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G.–C. Perng, B.S. Drolet, K.R. Mott, A.M. Lippa, S.L. Wechsler; Glycoprotein C of Herpes Simplex Virus Type 1 Is Required to Cause Corneal Disease at Low Infectious Doses In Intact Rabbit Corneas . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1655.
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Purpose: To determine whether the viral glycoprotein C (gC) plays a role in the ability of herpes simplex virus type 1 (HSV–1) to cause corneal disease in rabbits. Methods: A gC deletion mutant (ΔgC) was constructed and then rescued back to wild type (wt) for use as a control. Rabbits were ocularly infected with each virus, with or without prior corneal scarification and corneal disease was compared. Results: At low infection doses of 2x103 and 2x104 PFU/eye, in unscarified cornea , ΔgC produced significantly less corneal disease than did wt virus (p=0.007 and 0.03 respectively). In contrast, the corneal disease induced by ΔgC was similar to that induced by the wt virus (p>0.60) in scarified cornea. At high infection dose (2x105 PFU/eye), corneal disease induced by ΔgC was similar in scarified and unscarified cornea and the severity of disease was similar to that seen in scarified eyes at the low dose ΔgC infections. Interestingly, although ΔgC induced corneal disease with or without corneal scarification at high infection doses, the severity of disease was significantly less than that induced by wt infection. At all infection doses, corneal disease induced by wt infection was similar in scarified and unscarified eyes. Conclusions:These results suggest that (1)at low infection doses, in unscarified corneas, gC is required for HSV–1 induced corneal disease; (2)corneal scarification prior to infection can circumvent the need for gC at low doses but at higher doses, gC is required for wild type levels of corneal disease even in scarified cornea.
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