Anterior segment mechanisms of protection during herpes simplex virus 1 infection.
Anterior segment mechanisms of protection during herpes simplex virus 1 infection.
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DOI：
10.1007/s10384-010-0798-9
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发表时间：
2010-05
影响因子：
2.4
通讯作者：
Cathcart, Heather M.
中科院分区：
文献类型：
--
作者：
Atherton, Sally S.;Cathcart, Heather M.
Herpes simplex viruses (HSV) are linear double-stranded DNA viruses that are highly disseminated in nature and characterized by lifetime latency in their host; 1 they are also a leading cause of infectious corneal blindness in the United States 2 and a major cause of corneal opacity worldwide. One example is HSV-1, which causes herpes stromal keratitis (HSK), an infection of the corneal stroma that, if not appropriately treated, may result in vascularization and scarring that may eventually lead to blindness. 3 Herpesviruses may also cause visually devastating diseases in noncorneal sites, such as in acute retinal necrosis (ARN). 4, 5 While the clinical features of herpes ocular diseases have been described extensively, the pathogenesis of herpesvirus infection in humans is still poorly understood. For example, it is not known why patients with HSK who have HSV-1 in the anterior segment do not develop retinitis in the posterior segment, despite the absence of an anatomical barrier between the anterior and posterior segments. A similar phenomenon has been observed in a mouse model of ARN. 6 Following inoculation of HSV-1 (KOS strain) into the anterior chamber (AC) of one eye of a BALB/c mouse, the virus replicates in the anterior segment of the injected eye and then spreads via synaptically connected neurons through the central nervous system (CNS) to the optic nerve and retina of the uninoculated contralateral eye. Paradoxically, the retina of the injected eye is spared from destructive retinitis. Sequentially, the route and timing of the virus spread are as follows: anterior segment of the injected eye (day 0), ipsilateral ciliary ganglion (day 2), ipsilateral Edinger-Westphal nucleus (day 3), ipsilateral suprachiasmatic nucleus (day 5), and contralateral optic nerve and retina (day 7). 6–8 In an effort to discern the mechanisms involved in protection of the retina of the injected eye, previous studies have examined the roles of T cells, natural killer (NK) cells, and polymorphonuclear cells in preventing direct anteriorto-posterior transfer of virus in the mouse model of ARN. Although in T-cell-depleted mice, the virus infects the CNS and both optic nerves and bilateral infection of the retina is observed, there is no evidence of direct anterior-toposterior spread of the virus in the injected eye of these mice. 9–13 Neutrophils and NK cells have been implicated in protecting the ipsilateral retina from direct anterior-toposterior spread of HSV-1 after uniocular AC injection; however, the number of these cells peaks in the injected eye on postinjection (pi) day 4 or later. Additionally, the mechanisms by which these innate immune cells control virus spread in the injected eye have not been elucidated. 14–17 The goal of the studies described herein was to identify cells and cytokines involved in early protection (ie, before day 4) of the injected eye in the mouse model of ARN.
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影响因子：
5.4
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