Abstract
Herpes Simplex Virus (HSV) is a double-stranded virus that affects the skin and mucous membranes. There has been a long-standing dogma stating that the virus remains dormant and is reactivated from the dorsal root ganglia. However, more recent studies have established that there is a secondary mode of viral reactivation from the epidermis itself. These two distinct reactivation patterns help explain why prophylactic antivirals do not consistently prevent herpes outbreaks.
Highlights
Herpes Simplex Virus (HSV) is a common disease that belongs to the Herpesviridae family and primarily affects the skin and mucous membranes
Current dogma states that recurrent clinical symptoms of herpes simplex virus are the result of the activation of latent viral genome within the dorsal root ganglia
The ‘skin trigger’ hypothesis [6] states that HSV periodically sheds into the epithelium, and a change in the resistance of the epithelium is what allows lesions to develop
Summary
Herpes Simplex Virus (HSV) is a common disease that belongs to the Herpesviridae family and primarily affects the skin and mucous membranes. After the primary HSV infection, the virus enters an extended dormant phase within the dorsal root ganglia, during which the patient does not show signs or symptoms of the disease [2]. Current dogma states that recurrent clinical symptoms of herpes simplex virus are the result of the activation of latent viral genome within the dorsal root ganglia. The virus is stimulated to induce replication and subsequent anterograde transport of the virus along the peripheral sensory nerve to the cutaneous or mucosal surface. This, in turn, results in the production of vesicles on skin and mucosal surfaces [2]
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