STING deficiency leads to increased innate immune signaling during WNV infection.
(A-B) (A) WNV detection in BMDM by RT-qPCR, (B) innate immune response gene expression in WNV-infected BMDM over an infection time course. Bone marrow was harvested and differentiated into BMDM with mMCSF for 7 days. Cells were infected and harvested at the indicated time-points. Mock infected cells harvested at 12hpi. n = 3 infectious replicates. Results were reproducibly significant in multiple studies. Calculated as linear fold change over WT Mock. Unpaired students t-test; p = 0.05*; p = 0.005**, p = 0.0005***. (C) Splenic WNV titers at D4 and D8 post infection (PFU/g detected by plaque assay). n = 3–4. Graphed as stacking points. Limit of detection indicated by dashed line. Unpaired students t-test; p = 0.05*. (D) In vivo innate immune profile in splenic and CNS tissues. RT-qPCR detection of innate immune genes in the spleen, spinal cord and brain regions (brain stem, cerebellum, sub-cortex). Columns indicate individual mice; rows the different tissues. Calculated as log (WNV) or linear (immune) fold change over GAPDH in WT Mock. Dark red indicates values outside of (above) set scale.