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Fig. 1
The percentages of CSFV-infected cells in the parent cell line and cloned PK15 cells. A – mock-infected PK15 cells (negative control); B – high-permissive (clone 1A6); C – low-permissive (clone 3B1); D – infected parent PK15 cells; E – percentages of positively stained cells. The cells were infected with CSFV and stained with CSFV-specific monoclonal antibodies (400×). Five visual fields were randomly selected to be photographed in each group. The percentages of positively stained cells in the photos were counted and shown as mean ± SD. * P < 0.05, ** P < 0.01
Fig. 2
Growth curves of parent PK15, clone PK15-1A6, and PK15-3B1 cells. The cells were trypsinised and counted at 8, 12, 24, 36, and 48 h post seeding. The data represent the mean ± SD of three independent experiments performed. The differences between the number of parent cells and that of PK15-1A6 cells are shown above the squares. The differences between the number of parent cells and that of PK15-3B1 cells are shown below the triangles. * P < 0.05, ** P < 0.01
Fig. 3
Mean CSFV titres produced by the parent PK15, PK15-1A6, and PK15-3B1 cells. The replication abilities of CSFV in each type of PK15 cells (TCID50) were detected by the IPMA method. ** P < 0.01
Fig. 4
IPMA results demonstrating the replication abilities of CSFV in high- and low-permissive PK15 cells at different time points. Different cell lines were fixed at 6, 12, 18, 24, 36, and 48 h post CSFV infection and stained with CSFV-specific antibodies followed by HRP-conjugated secondary antibodies (400×)
Fig. 5
The synthesis of CSFV genome in parent PK15 cells and PK15-1A6 (HP) and PK15-3B1 (LP) cell lines. The genomic RNA extractions from infected cells were quantitated by RT-PCR (amplification of partial E2 gene). The copy numbers of CSFV were determined by referring to a standard curve. ** P < 0.01