Herpes simplex keratitis

The herpes simplex viruses (HSV) are responsible for a variety of infections of the central nervous system and mucocutaneous surfaces. Both subtypes, HSV-1 and HSV-2, are similar in structure. The viral core consists of a genome of linear, double-stranded DNA surrounded by a regular icosahedral protein capsid. The core and the protein shell are enveloped in an outer lipid-containing membrane. Humans are the only natural host and reservoir for the HSV virus. Viral entry occurs at mucous membranes or through compromised skin epithelium, allowing replication in host cells. Upon entry into sensory or autosomal nerve endings of the skin or mucous membranes, the viral capsid and nucleus progress by axonal transport to the nerve cell bodies. A unique feature of HSV infection is the ability of the viral genome to persist in a repressed state in the neuronal cell bodies of ganglia. In this state, known as latency, cell death does not occur and normal cellular activity continues, while a limited number of viral proteins are transcribed. At a later time, the viral genome may become reactivated, resuming fulminant replication. Upon subsequent release from the host neuron, the new virions can then reinvade the cells of mucosal surfaces.