Buckley Alexandra, Montiel Nestor, Guo Baoqing, Kulshreshtha Vikas, van Geelen Albert, Hoang Hai, Rademacher Christopher, Yoon Kyoung-Jin, Lager Kelly
U.S. Department of Agriculture, Oak Ridge Institute for Science and Education and National Animal Disease Center, Ames, IA, USA.
Present address: U.S. Department of Agriculture, Avian Viruses Section, Diagnostic Virology Laboratory, National Veterinary Services Laboratories, Animal and Plant Health Inspection Service, Ames, IA, USA.
BMC Vet Res. 2018 Nov 20;14(1):352. doi: 10.1186/s12917-018-1693-8.
Senecavirus A, commonly known as Seneca Valley virus (SVV), is a picornavirus that has been infrequently associated with porcine idiopathic vesicular disease (PIVD). In late 2014 there were multiple PIVD outbreaks in several states in Brazil and samples from those cases tested positive for SVV. Beginning in July of 2015, multiple cases of PIVD were reported in the United States in which a genetically similar SVV was also detected. These events suggested SVV could induce vesicular disease, which was recently demonstrated with contemporary US isolates that produced mild disease in pigs. It was hypothesized that stressful conditions may exacerbate the expression of clinical disease and the following experiment was performed. Two groups of 9-week-old pigs were given an intranasal SVV challenge with one group receiving an immunosuppressive dose of dexamethasone prior to challenge. After challenge animals were observed for the development of clinical signs and serum and swabs were collected to study viral shedding and antibody production. In addition, pigs were euthanized 2, 4, 6, 8, and 12 days post inoculation (dpi) to demonstrate tissue distribution of virus during acute infection.
Vesicular disease was experimentally induced in both groups with the duration and magnitude of clinical signs similar between groups. During acute infection [0-14 days post infection (dpi)], SVV was detected by PCR in serum, nasal swabs, rectal swabs, various tissues, and in swabs from ruptured vesicles. From 15 to 30 dpi, virus was less consistently detected in nasal and rectal swabs, and absent from most serum samples. Virus neutralizing antibody was detected by 5 dpi and lasted until the end of the study.
Treatment with an immunosuppressive dose of dexamethasone did not drastically alter the clinical disease course of SVV in experimentally infected nursery aged swine. A greater understanding of SVV pathogenesis and factors that could exacerbate disease can help the swine industry with control and prevention strategies directed against this virus.
A 型塞内卡病毒,通常称为塞内卡山谷病毒(SVV),是一种小核糖核酸病毒,与猪特发性水疱病(PIVD)的关联并不常见。2014 年末,巴西多个州爆发了多起 PIVD,来自这些病例的样本检测出 SVV 呈阳性。从 2015 年 7 月开始,美国报告了多起 PIVD 病例,其中也检测到了基因相似的 SVV。这些事件表明 SVV 可能诱发水疱病,最近用当代美国分离株在猪身上引发轻度疾病的实验证实了这一点。据推测,应激条件可能会加剧临床疾病的表现,因此进行了以下实验。两组 9 周龄的猪接受鼻内 SVV 攻击,其中一组在攻击前接受免疫抑制剂量的地塞米松。攻击后观察动物临床症状的发展,并收集血清和拭子以研究病毒脱落和抗体产生。此外,在接种后 2、4、6、8 和 12 天(dpi)对猪实施安乐死,以证明急性感染期间病毒的组织分布。
两组均通过实验诱发了水疱病,两组临床症状的持续时间和严重程度相似。在急性感染期间[感染后 0 - 14 天(dpi)],通过 PCR 在血清、鼻拭子、直肠拭子、各种组织以及破裂水疱的拭子中检测到 SVV。从 15 到 30 dpi,在鼻拭子和直肠拭子中检测到病毒的情况不太一致,大多数血清样本中未检测到病毒。在 5 dpi 时检测到病毒中和抗体,并且一直持续到研究结束。
用免疫抑制剂量的地塞米松治疗并未显著改变实验感染的保育猪中 SVV 的临床病程。对 SVV 发病机制以及可能加剧疾病的因素有更深入的了解,有助于养猪业制定针对该病毒的控制和预防策略。