Metcalf J F, Hamilton D S, Reichert R W
Infect Immun. 1979 Dec;26(3):1164-71. doi: 10.1128/iai.26.3.1164-1171.1979.
The inflammatory response to herpes simplex virus infection of the cornea was studied in athymic nude (nu/nu) and heterozygote (nu/+) BALB/c mice. Although athymic mice were highly susceptible to HSV infection and died 13 to 17 days after corneal inoculation, they failed to develop necrotizing keratitis of the cornea. Heterozygote mice survived the initial virual infection, but many of these mice developed necrotizing keratitis and permanent corneal scarring. Light and electron microscopy showed numerous inflammatory cells (polymorphonuclear leukocytes and lymphocytes) in the corneas of heterozygote mice, but not in the athymic mice. These studies suggest that the immune system plays a dual role in herpes simplex virus infection of the cornea: protection against dissemination of the virus and immunopathogenesis of necrotizing keratitis in the cornea.
在无胸腺裸鼠(nu/nu)和杂合子(nu/+)BALB/c小鼠中研究了对单纯疱疹病毒角膜感染的炎症反应。尽管无胸腺小鼠对单纯疱疹病毒感染高度敏感,在角膜接种后13至17天死亡,但它们并未发生角膜坏死性角膜炎。杂合子小鼠在初始病毒感染中存活下来,但其中许多小鼠发生了坏死性角膜炎和永久性角膜瘢痕形成。光镜和电镜检查显示,杂合子小鼠的角膜中有大量炎症细胞(多形核白细胞和淋巴细胞),而无胸腺小鼠的角膜中则没有。这些研究表明,免疫系统在单纯疱疹病毒角膜感染中起双重作用:防止病毒扩散以及角膜坏死性角膜炎的免疫发病机制。