journal of feline medicine and surgery, 2009Co-Authors: Alan D Radford, Diane Addie, Sándor Belák, Corine Boucraut-baralon, Herman Egberink, Tadeusz Frymus, Tim Gruffydd-jones, Katrin Hartmann, Margaret J Hosie, Albert LloretAbstract:Feline Calicivirus (FCV) is a highly variable virus. More severe, systemic forms of FCV infection have been observed recently. Sick, acutely infected or carrier cats shed FCV in oronasal and conjunctival secretions. Infection occurs mainly through direct contact. The main clinical signs are oral ulcers, upper respiratory signs and a high fever. Feline Calicivirus may be isolated from nearly all cats with chronic stomatitis or gingivitis. Cats with 'virulent systemic FCV disease' variably show pyrexia, cutaneous oedema, ulcerative lesions on the head and limbs, and jaundice. Mortality is high and the disease is more severe in adult cats. Diagnosis of FCV can be achieved by virus isolation or reverse-transcriptase PCR. Viral RNA can be detected in conjunctival and oral swabs, blood, skin scrapings or lung tissue using PCR. Positive PCR results should be interpreted with caution, as these may be a consequence of low-level shedding by persistently infected carriers. The diagnosis of virulent systemic FCV disease relies on clinical signs and isolation of the same strain from the blood of several diseased cats. Supportive therapy (including fluid therapy) and good nursing care are essential. Anorexic cats should be fed highly palatable, blended or warmed food. Mucolytic drugs (eg, bromhexine) or nebulisation with saline may offer relief. Broad-spectrum antibiotics may be administered to prevent secondary bacterial infections. Feline Calicivirus can persist in the environment for about 1 month and is resistant to many common disinfectants. Two injections, at 9 and 12 weeks of age, are recommended, followed by a first booster 1 year later. In high-risk situations, a third vaccination at 16 weeks is recommended. Boosters should be given every 3 years. However, cats in high-risk situations should be revaccinated annually. Cats that have recovered from caliciviral disease are probably not protected for life, particularly if infected with different strains. Vaccination of these cats is still recommended.
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The challenge for the next generation of Feline Calicivirus vaccines.
Veterinary microbiology, 2006Co-Authors: Alan D Radford, Karen P. Coyne, C. J. Porter, Susan Dawson, Rosalind M. GaskellAbstract:Feline Calicivirus (FCV) has been shown to evolve within individual cats and in the environment of colonies. This evolution and the diversity it creates has important clinical implications, not only for the disease in cats, but also for attempts to control disease by vaccination. Generally speaking, existing vaccines appear to be very effective at controlling the majority of clinical disease. However, some concerns remain including a failure to induce sterilising immunity, occasional vaccine breakdowns, and for live vaccines, occasional vaccine-induced disease. Key areas for future vaccine development include monitoring and broadening the cross-reactivity of vaccine immunity to field viruses, especially the recently evolved highly virulent strains, and attempting to reduce/eliminate field virus shedding by vaccinated cats.
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Recombination of Feline Calicivirus within an endemically infected cat colony
Journal of General Virology, 2006Co-Authors: Karen P. Coyne, F. C. Reed, C. J. Porter, Rosalind M. Gaskell, Susan Dawson, Alan D RadfordAbstract:To understand the evolution of the family Caliciviridae, the persistence of Feline Calicivirus (FCV) was studied within an endemically infected cat colony. Polymerase and capsid sequences were analysed for 34 FCV isolates obtained over a 4 year period. Initially, the colony was infected with one strain of virus, but a second distinct strain was later identified. Subsequently, the emergence of a recombinant virus was observed, containing elements of both of the strains circulating within the colony. The recombination event mapped close to the ORF1/ORF2 junction. This is consistent with recombination in other Caliciviruses, suggesting a common mechanism within this family. This is the first report of recombination within the genus Vesivirus in the family Caliciviridae and the first time that a recombination event has been observed where the parental strains have also been identified.
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Cessation of Feline Calicivirus shedding coincident with resolution of chronic gingivostomatitis in a cat.
The Journal of small animal practice, 2003Co-Authors: D. D. Addie, Alan D Radford, Philippa S. Yam, D. TaylorAbstract:Feline Calicivirus (FCV) shedding and oral bacterial flora were monitored over a period of 22 months in a case of Feline gingivostomatitis (FGS). The cat was treated daily with 50 mg thalidomide capsules by mouth, and 200 mg lactoferrin powder was applied directly to the lesions. Clinical signs began to resolve after 11 months when, in addition to treatment, the diet had been changed to an additive-free cat food supplemented with antioxidant vitamins A, D3 and E. Resolution of clinical signs of FGS coincided with the cessation of FCV shedding, and this is the first report documenting such an association. Which part of the treatment, if any, contributed to the cure requires further investigation.
Amanda D. Stuart - One of the best experts on this subject based on the ideXlab platform.
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Alpha2,6-linked sialic acid acts as a receptor for Feline Calicivirus.
The Journal of general virology, 2007Co-Authors: Amanda D. Stuart, T. David K. BrownAbstract:Feline Calicivirus (FCV) is a major causative agent of respiratory disease in cats. It is also one of the few cultivatable members of the family Caliciviridae. It has recently been reported that FCV binding is in part due to interaction with junction adhesion molecule-A. This report describes the characterization of additional receptor components for FCV. Chemical treatment of cells with sodium periodate showed that FCV recognized carbohydrate moieties on the surface of permissive cells. Enzymic treatment with Vibrio cholerae neuraminidase demonstrated that sialic acid was a major determinant of virus binding. Further characterization using linkage-specific lectins from Maackia amurensis and Sambucus nigra revealed that FCV recognized sialic acid with an alpha2,6 linkage. Using various proteases and metabolic inhibitors, it was shown that alpha2,6-linked sialic acid recognized by FCV is present on an N-linked glycoprotein.
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α2,6-Linked sialic acid acts as a receptor for Feline Calicivirus
Journal of General Virology, 2007Co-Authors: Amanda D. Stuart, T. David K. BrownAbstract:Feline Calicivirus (FCV) is a major causative agent of respiratory disease in cats. It is also one of the few cultivatable members of the family Caliciviridae. It has recently been reported that FCV binding is in part due to interaction with junction adhesion molecule-A. This report describes the characterization of additional receptor components for FCV. Chemical treatment of cells with sodium periodate showed that FCV recognized carbohydrate moieties on the surface of permissive cells. Enzymic treatment with Vibrio cholerae neuraminidase demonstrated that sialic acid was a major determinant of virus binding. Further characterization using linkage-specific lectins from Maackia amurensis and Sambucus nigra revealed that FCV recognized sialic acid with an α2,6 linkage. Using various proteases and metabolic inhibitors, it was shown that α2,6-linked sialic acid recognized by FCV is present on an N-linked glycoprotein.
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Entry of Feline Calicivirus is dependent on clathrin-mediated endocytosis and acidification in endosomes
Journal of virology, 2006Co-Authors: Amanda D. Stuart, T. David K. BrownAbstract:Feline Calicivirus is a major causative agent of respiratory disease in cats. It is also one of the few cultivatable members of Caliciviridae. We have examined the entry process of Feline Calicivirus (FCV). An earlier study demonstrated that acidification in endosomes may be required. We have confirmed this observation and expanded upon it, demonstrating, using drugs to inhibit the various endocytic pathways and dominant-negative mutants, that FCV infects cells via clathrin-mediated endocytosis. We have also observed that FCV permeabilizes cell membranes early during infection to allow the co-entry of toxins such as alpha-sarcin. Inhibitors of endosome acidification such as chloroquine and bafilomycin A1 blocked this permeabilization event, demonstrating that acidification is required for uncoating of the genome and access to the cytoplasm.
Kirsten Mattison - One of the best experts on this subject based on the ideXlab platform.
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Survival of Calicivirus in foods and on surfaces: experiments with Feline Calicivirus as a surrogate for norovirus.
Journal of Food Protection, 2007Co-Authors: Kirsten Mattison, Michael Abebe, J.m. Farber, K Karthikeyan, N Malik, Syed A Sattar, Sabah BidawidAbstract:Although there is a large body of evidence incriminating foods as vehicles in the transmission of norovirus, little is known about virus survival in foods and on surfaces. Feline Calicivirus was us...
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Survival of Calicivirus in foods and on surfaces: experiments with Feline Calicivirus as a surrogate for norovirus.
Journal of food protection, 2007Co-Authors: Kirsten Mattison, Michael Abebe, J.m. Farber, K Karthikeyan, N Malik, Syed A Sattar, Sabah BidawidAbstract:Although there is a large body of evidence incriminating foods as vehicles in the transmission of norovirus, little is known about virus survival in foods and on surfaces. Feline Calicivirus was used as a surrogate for norovirus to investigate its survival in representative foods of plant and animal origin and on metal surfaces. Known concentrations of Feline Calicivirus in a natural fecal suspension were deposited onto lettuce, strawberries, ham, or stainless steel and incubated for 7 days at refrigeration or room temperatures. Virus was recovered at 1-day intervals, and the titers of the virus were determined by plaque assay. Infectious virus was recoverable until day 7 from lettuce, ham, and stainless steel. Statistically higher titers of Feline Calicivirus (P < 0.05) were recovered from ham under all conditions than from lettuce, strawberries, or stainless steel. These data provide valuable information for epidemiological and monitoring purposes as well as for the development of food processing practices and appropriate strategies to inactivate norovirus and control its transmission via foods and surfaces.
