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P. M. Stuart, T. L. Keadle, Jr.; CCL3 Protects Mice From Corneal Pathology During Recurrent HSV-1 Infection. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5518.
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Previous studies in primary murine models of herpetic stromal keratitis (HSK) have demonstrated a role for the CCL2 and CCL3 chemokines. In general these studies indicated that these two chemokines had opposite effects with CCL2 associated with less disease and CCL3 associated with increased disease. This study was undertaken to evaluate the role that CCL2 and CCL3 play in a recurrent model of HSK in mice.
We infected CCL2 gene targeted and CCL3 gene targeted mice along with C57BL/6 parental controls with the McKrae strain of HSV-1 in the presence of pooled human sera containing anti-HSV-1 antibody to allow the virus to establish latency in the trigeminal ganglia. Six weeks following infection mice were irradiated with UV-B to stimulate reactivation. Mice were then evaluated for corneal pathology, viral production, rate of reactivation, and cyokine production in the cornea and in the trigeminal ganglia.
These studies did not demonstrate a significant role for CCL2 except at very early time points. In contrast, mice deficient in CCL3 displayed significantly enhanced disease as compared to wild-type C57BL/6 controls. Viral titers and reactivation rates were not significantly different between these strains of mice.
These data indicate that CCL2 plays little or no role during recurrent HSK. However, unlike what has been reported for CCL3 during primary herpetic disease, CCL3 plays a protective role for the cornea following UV-B induced reactivation.
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