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. 2014 Mar;88(5):2810–2820. doi: 10.1128/JVI.03205-13

FIG 2.

FIG 2

COX-1 is significantly upregulated by HP-PRRSV infection in PAMs. (A) Cells were inoculated with medium alone, HP-PRRSV strain JXnw06 (MOI, 2), or UV-inactivated HP-PRRSV JXnw06 (UV-JXnw06). COX-1 expression was analyzed using real-time PCR at 0, 4, 8, 12, 24, and 36 h postincubation. Results were normalized to those for cyclophilin and are shown as the fold induction compared to that for medium alone. (B) PAMs were infected with HP-PRRSV at an MOI of 0.25, 0.5, 1, or 2, and the level of COX-1 mRNA was analyzed at 24 hpi using real-time PCR; results were normalized to those for cyclophilin and are shown as the fold induction compared to that for medium alone. (C) COX-2 expression was analyzed as described for panel A. (D) COX-1 and COX-2 protein levels in PAMs infected with HP-PRRSV were analyzed using Western blotting at 0, 4, 8, 12, 24, and 36 hpi. β-Actin was set up as a loading control. (E) The levels of COX-1 and COX-2 expression in PAMs infected with HP-PRRSV (MOI, 2) were assessed by flow cytometry at 24 hpi. Levels of COX-1 and COX-2 expression are presented as the mean fluorescence intensity (MFI). Data are means ± SEMs from at least three independent experiments. Differences were evaluated by Student's t test (*, P < 0.05; **, P < 0.01; ns, not significant).