Fig. 4: LCMV-WE strain triggers robust pattern recognition receptor (PRR) activation.
From: Slow viral propagation during initial phase of infection leads to viral persistence in mice
GM-CSF induced BMDCs were infected with LCMV-WE, LCMV-Docile, or co-infected at a MOI of 1. a Whole-cell lysates from LCMV infected BMDCs were blotted for p-TBK1, total TBK1, p-IKKε, total IKKε, and loading control α-Tubulin (one representative blot of n = 4 is shown, uncropped blots scans in Supplementary Fig. 6). b p-TBK1, c p-IKKε quantification was analyzed by first normalizing to the corresponding loading control, followed by standardizing to the 3 h LCMV-WE infected BMDC group (n = 4). d Whole-cell lysates from infected BMDCs were blotted for RIG-I, MDA5, MAVS, and loading control α-Tubulin at the indicated timepoints post-infection (uncropped blots scans in Supplementary Fig. 8). e RIG-I (n = 4), f MDA5 (n = 4), g MAVS (n = 3) quantification was analyzed by first normalizing to loading control, followed by standardizing to the 3 h LCMV-WE infected BMDC group. h JAWSII immature DC cells were transfected with 100 ng of LCMV-WE or LCMV-Docile genomic RNA and 24 h post transfection, IFN-α levels were determined in the supernatant of transfected DC cells (n = 12). (Error bars show SEM, *p < 0.05, **p < 0.01, and ns indicates statistically not significant between the indicated groups).
