ABSTRACT
The three neurotropic herpesviruses vary in the clinical disorders they cause and in their molecular structure. However, they share several features that govern the biology of their infection in the human nervous system: (1) The primary infection involves the mucocutaneous surfaces, which serve as the portal of entry of the viral particles into the PNS; (2) the primary and the infectious recurrent diseases caused by the same virus usually occur within the same cutaneous distribution; (3) under normal (i.e., immunocompetent) conditions, the reactivation infection usually does not spread beyond the anatomic distribution and the vicinity of a single PSG; (4) although primary infection usually takes place during the first two to three decades of life, reactivation may occur at any time in the patient’s life, sometimes at a very advanced age. These features can be grouped under a unifying hypothesis that is now the dogma in herpes virology [1,2]: Following primary infection, the virus gets access to axon endings within the mucocutaneous surfaces and is transported to the PSG. The viral genome is maintained within the PSG, which serve as a reservoir for viral nucleic acids. Latent herpetic infection is a lifelong state. Under certain circumstances the virus can reactivate and travel to regions innervated by the respective PSG, causing recurrent disease there.
