Abstract
Purpose :
The innate immune response activated by acute retinal necrosis, a rapidly progressive herpes virus infection (herpes simplex virus [HSV] -1 or -2, or varicella-zoster virus) of the retina, is poorly understood. We aimed to create an experimental mouse model of acute retinal necrosis in which the retina is directly infected with herpes virus and that mimicks human disease.
Methods :
Using both male and female C57Bl/6J mice between 6-8 weeks of age consisting of 2 experiments of 2-3 mice per group. Mice receiving subretinal HSV-1 were compared 1, 3, and 5 days post-infection to subretinal sterile saline controls. Histology, OCT, fundus imaging and viral plaque assays were evaluated. A student's t test was then used to compare the two groups with statistical significance defined as a p value less than 0.05.
Results :
Following subretinal injection of herpes simplex virus -1, retinal whitening insues and results in full thickness retinal necrosis with overlying vitreous inflammation on OCT, histology, fundus imaging within 3 days of infection and progressively expands in size (n = 2-5 mice / group consisting of 2 independent experiments) [FIGURE]. Viral load was then compared at 5 days post infection and was significantly elevated when compared to PBS controls (3.94±0.332 versus 0±0; p <0.01) [FIGURE].
Conclusions :
We have created a reproducible mouse model of acute retinal necrosis similar to human disease and in which replicating virus can be isolated from the retina. This model will help us better understand the innate immune response to HSV infection of the retina and could be utilized to better understand innate immunity to other bacterial, viral, or viral-vector pathogens.
This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.