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S.S. Tuli, D.C. Bloom, A.S. Lewin, J. Liu, G.S. Schultz; Prevention of Ocular Herpes Using a Replication Defective Herpes Simplex Virus . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2617.
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Herpes simplex keratitis is the most common infectious cause of corneal blindness in developed nations. A large percentage of the population is infected with herpes simplex and, once infected, the virus remains latent in the nerve ganglia lifelong. It undergoes periodic reactivation resulting in corneal infection and scarring. Prevention of the initial infection by vaccination would be ideal but has been very elusive to date.
To evaluate the ability of a replication defective herpes simplex virus to prevent wild type herpes infection of the cornea and to determine the possible mechanisms of protection.
A replication defective herpes simplex type–1 (HSV–1) virus was injected by the intrastromal route into one cornea of New Zealand white rabbits. Four months later, 2 x 105 pfu of a wild type HSV–1 containing a lacZ reporter was topically applied to both corneas of the rabbits after scarification and blood was drawn for serology. Four days later, conjunctival swabs were taken and the corneas were harvested and stained for ß–galactoside activity.
The corneas previously injected with the vector showed a dramatic decrease in the number and extent of epithelial dendrites. In some cases, there was a complete absence of dendrites (bottom image). The contra lateral corneas, on the other hand, had extensive dendrites (top image). The dendrites were quantified using Sigma Scan Pro software. The difference in area infected was statistically significant by the paired t–test (P = 0.01). The serum antibody titre in these rabbits was very low (1:5 – 1:10 versus 1:100 for rabbits infected with the wild type virus) indicating a predominantly local immune response.
A replication defective herpes simplex virus confers local immunity to the cornea and has the potential to ‘vaccinate’ the cornea against herpes simplex infections. It is also a useful tool to study the pathophysiology of herpes infection and latency.
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