In two independent experiments, the MARC-nsp11 cells at the S phase constituted 28.5%) as compared to 12.6% for MARC-145 cells), which was more than a 2-fold increase for nsp11-expressing cells indicating that MARC-nsp11 cells were accumulating at the S phase by 24 h.
It can be seen from Figure 3 that the replication ability of GFP-PRRSV, similar to its parental PRRSV, was higher in Marc-145 cells than that in PAMs, and the GFP-PRRSV replication is slower than that of its parental PRRSV in either Marc-145 cells or PAMs, indicating that the gfp gene insertion likely decreases PRRSV replication in the host cells.
Both deletion mutants were non-viable in MARC-145 cells and porcine alveolar macrophages, indicating that both genes are essential for virus replication.
As shown in Figure 2(c), about 1100 bp DNA fragment was amplified from GFP-PRRSV-infected Marc-145 cells, but not from PRRSV-infected cells, indicating that the GFP-PRRSV has been successfully constructed in this study.
Repair of each of these regions identified 5 genes as responsible for nearly all of the increased isobutanol tolerance in this strain: including acrA, marC; their data also indicated that acrB was inactivated in this strain.
As shown in Figure 3, MARC-2a and MARC-N cells had significantly increased levels of SEAP than MARC-145 cells, which indicate the NF- κB and AP-1 activation in these cells.
Taken together, these data indicate that MARC-2a cells are more resistant to programmed cell death than to parent MARC-145 cells or MARC-N cells.
This indicates that nsp11 in MARC-nsp11 cells was biologically active and retained the modulatory activity for IFN induction.
However, increasing ROS didn't inhibit PRRSV replication in MARC-145 cells (Fig. 3), which indicated that infection and replication of PRRSV was independent with ROS.
In Table 4, the QTL positions and the flanking marker loci for the Hohenheim maps are indicated together with the corresponding USDA MARC map positions.
