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A. E. Buckner, C. O. Ekworomadu, S. Kaliappan, V. Lyzogubov, P. S. Bora, N. S. Bora; The Role of Complement in Herpes Stromal Keratitis. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2484. doi: https://doi.org/.
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Herpes simplex virus type 1 (HSV-1) infection in humans leads to a rapid induction of an innate immune response in the body that is spread from initial infection of the skin or mucosal surfaces. Infection can cause encephalitis, retinitis, and keratitis. Primary infection in the stromal layer of the cornea can cause herpes stromal keratitis (HSK), a common type of vision loss and blindness for adults in the United States. The complement system, a major component of innate immunity, functions as an early host response to viral infection. However, several viruses have evolved strategies to inhibit host defense mediated by complement. We propose to test our hypothesis that complement plays a key role in the development of herpes stromal keratitis.
BALB/c mice were infected with 1x 105 plaque forming units of HSV-1 and the animals were divided into two groups. Animals in one group received a daily injection of cobra venom factor to deplete the complement system of the host. Animals in the second group received a similar treatment with sterile phosphate buffered saline (PBS). Clinical examination and histological analysis were used to monitor the development and the severity of disease.
Histopathological analysis of the mouse eye showed that the corneal stroma was heavily infiltrated with inflammatory cells in PBS treated complement-sufficient animals. Most of the infiltrating cells were polymorphonuclear cells. Interestingly, the numbers of inflammatory cells differed significantly between complement-sufficient and complement-depleted mice.
The severity of HSV-1 induced stromal keratitis differed between complement-sufficient and complement-depleted animals suggesting a role for complement in the development of HSK.
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