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The porcine trophoblast cell line PTr2 is susceptible to porcine reproductive and respiratory syndrome virus-2 infection.
Suleman, M; Malgarin, C M; Detmer, S E; Harding, J C S; MacPhee, D J.
Afiliación
  • Suleman M; Department of Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK, Canada; Department of Microbiology, Faculty of Veterinary Sciences, University of Veterinary and Animal Sciences, Lahore, Pakistan.
  • Malgarin CM; Department of Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
  • Detmer SE; Department of Veterinary Pathology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
  • Harding JCS; Department of Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
  • MacPhee DJ; Department of Veterinary Biomedical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK, Canada. Electronic address: d.macphee@usask.ca.
Placenta ; 88: 44-51, 2019 12.
Article en En | MEDLINE | ID: mdl-31670096
INTRODUCTION: Porcine reproductive and respiratory syndrome virus-2 (PRRSV-2) breaches the maternal-fetal interface (MFI) to infect porcine fetuses, yet the exact mechanism(s) of transmission is not understood. The objective of this study was to determine the susceptibility of porcine trophoblast cell line (PTr2) to PRRSV-2 infection to understand the potential role of the trophoblast in viral transmission to fetuses in vivo. METHODS: PTr2 cells were exposed in vitro to PRRSV-2 and then subjected to immunofluorescence analysis (IF), flow cytometry (FCM), real-time quantitative PCR (RT-qPCR), transmission electron microscopy (TEM) and immunogold electron microscopy (IEM) to assess viral infection. The effects of PRRSV-2 on PTr2 cell cycle progression and apoptosis, as well as the ability of PTr2 cells to produce infectious viral particles were also examined. RESULTS: PRRSV-2 was readily detected in PTr2 cells by IF, FCM, RT-qPCR, TEM and IEM techniques. RT-qPCR and FCM results of a time course of infection of PTr2 cells indicated PRRSV-2 load decreased over time after initial infection up to 72 h. PRRSV-2 infection altered PTr2 cell cycle with a selective increase of cells within the G2/M phase and also induced apoptosis. TEM and IEM demonstrated PRRSV-2 within and on the surface of PTr2 cells and PRRSV-2 virions released from PTr2 cells infected naïve MARC-145 cells inducing cytopathic effects. DISCUSSION: Trophoblast cells are susceptible to PRRSV-2 infection and release live virions capable of inducing cytopathic effects in naïve cells. This suggests a possible mechanism by which PRRSV-2 can breach the MFI resulting in fetal infection and death.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Trofoblastos / Virus del Síndrome Respiratorio y Reproductivo Porcino / Interacciones Huésped-Patógeno Límite: Animals Idioma: En Revista: Placenta Año: 2019 Tipo del documento: Article País de afiliación: Pakistán Pais de publicación: Países Bajos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Trofoblastos / Virus del Síndrome Respiratorio y Reproductivo Porcino / Interacciones Huésped-Patógeno Límite: Animals Idioma: En Revista: Placenta Año: 2019 Tipo del documento: Article País de afiliación: Pakistán Pais de publicación: Países Bajos