Figure 2
From: Resistance to HSV-1 infection in the epithelium resides with the novel innate sensor, IFI-16
Unaltered IFN response despite a loss of TLR signaling. (a) WT, Trif−/−, MyD88−/−, and CD118−/− mice were infected with 1,000 p.f.u. HSV-1 per eye. Forty-four to forty-eight hours pi, IFN production (green) was examined by confocal imaging relative to HSV-1 lesions (red) in the cornea (n=3–6 corneas per group). Images are representative of two independent experiments acquired using a × 400 objective with a digital zoom of × 10. White arrows depict uninfected IFN-α-expressing cells; yellow arrows depict HSV-infected IFN-α-expressing cells; white bars, 50 μm. (b) Mice were infected with HSV-1 and 24 or 48 h pi, corneas were evaluated for mRNA expression of ISG54 and OAS1a by RT-PCR. Bars are normalized to uninfected controls and represent 2 independent experiments of 2–4 corneas per group plotted as relative expression±s.e.m. HSV, herpes simplex virus; IFN, interferon; ISG54, IFN-stimulatory gene-54; pi, post infection; OAS1a, oligosynthetase 1a; RT-PCR, reverse transcriptase-PCR; TLR, Toll-like receptor; WT, wild type.
