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At least 325 records · Page 18Linked to original sources
PubMed1995

[Study on animal models of immune mediate motoneuron disease].

Swine motoneurons (SMN) were isolated from fresh spinal cords of pigs. Homogenates of these SMN or fresh anterior horns of pigs (SAH) as immunogens were inoculated to guinea pigs or Lewis rats and Wistar rats respectively. The impairments of motion were observed in the immunized guinea pig four months after the fifth inoculation of SMN, in the immunized Lewis rats after the first or second inoculation of SAH and in the Wistar rat after the third inoculation of SAH respectively. Degeneration and loss of motoneurons in the spinal cords of these symptomatic animals were found histologically. Antibodies against motoneurons of guinea pig and rat can be detected in sera of these symptomatic animals with immunocytochemical method respectively. In control guinea pigs, Lewis rats and Wistar rats there were no symptom, and did not found degeneration of motoneurons in the spinal cords of these control animals. Antibodies against motoneurons can not be detected in the sera of these control animals. The results indicated immune mediate guinea pig or rat models for MND can be established with pure SMN or impure SMN as immunogens. It was shown the conservative homology between antigenic structures of lower motoneurons in pigs and guinea pigs or rats. The pathogenesis in immunized animals with SAH is faster than that in immunized animals with SMN at least in terms of the appearance of symptoms. The Lewis rats produced symptoms first and the incidence ratio of symptomatic animals in Lewis rats was the highest. The immunized Wistar rats produced symptoms a little bit slower.

Animals↗
PubMed1987

Embryo transfer as a means of controlling the transmission of viral infections. IX. The in vitro exposure of zona pellucida-intact porcine embryos to swine vesicular disease virus.

When zona pellucida-intact porcine embryos were exposed to 10(7) plaque-forming units (pfu)/ml of swine vesicular disease virus (SVDV) and then washed, infectious virus could be isolated from all of the embryos. Culturing the embryos for 24 or 48 h or treating the embryos with pronase, trypsin, or antiserum after virus exposure and washing reduced the number of embryos carrying virus and lessened the amount of virus on each of the embryos. None of the treatments, however, was capable of disinfecting every embryo.

Journal Article↗
PubMed2004

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

Heparan sulphate (HS) has been found to serve as receptor for initial cell binding of numerous viruses. Different glycosaminoglycans (GAGs), including heparin and HS, were analysed for their ability to bind swine vesicular disease virus (SVDV), a picornavirus with close homology to human coxsackie B5 virus. Binding of SVDV was established by heparin-affinity chromatography. In addition, infection of IB-RS-2 epithelial porcine cells was inhibited by treating the virus with soluble HS, heparin, and chondroitin sulphate B (CS-B), as well as by enzymic digestion of cell surface GAGs. Analysis of the infection course showed that SVDV uses cellular HS for its binding to the cell surface and that this interaction occurs during attachment of the virus, prior to its internalization into the cell. Sequence analysis of SVDV variants selected for their lack of sensitivity to heparin inhibition in vitro led to the identification of two residues (A2135V and I1266K) potentially involved in heparin/HS interaction. The location of these residues in a three-dimensional model shows that they are clustered in a well-exposed region of the capsid, providing a physical mechanism that could account for the heparin-binding phenotype.

Amino Acid Sequence↗
PubMed1976

[Participation of Aujeszky's disease virus in the respiratory diseases of swine].

Clinical, virologic and seroligic investigations on vaccinated and unvaccinated pigs fattened on two farms with a record of a stationary Aujeszky's disease infection were carried out. Aujeszky's virus was isolated from the lungs of all pigs and partially of other viscera of some of the animals. The serologic studies revealed the dynamics of the antibody titer reise which spoke of the development of an infectious process. The clinical signs observed along with the morphologic changes characteristic of pneumonia, coupled with the advancement of the Aujeszky's disease infection demonstrated that on stationary fattening pig farms Aujeszky's disease assumed the course of a respiratory affection. The discripancy between the results obtained with vaccinated and unvaccinated animals, which were negligible on one of the farms and considerable on the other, was due to variations in the intensity of the infection as well as to the level of passive immunity.

Animals↗
PubMed2001

Virulence of swine vesicular disease virus is determined at two amino acids in capsid protein VP1 and 2A protease.

To identify the genetic determinants of virulence for swine vesicular disease virus, a panel of recombinant and site-directed mutant viruses were constructed from cDNA clones of a virulent J1'73 strain and an avirulent H/3'76 strain. Initial studies mapped the genetic determinants of virulence to either or both of the two sites at nucleotide (nt) 2842, encoding VP1-132, and nt 3355, encoding 2A-20. To determine their relative importance with regard to virulence, viruses mutated at either of these two sites from the avirulent to the virulent genotype and vice versa were tested in pigs. Viruses, mutated at nt 2842 to the virulent genotype (vSVLS104MJ1) or mutated at nt 3355 to the virulent genotype (vSVLS201MJ1), slightly recovered virulence but were very weak compared with viruses with site-directed mutations at both sites (vSVLS104/201MJ1). On the other hand, viruses, mutated at nt 2842 to the avirulent genotype (vSVLS104M00) or mutated at nt 3355 to the avirulent genotype (vSVLS201M00), did not have attenuated virulence. Sequence analysis of viruses recovered from inoculated pigs revealed that reversion at nt 3355 to the virulent genotype occurred in pigs which had been inoculated with vSVLS201M00. These results suggested that both amino acids determined the virulent phenotype, but that the 2A-20 site might be the major determinant for virulence.

Animals↗
PubMed2005

More recent swine vesicular disease virus isolates retain binding to coxsackie-adenovirus receptor, but have lost the ability to bind human decay-accelerating factor (CD55).

Swine vesicular disease virus (SVDV) evolved from coxsackie B virus serotype 5 (CVB5) in the recent past, crossing the species barrier from humans to pigs. Here, SVDV isolates from early and recent outbreaks have been compared for their capacity to utilize the progenitor virus receptors coxsackie-adenovirus receptor (CAR) and decay-accelerating factor (DAF; CD55). Virus titre of CVB5 and SVDV isolates It'66 and UK'72 on human HeLa cells was reduced by pre-incubation with either anti-DAF or anti-CAR antibodies; however, recent SVDV isolates R1072, R1120 and SPA'93 did not infect HeLa cells lytically. CVB5 and SVDV infection of the pig cell line IB-RS-2 was inhibited completely by anti-CAR antibodies for all isolates, and no reduction was observed following pre-incubation of cells with anti-pig DAF antibodies. Expression of human DAF in the pig cell line IB-RS-2 enhanced the virus titre of early SVDV isolates by 25-fold, but had no effect on recent SVDV isolate titre. Binding of radiolabelled CVB5 to IB-RS-2 cells was increased seven- to eightfold by expression of human DAF and binding of early SVDV isolates was increased 1.2-1.3-fold, whereas no increase in binding by recent SVDV isolates was mediated by human DAF expression. Addition of soluble hDAF-Fc inhibited CVB5, but not SVDV, infection of pig cells. Pre-incubation of all viruses with soluble hCAR-Fc blocked infection of IB-RS-2 pig cells completely; titration of the amount of soluble hCAR-Fc required to block infection revealed that early isolate UK'72 was the least susceptible to inhibition, and the most recent isolate, SPA'93, was the most susceptible.

Amino Acid Sequence↗
PubMed1969

Glasser's disease of swine produced by the intracheal inoculation of haemophilus suis.

The intracheal inoculation of pigs with Haemophilus suis led to the production of Glasser's disease at every attempt without significant pulmonary involvement. Isolation of this organism from the experimental animals was possible only in the acute phase of the disease. The indirect fluorescent antibody technique when applied to frozen sections of tissues obtained from the experimentally infected pigs at autopsy, revealed a few rod forms but mostly "round bodies" of H. suis in animals from which the organism was isolated, and "round bodies" only in the pigs from which the organism was not isolated. Attention is drawn to the similarities between the lesions caused by H. suis and Mycoplasma hyorhinis, and to the confusion which may result therefrom. It is stressed that the laboratory diagnosis of these two diseases is complicated by the fact that both agents may not be isolated on the media commonly used in diagnostic laboratories. Both organisms necessitate the use of special media where the clinical and autopsy results indicate polyserositis and arthritis.

Animals↗