Abstract
Abstract: :
Purpose: Following primary infection, HSV–1 establishes latency in sensory neurons of its host for life. Recurrent infections are due to the reactivation of the latent virus. In rare events, an eye appearance of "dark pupils" is observed due to recurrent infections, but the reasons for this are unclear. An HSV–1 mutant virus was generated to investigate the cause of "dark pupils" observed in latently–infected rabbit eyes. Methods: Study rabbits (20/group) were topically inoculated with either the HSV–1 mutant or the wild type virus strain at 2 X 105 PFU/eye. 20 control rabbits were inoculated with culture media only. Rabbits surviving at least 30 days post infection (PI) were visually assessed daily by extermal, unaided examination, and the appearance of their eyes was recorded for 26 consecutive days. At 56 days PI, all rabbit eyes were enucleated, formalin–fixed, paraffin–embedded, and sectioned for H&E staining. Results: A high percentage (75%) of rabbit eyes infected with the mutant strain developed observable "dark pupils". Their histology revealed that the retina from these eyes was remarkably thin and consistently lost, as shown in the figure. Interestingly, very few infiltrating cells were observed and only a vesicular layer remained in these eyes. In contrast, the morphologies of the retina in control eyes and wild type infected eyes were grossly intact. Moreover, the density of photoreceptor layer appeared to be less and the vascular layer slightly thicker in wild type infected eyes than in control rabbit eyes. Conclusions: The appearance of dark pupils in rabbits infected with this HSV–1 mutant in latently–infected rabbits was due to loss of the retina, and the mechanisms involved are yet unclear. However, our HSV–1 mutant–infected rabbit model may provide a useful tool in the study of mechanisms related to diseases caused by retinal degeneration.
Keywords: herpes simplex virus • retinal degenerations: cell biology • retinal detachment