Characterization of three antigenic particles of swine vesicular disease virus.
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Three distinct particles were isolated from cell culture harvests of swine vesicular disease virus (SVDV) by sucrose and CsCl gradient centrifugation. Virions (148S), RNA-free empty capsids (81S), and a third particle (49S) also free of RNA showed immune reactivity with SVDV antiserum. The 81S and 49S particles had polypeptides typical of naturally occurring empty capsids. Injection of purified antigens into guinea pigs produced antisera which distinguished empty capsids from virions on immunodiffusion; the 49S antigen appeared similar to virions. Antisera produced to freshly prepared virus antigen grown in brains of baby mice distinguished SVDV from the serologically related Coxsackie B-5 virus but did not distinguish the individual S particle antigens. Partly purified virus preparations degraded to empty capsids when incubated in guinea pig serum. The possible origin of empty capsids and 49S particles and their relationship to antigenicity of virus preparations are discussed. (+info)
Swine vesicular disease: pathways of infection.
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The pathways of infection in swine vesicular disease have been studied by (i) an estimation of the amounts of virus required to produce infection by different artificial inoculation procedures; (ii) the distribution and amounts of virus in various tissues of pigs killed at intervals after contact infection; (iii) an investigation of the susceptibility to virus infection of pig tissue explants. The results show that pigs can be infected by a number of pathways and that the skin, as the most susceptible tissue, is probably the most frequent route of infection. (+info)
Swine vesicular disease in Great Britain.
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The State Veterinary Service in Great Britain has encountered considerable difficulty in eradicating SVD. For the last four years confirmed outbreaks have been mainly confined to one region, linked directly to outbreaks in that region, or have occurred as isolated cases related to the feeding of swill. The surveillance effort to locate subclinical disease has far surpassed that of any other country. There is no doubt that the introduction of SVD into any country which adopts a stamping-out policy for FMD and does not vaccinate, could present similar problems to those experienced by Great Britain. (+info)
Complete nucleotide sequence of a coxsackie B5 virus and its relationship to swine vesicular disease virus.
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We report the first complete nucleotide sequence of the picornavirus coxsackievirus B5 (CB5), strain 1954/UK/85, an isolate from a case of hand-foot-and-mouth disease. We have compared the sequence with those of other coxsackie B viruses, coxsackievirus A9, poliovirus and swine vesicular disease virus (SVDV). The genes encoding the three major capsid proteins are most closely related to those of SVDV but the 5' and 3' noncoding regions and the P3 gene are more similar to the corresponding regions in the other coxsackie B viruses than to those of SVDV. These observations are considered in the light of the antigenic and biochemical relationships between SVDV and CB5. (+info)
Molecular epidemiology of recent outbreaks of swine vesicular disease: two genetically and antigenically distinct variants in Europe, 1987-94.
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Viruses from the recent epidemic of swine vesicular disease (SVD) in Europe have been isolated and characterized by antigenic and genetic methods to examine the likely epidemiological origins of the disease. Antigenic analysis was performed on 77 SVD viruses (SVDV) isolated in Europe between 1966 and 1994 using two panels of monoclonal antibodies (MAb) in a trapping ELISA. Genetic analysis of 33 of the SVD viruses by reverse transcription-polymerase chain-reaction (RT-PCR) amplification and nucleotide sequencing of the ID (VP1) coding region was also performed. Comparison of the nucleotide sequences with each other and with three other previously published SVDV sequences revealed four distinct groups which correlated exactly with the results of the pattern of reactivity with MAbs. The first group consisted solely of the earliest SVD virus isolated (ITL/1/66) while the second group comprised viruses present in Europe and Japan between 1972 and 1981. The third group consisted of viruses isolated from outbreaks of SVD in Italy between December 1988 and June 1992. Viruses isolated between 1987 and 1994 from Romania, the Netherlands, Italy and Spain formed a fourth group. The genetic and antigenic similarity of the most recent virus isolates from Western Europe to a virus isolated in Romania 5 years previously suggests that the possible origin of the recent epidemic of swine vesicular disease in Western Europe was in Eastern Europe. (+info)
Effects of quaternary ammonium compounds with 0.1% sodium hydroxide on swine vesicular disease virus.
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The effects of quaternary ammonium compounds (QACs) with sodium hydroxide on swine vesicular disease virus (SVDV), an enterovirus were studied. Didecyldimethylammonium chloride (DDAC) with 0.1% NaOH showed a stronger effect against SVDV than other QACs with 0.1% NaOH. The effect of DDAC with 0.1% NaOH was strong at 40 degrees C. DDAC was effective against SVDV at pH values around 11.0, but not in the distilled water control. The effect of DDAC with 0.1% NaOH was already observed at 1 min after mixing of the DDAC with SVDV. Observation under an electron microscopy revealed that the probable mechanism of inactivation of DDAC with 0.1% NaOH is as follows: The virus particles were partially destroyed by 0.1% NaOH. DDAC gathered these affected particles and formed a micelle, then SVDV lost its infectivity. From these results, QACs with 0.1% NaOH are considered to be very effective against SVDV representing enteroviruses. (+info)
General pathology of experimental swine vesicular disease.
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Twenty-four minimal disease pigs were inoculated intracerebrally, intravenously or intradermally with an English strain of swine vesicular disease virus. In the skin, snout, tongue and tonsil the main lesion was a full-thickness coagulative necrosis of the stratified squamous epithelium. In the renal pelvis, bladder, tonsillar crypts and the collecting ducts of salivary glands and pancreas, epithelial degeneration with the formation of periodic acid-Schiff-positive material were consistent features of this disease. Histopathological examination alone could not be relied upon to differentiate between well-established skin lesions caused by swine vesicular disease and foot and mouth disease. The relationship between vesicular disease and Coxsackie B5 is discussed briefly. (+info)
The persistence of swine vesicular disease virus infection in pigs.
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Two groups of pigs were infected with a recent Italian isolate of swine vesicular disease virus (SVDV). Blood, nasal swabs and faeces were collected for up to 6 months after exposure to infection and animals were killed at regular intervals to obtain tissues post-mortem. These samples were examined for virus by conventional means and for viral RNA (vRNA) by reverse transcription-nested polymerase chain reaction (RT-nPCR). Virus was identified intermittently from both clinically and subclinically infected animals in nasal swabs, faeces and tonsillar tissue by either virus isolation or RT-nPCR up to 63 days post infection (dpi). Between 63 and 119 dpi virus was not detected in the secretions, excretions or tissues of any pigs. Following mixing of the two groups of animals at 119 dpi, SVDV was again identified in faeces for up to 7 days suggesting that the stress of mixing reactivated the excretion of virus in pigs from which the agent could no longer be identified. Minor antigenic changes were identified between the parental virus and isolates recovered late in the course of infection. Altered antigenicity corresponded with deduced amino acid substitutions identified from differences in nucleotide sequence between early and late isolates. This investigation demonstrates that SVDV and vRNA can be present in pigs for considerably longer after exposure to infection than has previously been recognized and provides preliminary evidence for a carrier state in swine vesicular disease. (+info)