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B.J. Reiser, G.–C. Perng; A Herpes Simplex Virus–Type 1 Antigen Detected in Latently–infected Rabbit Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2798.
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Following a primary infection, human simplex virus type 1 (HSV–1) establishes latency in sensory neurons of its host for life. Reactivation of the latent virus causes recurrent infections which may lead to a loss of retinal architecture in study animals. While HSV has been suggested to play a role in the development of acute retinal necrosis (ARN), its pathogenesis has been unclear due to two reasons: ARN is rare and no specific viral antigens or peptides have been identified. The purpose of this study was to identify any viral antigen or peptide in latently infected rabbit eyes.
Study rabbits (20/group) were topically inoculated with either an HSV–1 mutant or the wild type virus strains at 2 X 105 PFU/eye. 5 control rabbits were inoculated with culture media only. Rabbits surviving at least 30 days post infection (PI) were visually assessed daily by external, 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 and immunohistochemical studies.
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. In contrast, the morphologies of the retina in control eyes and wild type infected eyes were grossly intact. Using immunohistochemical studies, we observed that in one of the mutant–infected rabbit eyes with a preserved retinal architecture, an HSV antigen was detected in the inner and outer plexiform layers (Figure 1).
The identification of an HSV antigen suggests a relationship of HSV–1 to the loss in retinal architecture. This study further suggests that detection may be antigen–specific and a matter of timing.
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