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An animal model of ocular herpes. Keratitis retinitis and cataract in the mouse.

机译:眼疱疹的动物模型。小鼠的角膜炎视网膜炎和白内障。

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摘要

Acute ocular infection followed both intracerebral and intranasal inoculation of herpes simplex type I virus (HSVI) in mice. Eye infections were a terminal complication of fatal encephalitis. After intracerebral inoculation HSVI spread directly along the optic nerves to infect the retina provoking a necrotizing retinitis. In contrast after intranasal inoculation, HSVI spread via the fifth cranial nerve to the anterior chamber of the eye producing keratitis and uveitis. Necrotizing retinitis was also produced by intracerebral inoculation of mice with a drug-resistant mutant HSVI known to have relatively low neurovirulence. These animals developed only mild encephalitis but this was associated with florid retinitis. The mice survived cerebral infection with the mutant virus and several weeks after initial inoculation cataracts were observed. There was no evidence, at any time, of virus infection of lens epithelium and cataracts appeared to be a non-specific consequence of retinal injury. It is suggested that these examples of murine ocular infection provide animal models for herpetic eye lesions in man and thus may elucidate the pathogenesis of herpetic keratitis, retinitis and cataract.
机译:在小鼠的脑内和鼻内接种I型单纯疱疹病毒(HSVI)后进行急性眼部感染。眼部感染是致命性脑炎的晚期并发症。脑内接种后,HSVI直接沿视神经传播,感染视网膜,引起坏死性视网膜炎。相比之下,鼻内接种后,HSVI通过第五颅神经扩散到眼睛的前房,从而引起角膜炎和葡萄膜炎。通过脑内接种已知具有相对较低神经毒力的抗药性突变体HSVI的小鼠,也可产生坏死性视网膜炎。这些动物仅发展为轻度脑炎,但这与小花性视网膜炎有关。小鼠在脑部感染突变病毒后幸存下来,观察到最初接种白内障几周后。在任何时候都没有证据表明晶状体上皮被病毒感染,白内障似乎是视网膜损伤的非特异性结果。提示这些鼠眼感染的例子为人的疱疹性眼病提供了动物模型,因此可以阐明疱疹性角膜炎,视网膜炎和白内障的发病机理。

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