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. 2013 Apr 24;8(4):e61967. doi: 10.1371/journal.pone.0061967

Figure 5. Inhibition of PRRSV-mediated STAT1 phosphorylation by methylthioadenosine (MTA).

Figure 5

A. MTA treatment leads to blockage of VR-2385-induced STAT1 phosphorylation. MARC-145 cells were infected with VR-2385 and treated with MTA. The cells were harvested at 24 hpi for Western blotting with antibodies against pSTAT1-S727, STAT1, and tubulin. Relative levels of pSTAT1 in comparison to the mock-treated and uninfected cells are shown as folds below the images. B. PRRSV yield remains stable in the presence of MTA. The virus samples were titrated and the result is shown as log10 TCID50/ml. C. MTA treatment reduces PRRSV-induced expression of proinflammatory cytokine genes. MARC-145 cells were infected with VR-2385 and treated with MTA. The cells were harvested at 48 hpi for RNA isolation and RT-qPCR. “*” indicates significant differences (P<0.05) between MTA-treated and mock-treated cells. D. Cell viability assay of MTA-treated MARC-145 cells. The cells were subjected for the assay 24 h after treatment. Relative percentages in comparison with mock-treated cells are shown.