Theories on Varicella Zoster Virus Reactivation Based on Shingles Patterns

Abstract

Herpes zoster, a disease also known as shingles or as zoster, infects the sensory nerve ganglion and the peripheral nerve and its branches, resulting in pain to the affected dermatomes. Infection results from reactivation of the varicella-zoster virus, the same virus which causes varicella, or chickenpox. The varicella-zoster virus usually causes chickenpox to its host at an early age and then withdraws to the dorsal root ganglia where it enters a latency stage. The virus may reemerge at any time and infect its host with shingles. As shingles is most common in ages 50 and above, it is assumed that cell-mediated immunity plays a role in suppressing the virus, and, therefore, a decline in this immunity allows the virus to reemerge from latency. Shingles also appears to be more common in temperate regions than in tropical regions, leading to a suggestion that certain genotypes of the varicella-zoster virus are more prone to reactivation than others. Decreased herpes zoster incidence in the African American population and the detection of increased presence of the ATA and GCC haplotypes in herpes zoster patients may point to a genetic predisposition to reactivation of varicella-zoster virus. Evidence of increased female shingles incidence has lead to numerous hypotheses, some of which may shed some light on the mechanism of varicella-zoster reactivation, a phenomenon which is still poorly understood.