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  • ISSN 1674-8301
  • CN 32-1810/R
Volume 25 Issue 2
Feb.  2011
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Christopher D. Conrady, Heather Jones, Min Zheng, Daniel J.J. Carr. A functional type I interferon pathway drives resistance to cornea herpes simplex virus type 1 infection by recruitment of leukocytes[J]. The Journal of Biomedical Research, 2011, 25(2): 111-119. DOI: 10.1016/S1674-8301(11)60014-6
Citation: Christopher D. Conrady, Heather Jones, Min Zheng, Daniel J.J. Carr. A functional type I interferon pathway drives resistance to cornea herpes simplex virus type 1 infection by recruitment of leukocytes[J]. The Journal of Biomedical Research, 2011, 25(2): 111-119. DOI: 10.1016/S1674-8301(11)60014-6
shu

A functional type I interferon pathway drives resistance to cornea herpes simplex virus type 1 infection by recruitment of leukocytes

  • 1.

    Departments of Microbiology, Immunology,The University of Oklahoma Health Science Center, Oklahoma City, OK 73104, USA

  • 2.

    Ophthalmology, The University of Oklahoma Health Science Center, Oklahoma City, OK 73104, USA

  • 3.

    Departments of Microbiology, Immunology, and Ophthalmology, The University of Oklahoma Health Science Center, Oklahoma City, OK 73104, USA

Funds: 

This work was supported by USPHS grant (No. AI053108) to Daniel J.J. Carr. Additional support includes P20 (No. RR017703) and an unre-stricted grant from Research to Prevent Blindness. Daniel J.J. Carr. is an OUHSC Presbyterian Health Foundation President

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    • 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 susceptibil-ity 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.
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