Figure 6. Loss of MDA5 function results in increased replication of HRV in respiratory epithelial cells and fibroblasts. (A) HRV transcripts, normalized to father control at 48 h. Primary nasal epithelial cells from the patient, parents, and six normal healthy controls were infected with HRV-B14 (MOI: 1) as indicated. (B) HRV transcripts in maternal fibroblasts, gene-edited to have IFIH1 genotypes WT/- (2 clones), WT/K365E (1 clone), K365E/- (2 clones), −/− (3 clones), after infection with HRV-B14 (MOI: 1). (C) HRV transcripts in A549 cells previously transduced with empty vector (EV), WT, or K365E MDA5, at 72 h after infection with HRV-B14 (MOI:1). (D) Immunoblot showing MDA5 overexpression and comparable RIG-Iexpression in C. 10.5 µg of lysates were run per lane. Data show means ± SD from two (A), six (B), and five experiments (C). *, P < 0.05; ***, P < 0.001 by Kruskal-Wallis test; comparisons in B and C were nonsignificant.
Figure 6.

Loss of MDA5 function results in increased replication of HRV in respiratory epithelial cells and fibroblasts. (A) HRV transcripts, normalized to father control at 48 h. Primary nasal epithelial cells from the patient, parents, and six normal healthy controls were infected with HRV-B14 (MOI: 1) as indicated. (B) HRV transcripts in maternal fibroblasts, gene-edited to have IFIH1 genotypes WT/- (2 clones), WT/K365E (1 clone), K365E/- (2 clones), −/− (3 clones), after infection with HRV-B14 (MOI: 1). (C) HRV transcripts in A549 cells previously transduced with empty vector (EV), WT, or K365E MDA5, at 72 h after infection with HRV-B14 (MOI:1). (D) Immunoblot showing MDA5 overexpression and comparable RIG-Iexpression in C. 10.5 µg of lysates were run per lane. Data show means ± SD from two (A), six (B), and five experiments (C). *, P < 0.05; ***, P < 0.001 by Kruskal-Wallis test; comparisons in B and C were nonsignificant.

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