Investigative ophthalmology & visual science · 2026
A Murine Model of HSV-1-Induced Corneal Endotheliitis: Primary Infection, Latency, and Recurrence.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Sun Yu, Cao Dingwen, Meng Jiayu, Wang Liuli, Ma Li, Zhou Qingjun, Wei Chao, Xie Lixin
Аннотация
PURPOSE: HSV-induced corneal endotheliitis (HSV endotheliitis) is a sight-threatening ocular disease, with poor underlying its pathogenesis due to the lack of suitable animal models, we therefore aimed to develop a murine HSV endotheliitis model.
METHODS: Herpes simplex virus type 1 (HSV-1) was injected into the anterior chamber (AC) of C57BL/6 mice to establish primary and latent infection. Recurrence was induced at least 5 weeks post-infection via ultraviolet B (UVB) corneal exposure. Clinical manifestations were dynamically monitored. The histopathology and molecular changes were assessed using transmission electron microscopy, immunofluorescence (IF) staining, hematoxylin and eosin (H&E) staining and multiple cytokines and chemokines analysis. HSV-1 load in corneas and trigeminal ganglia (TG) was detected via plaque assay, quantitative real-time PCR and IF staining.
RESULTS: Compared with controls, the primary HSV-1-infected mice exhibited characteristic manifestations of viral endotheliitis, including corneal and iris edema, AC inflammation, keratic precipitates (KPs), elevated intraocular pressure, and corneal endothelial cell damage and loss. Early after infection, viral loads were elevated both in corneas and TGs. By day 28, however, a latency-associated transcript (LAT) in TGs increased markedly, while HSV-1 titers became undetectable, indicating viral latency. Following UVB corneal exposure, the recurrent mice showed significant stromal edema, increased KPs, extensive endothelial cell loss, and elevated viral loads, confirming the successful induction of recurrence.
CONCLUSIONS: We successfully established a murine model of primary infection, latency and recurrence of HSV endotheliitis, providing a reliable platform for investigating pathological mechanisms and potential treatments.
METHODS: Herpes simplex virus type 1 (HSV-1) was injected into the anterior chamber (AC) of C57BL/6 mice to establish primary and latent infection. Recurrence was induced at least 5 weeks post-infection via ultraviolet B (UVB) corneal exposure. Clinical manifestations were dynamically monitored. The histopathology and molecular changes were assessed using transmission electron microscopy, immunofluorescence (IF) staining, hematoxylin and eosin (H&E) staining and multiple cytokines and chemokines analysis. HSV-1 load in corneas and trigeminal ganglia (TG) was detected via plaque assay, quantitative real-time PCR and IF staining.
RESULTS: Compared with controls, the primary HSV-1-infected mice exhibited characteristic manifestations of viral endotheliitis, including corneal and iris edema, AC inflammation, keratic precipitates (KPs), elevated intraocular pressure, and corneal endothelial cell damage and loss. Early after infection, viral loads were elevated both in corneas and TGs. By day 28, however, a latency-associated transcript (LAT) in TGs increased markedly, while HSV-1 titers became undetectable, indicating viral latency. Following UVB corneal exposure, the recurrent mice showed significant stromal edema, increased KPs, extensive endothelial cell loss, and elevated viral loads, confirming the successful induction of recurrence.
CONCLUSIONS: We successfully established a murine model of primary infection, latency and recurrence of HSV endotheliitis, providing a reliable platform for investigating pathological mechanisms and potential treatments.