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Abnormal immune response of CCR5-deficient mice to ocular infection with herpes simplex virus type 1

¹ Department of Ophthalmology, University of Oklahoma Health Sciences Center, DMEI #415, 608 Stanton L. Young Blvd, Oklahoma City, OK 73104, USA
² Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, DMEI #415, 608 Stanton L. Young Blvd, Oklahoma City, OK 73104, USA
³ Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92037, USA
⁴ Protein Design Labs Inc., Fremont, CA 94555, USA

Correspondence
Daniel J. J. Carr
dan-carr{at}ouhsc.edu

Ocular herpes simplex virus type 1 (HSV-1) infection elicits a strong inflammatory response that is associated with production of the chemokines CCL3 and CCL5, which share a common receptor, CCR5. To gain insight into the role of these molecules in ocular immune responses, the corneas of wild-type (WT) and CCR5-deficient (CCR5–/–) mice were infected with HSV-1 and inflammatory parameters were measured. In the absence of CCR5, the early infiltration of neutrophils into the cornea was diminished. Associated with this aberrant leukocyte recruitment, neutrophils in CCR5–/– mice were restricted to the stroma, whereas in WT mice, these cells trafficked to the stroma and epithelial layers of the infected cornea. Virus titres and cytokine/chemokine levels in the infected tissue of these mice were similar for the first 5 days after infection. However, by day 7 post-infection, the CCR5–/– mice showed a significant elevation in the chemokines CCL2, CCL5, CXCL9 and CXCL10 in the trigeminal ganglion and brainstem, as well as a significant increase in virus burden. The increase in chemokine expression was associated with an increase in the infiltration of CD4 and/or CD8 T cells into the trigeminal ganglion and brainstem of CCR5–/– mice. Surprisingly, even though infected CCR5–/– mice were less efficient at controlling the progression of virus replication, there was no difference in mortality. These results suggest that, although CCR5 plays a role in regulating leukocyte trafficking and control of virus burden, compensatory mechanisms are involved in preventing mortality following HSV-1 infection.

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