ABSTRACT
Herpes simplex viruses 1 and 2 belong to the herpesviridae family. The viruses infect at mucosal surfaces and replicate within epithelial cells resulting in cell lysis. Virus also enters nerve terminals and is transported to the nerve-cell body, the site of latency of HSV. Activation of pattern recognition receptors leads to a potent innate immune response with production of interferons and other inflammatory cytokines. The adaptive immune response, particularly cytotoxic T cells, is important for maintaining HSV in latency, as T-cell immunodeficient patients are prone to frequent and aggressive reactivations. Infection at mucosal sites gives rise to orolabial or genital herpes. Spread to the cornea leads to herpetic keratitis. Herpes-simplex encephalitis is the most serious form of disease, with a high mortality in the absence of appropriate antiviral therapy. Diagnosis of active infection is by detection of viral genome from swabs or cerebrospinal fluid (CSF). Treatment is with aciclovir or derivatives thereof. This molecule is first phosphorylated by viral thymidine kinase and, in the triphosphate form, acts as a viral DNA polymerase inhibitor. There is currently no vaccine available for prophylaxis.
