Labetoulle M, Kucera P, Ugolini G, Lafay F, Frau E, Offret H, Flamand A
Laboratoire de Génétique des Virus, Centre National de la Recherche Scientifique, Gif-sur Yvette, France.
Invest Ophthalmol Vis Sci. 2000 Aug;41(9):2600-6.
To identify possible neuronal pathways leading to herpetic ocular disease after primary oral infection in mice.
The SC16 strain of herpes simplex virus (HSV)-1 (10(6) plaque-forming units) was injected into the mucocutaneous border of the left upper lip. Animals were killed 2 to 10 days postinoculation (DPI). Spread of the virus in neural structures was studied by immunochemistry.
HSV1 first replicated at the site of inoculation and then at the superior cervical ganglion (at 2 DPI). The trigeminal ganglion and the facial nerve fibers were infected by 4 DPI. Infection of the ciliary body and iris occurred at 6 DPI, together with several brain stem nuclei belonging to the autonomic or sensory pathways. Between 8 and 10 DPI, the neural infection gradually cleared up, except for the ipsilateral sympathetic ganglion, and ipsilateral keratitis appeared in some animals.
The pattern of viral dissemination in this mouse model suggests that infection of iris and ciliary body results from transfer of virus in the superior cervical ganglion from sympathetic neurons innervating the lip to neighboring neurons innervating the anterior uvea. Later, zosteriform spread of virus from the trigeminal system may have contributed to the clinical and histologic findings.
确定小鼠原发性口腔感染后导致疱疹性眼病的可能神经通路。
将单纯疱疹病毒(HSV)-1的SC16株(10⁶ 蚀斑形成单位)注射到左上唇的黏膜皮肤交界处。在接种后2至10天处死动物。通过免疫化学研究病毒在神经结构中的传播。
HSV1首先在接种部位复制,然后在颈上神经节(接种后2天)复制。三叉神经节和面神经纤维在接种后4天被感染。睫状体和虹膜在接种后6天被感染,同时一些属于自主神经或感觉通路的脑干核也被感染。在接种后8至10天,除同侧交感神经节外,神经感染逐渐消退,一些动物出现同侧角膜炎。
该小鼠模型中病毒传播模式表明,虹膜和睫状体感染是由于颈上神经节中病毒从支配唇部的交感神经元转移到支配眼前葡萄膜的相邻神经元所致。后来,病毒从三叉神经系统的带状疱疹样传播可能导致了临床和组织学表现。