Herpetic eye disease is one of the most common infections that cause corneal blindness. The incidence of HSV keratitis is approximately 1.5 million, worldwide, including 40,000 new cases of related blindness each year [1-3]. The disease is caused by HSV, which is widely spread in the human population. About 90 percent of the population over the age of 50 is infected with HSV. Herpetic eye disease mostly affects the anterior segment and manifests as an epithelial or stromal keratitis, endotheliitis, and/or iritis.
HSV is a linear, double-stranded deoxyribonucleic acid (DNA) virus belonging to the Herpesviridae family. During the first episode of HSV-1 infection, the virus replicates in the corneal epithelium cells, which are vulnerable to the direct viral cytopathic effect. When the infection recurs, the corneal stroma is exposed. Due to an inflammatory response, the cornea becomes cloudy and cicatrized. Stromal tissue swelling and loss of integrity is influenced by inflammatory cell infiltration, which is detected in the cornea .
Corneal cell interaction with HSV causes an inflammatory cascade with anti-inflammatory cell infiltration, which is responsible not only for clearance of the virus but also determines corneal damage due to corneal opacification, neovascularization, and corneal nerve loss.
The virus enters the cell by fusing with the cell membrane. After the entrance, the synthesis of cytokines begins: cells involved in the immune response, such as natural killers (NK), dendritic cells (DC), neutrophils, macrophages and lymphocytes, are attracted to the site of inflammation. Corneal epithelial cells and plasma dendritic cells (pDC) express toll-like receptors, which detect virus DNA . Inflammatory cascade with anti-inflammatory cell infiltration is responsible not only for clearance of the virus but also determines corneal damage due to corneal opacification, neovascularization and corneal nerve loss .
DC are the most potent antigen presenting cells of the immune system to induce antiviral immune responses. They phagocytose viral particles and infected cells and deliver to the draining lymph nodes to generate an adaptive immune response . A decrease of DC in the cornea determines later NK, monocytes, and chemokines migration to the site of infection, resulting in delayed virus removal . LC are a population of DC that mediate antigen presentation. LC are discrete leukocyte population of professional, specialized antigen presenting cells (APCs) with an exceptional capacity for initiating T-lymphocyte responses and expression of major histocompatibility complex (MHC) class II antigens in the corneal epithelium [1-3].
In the acute phase of HSV keratitis LC are located at the level of the lower intermediate cells, basal cells, and sub-basal nerve plexus. During the active infection, a wide net with infiltration of LC can be found [7,8].
Corneal endothelium is a single layer of cells on the inner surface of the cornea. Endothelial cells (EC) form a monolayer located at the Descemet's membrane in the posterior cornea. It plays a significant role in maintaining visual function: controls cornea hydration and transfers nutrients and other molecules from the aqueous humour . As a result of aging, diseases, injury, or surgeries EC could be damaged and influence corneal blindness . The minimum density of corneal EC for normal functioning is thought to be around 500 cells/mm .
The main purpose of our study is to describe corneal morphological changes including LC and EC density in patients with herpetic eye disease and compare with data of contralateral, clinically unaffected eyes and control groups during acute phase of the disease and in 6 months. We compare the results not only with healthy controls, but also with patients, who previously have had herpes labialis.