Isolation and Identification of Type F Bovine Enterovirus from Clinical Cattle with Diarrhoea

Figures

• 

  Figure 1. Isolation and identification of BEV HB19-1. CPE, plaque purification, electron microscopy, and growth curve of BEV HB19-1 in MDBK cells: (a) CPE caused by BEV HB19-1 in MDBK cells was characterised at 24 hpi; (b) plaques of impurified and purified BEV HB19-1 strain; (c) electron microscopy of purified BEV HB19-1 virions; (d) growth curve of BEV HB19-1 in MDBK cells.

• 

  Figure 2. Phylogenetic analyses of the BEV HB19-1 strain. Phylogenetic analyses were based on the amino acid sequences. Phylogenetic trees were constructed using the neighbour-joining method with 1000 bootstrap replicates in the MEGA 7.0 software. The scale bars indicate the amino acid or nucleotide substitutions at each site: (A) VP1 of the BEV HB19-1 strain; (B) the polyprotein of the BEV HB19-1 strain.

• 

  Figure 3. Replication kinetics of HB19-1-infected mice. Detection and quantification of the BEV HB19-1 strain in ICR mice. Heart, liver, spleen, lungs, kidneys, brain, intestines, and muscle tissues of the BEV HB19-1-infected mice were obtained in triplicate. The total cellular RNA was extracted from the tissues and then analysed by RT-qPCR. The data are expressed as mean ± SD of three samples. Error bars represent the SD from triplicate within an experiment.

• 

  Figure 4. Histopathology analysis of HB19-1-infected ICR mice after 3 days infection. Heart, liver, spleen, lungs, kidneys, brain, intestines, and muscle tissues of the BEV HB19-1-infected mice were obtained. At the indicated time points post-infection, the paraffin sections of tissues were stained with haematoxylin–eosin (HE) and observed under a light microscope. All observations were performed at 200× magnification. Black arrows indicate the typical lesion.

• 

  Figure 5. BHK-21 cells inoculated with tissues obtained from HB19-1-infected ICR mice showed many BEV-positive cells by IFA at 36 hpi.