Herpetic Keratitis in Humans: Interaction between Virus and Host

Our first knowledge of human herpes can be traced back to the ancient Greeks, who coined the phrase: ‘herpes’. Hippocrates used this term to describe lesions that appeared to creep or crawl along the skin. The virus that causes this condition, herpes simplex virus (HSV), has been described in more detail over the past 3 decades. The spectrum of herpetic disease continues to expand. Nowadays, the structure of this virus is well documented. Herpesviruses are linear double-stranded DNA viruses, consisting of an envelope, a tegument, a nucleocapsid, and a core. The size of herpesvirus virions varies from 125-260 nm, and the shape varies from spherical to pleomorphic. Virus-encoded glycoproteins, exhibited as spikes are embedded in the envelope, which wraps the capsid. Herpesviruses encode a large group of enzymes involved in nucleic acid metabolism, DNA synthesis, and assembling capsid into the cell nucleus. Virions are processed in the cytoplasm. Production of infectious virus accompanies the destruction of the infected cells. All herpesviruses are able to remain latent in the host. More than 100 different herpesviruses are known to infect vertebrates. Only 8 of them can infect humans: human herpesvirus 1 to 8 (HHV1-HHV8). They are classified into three subfamilies based on their biological properties and DNA sequence homology: alpha-, beta-, gamma-herpesvirinae.