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. 2017 Jan 26;47(3):351–360. doi: 10.1111/cea.12879

Figure 5.

Figure 5

Type I IFN receptor blockade and the effect of exogenous IFN treatment of CBMCs during RV16 infection. CBMCs were pretreated with anti‐IFNAR2 (1 μg/mL) or IgG2a isotype (1 μg/mL) prior to RV16 MOI 7.5 or UV‐RV16 MOI 7.5 exposure. Twenty‐four h post‐infection cell pellets were harvested for gene expression and viral RNA by RT‐qPCR and cell‐free supernatants were harvested for infectious virus particles by TCID 50 assay. (a) IFNB1 and IFNL1 mRNA expression. (b) RV16 copy number and TCID 50/mL. CBMCs were exposed to RV16 MOI 7.5 or UV‐RV16 MOI 7.5 in the presence or absence of IFN‐β (100 IU/mL) or IFN‐λ (100 IU/mL). (c) IFNB1 and IFNL1 mRNA expression. (d) RV16 copy number and TCID 50/mL. Results are % of control (RV16 alone) means ± SEM, n = 2–3. *P ≤ 0.05, **P ≤ 0.01 vs. control (n = 3). Anti‐IFNAR2, anti‐IFN‐α/βR 2 antibody; MOI, multiplicity of infection.