Welch Michael, Krueger Karen, Zhang Jianqiang, Neveau Megan, Piñeyro Pablo, Magstadt Drew, Main Rodger, Gauger Phillip
Department of Veterinary Diagnostic and Production Animal Medicine, Iowa State University, Ames, IA 50011, USA.
Vet Sci. 2022 Dec 28;10(1):18. doi: 10.3390/vetsci10010018.
Porcine parainfluenza virus 1 (PPIV1) is a newly characterized porcine respiratory virus. Recent experimental challenge studies in three-week-old nursery pigs failed to cause disease. However, it remains unclear how genetic differences contribute to viral pathogenesis. To characterize the pathogenesis of different PPIV1 isolates, three-week-old nursery pigs were challenged with either PPIV1 isolate USA/MN25890NS/2016 (MN16) or USA/IA84915LG/2017 (IA17). A human parainfluenza virus 1 (HPIV1) strain C35 ATCC VR-94™ was included to evaluate swine as a model for human parainfluenza. All viruses were successfully re-isolated from bronchoalveolar lavage fluid and detected by RT-qPCR at necropsy. Microscopic lung lesions were more severe in the IA17 group compared to the non-challenged negative control (Ctrl) group whereas differences were not found between the MN16 and Ctrl groups. Immunohistochemistry staining in respiratory samples showed a consistent trend of higher levels of PPIV1 signal in the IA17 group followed by the MN16 group, and no PPIV1 signal observed in the HPIV1 or Ctrl groups. This study suggests potential pathogenesis differences between PPIV1 isolates. Additionally, these results indicate that HPIV1 is capable of replicating in nursery pigs after experimental inoculation. However, clinical disease or gross lung lesions were not observed in any of the challenge groups.
猪副流感病毒1型(PPIV1)是一种新鉴定的猪呼吸道病毒。最近在3周龄保育猪中进行的实验性攻毒研究未能引发疾病。然而,基因差异如何影响病毒发病机制仍不清楚。为了阐明不同PPIV1分离株的发病机制,用PPIV1分离株美国/MN25890NS/2016(MN16)或美国/IA84915LG/2017(IA17)对3周龄保育猪进行攻毒。纳入一株人副流感病毒1型(HPIV1)C35 ATCC VR-94™毒株,以评估猪作为人副流感模型的情况。所有病毒均成功从支气管肺泡灌洗液中再次分离出来,并在尸检时通过RT-qPCR检测到。与未攻毒的阴性对照组(Ctrl)相比,IA17组的肺部微观病变更严重,而MN16组和Ctrl组之间未发现差异。呼吸道样本的免疫组织化学染色显示,IA17组的PPIV1信号水平高于MN16组,呈一致趋势,而在HPIV1组或Ctrl组中未观察到PPIV1信号。本研究提示PPIV1分离株之间可能存在发病机制差异。此外,这些结果表明,实验接种后HPIV1能够在保育猪中复制。然而,在任何攻毒组中均未观察到临床疾病或明显的肺部病变。