Abstract
Type I interferons are critical antiviral cytokines produced following herpes simplex virus type-1 (HSV-1) infection that act to inhibit viral spread. In the present study, we identify HSV-infected and adjacent uninfected corneal epithelial cells as the source of interferon-α. We also report mice deficient in the A1 chain of the type I IFN receptor (CD118 −/−) are extremely sensitive to ocular infection with low doses (100 PFU) of HSV-1 as seen by significantly elevated viral titers in the cornea compared to wild type (WT) controls. The enhanced susceptibility correlated with a loss of CD4 + and CD8 + T cell recruitment and aberrant chemokine production in the cornea despite mounting an adaptive immune response in the draining mandibular lymph node of CD118 −/− mice. Taken together, these results highlight the importance of IFN production in both the innate immune response as well as eliciting chemokine production required to facilitate adaptive immune cell trafficking.
Highlights
Herpes simplex virus type 1 (HSV-1) is a highly successful double-stranded DNA virus of which 60%90% of the adult human population is seropositive[1]
In order to define the site of type I IFN production relative to HSV-1, imaging analysis was conducted on the cornea following virus infection
Ectopic expression of IFN-α or IFN-β markedly suppresses HSV-1 replication and spread associated with a reduction in lytic gene expression . [39,40] indirect evidence suggests type I IFNs are active within the cornea[3], up to this point there are no studies that have described the location of IFN-α or IFN-β expression in response to HSV-1 infection
Summary
Herpes simplex virus type 1 (HSV-1) is a highly successful double-stranded DNA virus of which 60%90% of the adult human population is seropositive[1]. The lytic nature of the virus is driven by a sequential cascade of genes (referred to as lytic genes) expressed collectively over the course. Additional support includes P20 (No RR017703) and an unrestricted grant from Research to Prevent Blindness. Is an OUHSC Presbyterian Health Foundation Presidential Professor recipient. *Corresponding author: Daniel J.J. Carr, Ph.D., Department of Ophthalmology, DMEI #415, OUHSC, 608 Stanton L. The authors reported no conflict of interests
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