title: A Functional Type I Interferon Pathway Drives Resistance to Cornea Herpes Simplex Virus Type 1 Infection by Recruitment of Leukocytes.
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.
authors.affiliation: Departments of Microbiology, Immunology, The University of Oklahoma Health Science Center, Oklahoma City, Oklahoma, 73104, USA.
authors.forename: Christopher D
authors.initials: CD
authors.lastname: Conrady
authors.forename: Heather
authors.initials: H
authors.lastname: Jones
authors.forename: Min
authors.initials: M
authors.lastname: Zheng
authors.forename: Daniel J J
authors.initials: DJ
authors.lastname: Carr