Herpes stromal keratitis: erosion of ocular immune privilege by herpes simplex virus

被引:5
作者
Knickelbein, Jared E. [1 ]
Buela, Kristine-Ann [1 ]
Hendricks, Robert L. [1 ]
机构
[1] Univ Pittsburgh, Sch Med, Pittsburgh, PA 15213 USA
关键词
angiogenesis; CD4 T cells; herpes simplex virus; herpetic stromal keratitis; REGULATORY T-CELLS; ENDOTHELIAL GROWTH-FACTOR; HUMAN-IMMUNODEFICIENCY-VIRUS; HUMAN TRIGEMINAL GANGLIA; IMMUNOINFLAMMATORY LESIONS; CORNEAL INFECTION; MACROMOLECULAR-SYNTHESIS; HSV-1; REACTIVATION; MOLECULAR MIMICRY; LANGERHANS CELLS;
D O I
10.2217/FVL.10.57
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Herpes stromal keratitis (HSK) is a potentially blinding disease caused by herpes simplex virus corneal infection. Most cases of HSK are due to reactivation of the virus from latency leading to recurrent bouts of corneal inflammation and scarring with progressive loss of vision. Replicating virus is required to initiate HSK, and CD4 T cells of the adaptive immune system appear requisite for stromal inflammation. Corneal neovascularization also contributes significantly to HSK pathogenesis. Combination therapy with topical antivirals and corticosteroids is the current standard of care for human HSK. Future therapies will probably target angiogenesis with anti-VEGF agents to inhibit blood vessel growth into the normally avascular cornea, and target viral reactivation with therapeutic vaccination strategies to inhibit subsequent attacks.
引用
收藏
页码:699 / 708
页数:10
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