Herpes Zoster or Shingles represents reactivation and replicationn of Latent infection in:

Herpes zoster (shingles) is caused by the reactivation and multiplication (Replication) of the Varicella -zoster virus (VZV) in the dorsal root ganglion. Herpes zoster, is a localized disease characterized by unilateral radicular pain and a vesicular rash limited to the area of skin innervated by a single dorsal root or cranial sensory ganglion. Reactivation of Latent Varicella Zoster: Varicella Zoster Virus remains latent in sensory ganglia including dorsal root ganglia of the spinal cord (most frequently) and other ganglion including trigeminal ganglion and/or geniculate ganglion. Chicken Pox: Virus enters sensory nerve endings and travels in retrograde fashion to sensory ganglia where it remains latent. Reactivation/replication in dorsal root ganglion: Virus travels back from ganglia along sensory nerves to the peripheral nerves of sensory dermatomes causing &;shingles&; = Herpes Zoster/Shingles: Unilateral vesicular eruption within a dermatome associated with severe pain. (The dermatomes from T3 and L3 are most frequently involved) Reactivation/replication in Trigeminal Ganglion: Virus travels back from trigeminal ganglia, most often along first division of cranial nerve V causing Zoster Ophthalmicus. Other divisions may also be involved & lesions may appear on the face, in the mouth or on the tongue. = Herpes Zoster Ophthalmicus Reactivation/replication in geniculate ganglion: Virus travels back from the geniculate ganglion along the sensory distribution of facial nerve causing Herpes Zoster Oticus or the &;Ramsay Hunt Syndrome&; = Ramsay Hunt Syndrome: Pain and vesicles appear in the external auditary canal. Patients lose their sense of taste in anterior 2/3rd of the tongue and develop ipsilateral facial nerve palsy. Ref: Harrison, Jawetz Microbiology, Rubin&;s Pathology