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[Histological and ultrastructural studies of experimental herpetic keratitis in the rabbit]
1Department of Ophthalmology, Ist Affiliated Hospital, China Medical University, Shenyang.
Objective:
In order to investigate the histological and ultrastructural changes at different post infection days in herpes simplex keratitis (HSK).
Methods:
The corneas of New Zealand white rabbit eyes experimentally infected with primary HSK were studied by light microscopy and electron microscopy. The histological and ultrastructural changes in the rabbit corneas at 3, 7, 14, 21, 60 post infection days were investigated by light microscopy with HE, Mallory dyes and electron microscopy.
Results:
Infiltration of corneas with inflammatory cells was found in rabbit eyes infected with HSK, polymorphonuclear leukocytes being predominant. Contact of inflammatory cells with fibroblast cells and corneal edema were seen in the stroma on acute post infection days 3 and 7. In severe cases inflammatory cells incarcerated in the endothelium. Only did two cases of the specimens present with herpes simplex virus type I granules in the acute stage under electron microscopy.
Conclusion:
The direct HSK-1 destruction together with immunopathogenetic injury caused by the body immune system may serve as the pathologic base of HSK. Decompensation of corneal endothelial function due to infiltration with inflammatory cells may be responsible for corneal edema.
Insights
Herpes simplex keratitis (HSK) causes corneal inflammation and edema due to direct viral damage and immune responses. Inflammatory cell infiltration, particularly polymorphonuclear leukocytes, is a key feature in HSK pathogenesis.
Area of Science:
- Ophthalmology
- Virology
- Immunology
Context:
- Herpes simplex keratitis (HSK) is a significant cause of corneal blindness worldwide.
- Understanding the temporal histological and ultrastructural changes is crucial for effective treatment strategies.
Purpose:
- To investigate the histological and ultrastructural changes in rabbit corneas at various post-infection days following experimental herpes simplex keratitis (HSK).
- To elucidate the cellular mechanisms underlying HSK progression and corneal pathology.
Summary:
- Light and electron microscopy revealed inflammatory cell infiltration, predominantly polymorphonuclear leukocytes, in HSK-infected rabbit corneas.
- Corneal edema and stromal fibroblast interaction with inflammatory cells were observed in acute stages (days 3-7).
- Herpes simplex virus type I granules were rarely detected, suggesting indirect immunopathogenetic mechanisms contribute significantly to HSK.
Impact:
- Findings suggest that combined direct viral injury and immunopathogenetic mechanisms drive HSK.
- Corneal endothelial dysfunction, resulting from inflammatory cell infiltration, is implicated in the development of corneal edema.
- This study provides a detailed cellular basis for HSK, aiding in the development of targeted therapies.