The Effects of Chemokines on Acute Infections of Herpes Simplex Virus-1

Manjaap Sidhu and Patrick Stuart

Department of Ophthalmology and Visual Science, Washington University School of Medicine

 

Herpes simplex virus-1 of the eye, better know as ocular herpes, is the leading cause of blindness in the United States with approximately 500,000 cases every year. It is also estimated that about 3% of the 40,000 corneal transplants are a result of Herpetic Stromal Keratitus, a disease which causes the inflammation of the cornea because of the ocular HSV-1 infection. The infection of HSV-1 follows a recurrent model, which begins with an acute infection. Then HSV-1 becomes latent and becomes reactivated due to outside forces such as stress, psychological and emotional trauma, and UV light. During the acute infection, the severity of it is characterized by taking into account three aspects of the infection: corneal opacity (cloudiness of the cornea), neovascularization (creation of new blood vessels to the site of the infection), and blepharitis (swelling around the eye). For some time now, researchers have believed that the acute infection depends on the amount of neutrophils close to the virus. In addition to eating away at the virus, neutrophils end up damaging viable around the site of the infection. These neutrophils congregate because of chemokines and cause swelling, deteriorating the cornea. In order to see how the acute infection of ocular HSV-1 would differ with the lack of presence of neutrophils, we decided to infect normal control mice and CCL3 knock out mice, the specific chemokine which helps bring neutrophils to HSV-1. Every seven days after we first the mice, we examined the mice for the three aforementioned characteristics. Our results show us that there was no difference in the infection of both the mice. However, in order to make sure that there were no neutrophils in the CCL3KO mice, we are currently doing histological examination on the eyes.