Physico-chemical properties of swine vesicular disease virus]

Titration of SVDV on primary pig kidney cell cultures revealed a plating efficiency of less than or equal to 0,9 X 10(-3). Concentration and purification of the SVD-Virus propagated on pig kidney cell cultures were done by chloroform treatment, adsorption, differential- and density gradient centrifugation. The following physical parameters were found: SVDV is an isometrical RNA-virus having a diameter of 25,1 +/- 1,0 nm. It is resistent to the action of chloroform, ether and pH. The virus has a sedimentation coefficient of 156 +/- 3S and a bouyant density in CsCl of 1,33 +/- 0,01 g/ml. Within the family of picornaviruses the SVDV belongs to the subgroup of enteroviruses and can be distinguished from the foot-and-mouth disease virus by the difference in pH-sensitivity and bouyant density in CsCl.     

Experimental swine vesicular disease, pathology and immunofluorescence studies.

Two day old piglets were inoculated intravenously with 1 ml of swine vesicular disease virus UK-G 27-72 isolate. Using infectivity tests, immunofluorescent staining and gross and histopathological examination, pathogenesis of the infection was studied in tissue specimens collected daily from one through seven days postinoculation. Swine vesicular disease virus had a strong affinity for the epithelia of the tongue, snout, coronary band and lips, the myocardium and the lymphoid elements of the tonsil and the brain stem. The virus had the greatest affinity for the epithelium of the tongue. However, there was no evidence that the tongue was the initial replication site for swine vesicular disease virus. Prickle cells in the stratum spinosum appear to be the primary targets for the virus. The necrotic foci in the stratum spinosum appeared first, followed the next day by reticular degeneration and multilocular intraepidermal vesicular formation. In the digestive tract and most of the other visceral organs the short duration and sudden drop of the virus titres and the negative fluorescence and pathological findings suggest that these are not important sites for the replication of swine vesicular disease virus in this experiment. The virus was recovered from most of the central nervous tissue specimens. Although the piglets had significant central nervous system lesions, signs of impaired central nervous system function were not detected. However, subtle nervous signs could have been obscured by difficulties in locomotion resulting from severe lesions of the feet.     

Comparative studies on three isolates of Breda virus of calves

Three isolates of Breda virus of calves were compared morphologically and antigenically. The isolates demonstrated similar morphology and shared common antigens, as determined by enzyme-linked immunosorbent assay and immunoelectron microscopy. On the basis of results of the hemagglutination-inhibition test, enzyme-linked immunosorbent assay, and immunoelectron microscopy, the 3 isolates were further subdivided into 2 serotypes: serotype 1 (Breda virus 1) represented by the Iowa isolate 1; and serotype 2 (Breda virus 2), by the Ohio isolate and the Iowa isolate 2. The 3 isolates caused diarrhea in gnotobiotic calves.     

Pathogenesis of swine vesicular disease in pigs.

Pigs exposed to swine vesicular disease virus developed vesicular lesions by postinoculation day 2. Lesions first appeared on the coronary band and then on the dewclaw, tongue, snout, lips, and bulbs of the heels. The onset of viremia coincided with febrile response and the appearance of vesicles. Virus was isolated from the nasal discharge, esophageal-pharyngeal fluid, and feces as early as postinoculation day 1. Greater amounts of virus were isolated from samples collected during the first week of infection, and lesser amounts from samples collected during the second week. The appearance and the distribution of specific fluorescence in various tissues indicated that during the development of swine vesicular disease virus infection, the epithelial tissues were initially involved, followed by a generalized infection of lymph tissues, and subsequently, a primary viremia. Seroconversion was detectable as early as postinoculation day 4. A mild nonsuppurative meningoencephalomyelitis throughout the CNS was observed in both inoculated and contact-exposed pigs. The olfactory bulbs were most severely and were frequently affected, particularly in contact pigs. The most severe brain lesions were found in pigs 3 to 4 days after the onset of viremia; contact pigs showed more severe brain lesions than inoculated pigs. Microscopic changes were also found in the coronary band, snout, tongue, and heart.     

The pathogenesis of vesicular exanthema of swine virus and San Miguel sea lion virus in swine

Vesicular exanthema of swine virus type A48 or San Miguel sea lion virus type 2, when inoculated intradermally into swine, resulted in fluid-filled vesicles at the sites of inoculation in the snout, coronary band, and tongue. Pigs that developed vesicles also had fevers. Secondary vesicle formation varied, depending on virus serotype. Viremia was found in one pig infected with San Miguel sea lion virus five days after infection. Virus was recovered from nasal-oral passages for up to five days after infection in both groups of pigs and from the gastrointestinal and urinary tracts of pigs infected with San Miguel sea lion virus. Neutralizing antibodies began to increase three days after inoculation and reached peak titers in seven to ten days. In the absence of secondary bacterial infection, healing was well advanced by ten days after inoculation. Lesions usually were limited to nonhaired portions of the integument and tongue. Individual epithelial cells became infected when a break in the skin allowed virus access to susceptible epithelial cells from either exogenous or endogenous sources. Individual infected cells ruptured and adjacent cells were infected, resulting in the formation of multiple microvesicles. Centrifugal coalescence of microvesicles led to formation of grossly visible macrovesicles. Lesions rarely developed from viral contamination of intact hair follicles. A mild virus-induced encephalitis was seen in pigs infected with vesicular exanthema of swine virus, and virus was recovered from brain tissue of pigs infected with San Miguel sea lion virus.     

No serological evidence for the presence of swine vesicular disease virus in South Africa.

An indirect ELISA incorporating a protein A-peroxidase conjugate was developed for detecting antibodies to swine vesicular disease virus (SVDV) in pig sera. This test and a conventional virus neutralization test were found to be equally sensitive. A total of 2846 pig sera collected from various abattoirs in South Africa were tested using the indirect ELISA. No serological evidence of infection with SVDV in pigs in South Africa was found.     

猪水泡病病毒的分子生物学研究进展

猪水泡病(Swine vesicular d isease,SVD)是猪的一种高度接触性传染病,其临床表现以口鼻腔粘膜、蹄部等出现水泡或溃烂为特征,与猪口蹄疫极其相似,常以流行形式发病,对养猪业的危害较大,因而其防治问题极受重视,世界动物卫生组织(OIE)将其列为动物A类传染病。猪水泡病病毒(Swin     

9株猪瘟分离毒株的致病特性

采用9株临床表现强、中、低致病特点的猪瘟野毒分离株第3代细胞毒作为种毒,按3mL/头剂量分别注射猪瘟抗原及抗体阴性猪,再用上一代传代猪发病后的血毒作为下一代接毒用种毒接种试验猪1头或2头,或上一代传代猪发病后,同圈放入1头或2头试验猪进行同居感染.如此进行,GDGZ1/95、BJCY1/96和JL1/94传至8代;FJFQ1/99传至7代;HeBHH1/95、HeNBY1/96、BJTX3/96、GXBH1/98和HeNXH2/98传至3代.结果显示:上述分离株传至3～5代过程中均表现出毒力增强的趋势,从3～5代传代到8(7)代的过程中毒力进一步增强并保持稳定,且均超过了标准石门强毒株的发病特点.所有试验猪均出现较典型的猪瘟临床症状,解剖后均表现出不同程度的病理变化,死后或解剖后的各种脏器经HCFA检查均为强阳性,这种现象进一步证实了猪是猪瘟病毒的敏感动物,各毒株之间毒力没有明显差异.对其中7株分离株传代血毒部分代次E2基因主要区域进行序列分析,结果仅GDGZ1/95株从F1～F8代中的F6代有2个核苷酸的差异,引起1个相应氨基酸的变异,其余毒株的不同代次没有碱基发生变异,初步说明猪瘟病毒基因型表现相对的稳定性.     

猪水疱病病毒研究进展

猪水疱病是猪的一种急性传染病,与口蹄疫和水疱性口炎等水疱类疫病具有同等的重要性,被世界动物卫生组织(OIE)列为A类疾病。文章主要介绍了本病病原近年来在分子生物学方面的研究概况,主要包括RNA基因组的结构和功能的研究、结构蛋白功能的新发现、抗原结构的研究、病毒的诊断研究以及与柯萨奇病毒B5的关系等方面的研究现状。     

猪水泡病病毒5''和3''非编码区一级和二级结构分析

应用RT-PCR技术,用特异性引物扩增出SVDV HK’70 5’和3’非编码区,并将目的片段连接于pMD18-T载体,转化JM109感受态细胞。重组质粒经双酶切、PCR鉴定后测序。核苷酸序列比较结果表明,SVDV HK’70 5’非编码区与参考毒株SVDV J1’73、SVDV H/3’76核苷酸的差异率分别为1.6％、1.9％;SVDV HK’70 3-NCR与参考毒株SVDV J1’73、SVDV H/3’76核苷酸的差异率分别为1.0％、1.0％。应用计算机软件对3个SVDV毒株非编码区的二级结构进行预测,结果表明,SVDV HK’70 5’非编码IX-"级结构中存在13个结构域,SVDV J1’73 5’非编码区二级结构中存在9个结构域,SVDV H/3’76 5’非编码区二级结构中存在10个结构域;SVDV HK’70 3’非编码区二级结构中存在3个结构域,且与其他的两个毒株SVDV J1’73、SVDV H/3’76基本相同。