Introduction

The varicella-zoster virus (VZV) causes two distinct diseases:varicella (i.e. “chickenpox”) and herpes zoster (i.e. “shingles”) [1].Chickenpox, which primarily occurs during childhood, causes anitchy rash for about a week. Complications from chickenpox are relatively infrequent and include pneumonia, bacterial surinfection and encephalitis. Shingles predominantly occurs at older age. It isthe result of a reactivation of VZV, which after chickenpox remains latently present in neural ganglia. This reemergence of the viruscan be assumed to be a consequence of waning cellular immunity.Shingles is characterized by a painful rash on the body and causes on average a more severe and longer-lasting loss of quality of lifethan chickenpox.

 Conclusion

Evidence increasingly suggests that chickenpox vaccination of children risks redistributing health risks toward older generations.  Varicella-ShinglesStudy

Dr. Gary Goldman:  The reason why we are getting SHINGLES

The only reason that “children who get the chickenpox vaccine APPEAR to have a much lower risk of shingles” is that the live vaccine has provided these children with a recent boost to their immunity. However, the vaccine-strain of varicella zoster virus (VZV)–also known as the Oka strain–is genetically different from the wild-type U.S. strain. When a vaccinated child is exposed to an adult with shingles or a child with wild-type varicella, if the strains are sufficiently heterologous, the vaccinated child will break out in chickenpox. It is also possible for the weakened vaccine-strain to revert to a more virulent strain that manifests wild-type pathology. This means when children are exposed to the wild-type strain, even though they may not have a breakthrough infection with chickenpox, they now harbor two heterologous (genetically different) strains of VZV–both of which are at a later time subject to reactivation as shingles. Thus, as they age, they will be even more likely to reactivate with shingles (unless periodically administered booster vaccine doses for life in order to maintain the immunity)–especially if they do not receive exogenous (outside) boosts to their cell-mediated immunity which, in the pre-vaccine era, came from expostures to other children infected with wild-type varicella which provided the adult with a subclinical boost that helped to suppress or postpone reactivattion of shingles.

I would also like to clear up the point that shingles has always been increasing–even prior to the licensing of the varicella vaccine. This statement is true; however, the increases were on the order of 2 to 4% per year (which were likely due to an aging population, or greater access to healthcare). Once a community had widespread distribution of varicella vaccine, increases in herpes zoster were on the order of 20% per year. For example, this source [Yih WK, Brooks DR, Lett SM, et al. The incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccine coverage, 1998-2003. BMC Public Health 2005; 5:68.
32. Schmid DS, Jumaan AO. Impact of varicella vaccine on varicella-zoster virus dynamics. Clin Microbiol Rev 2010; 23(1):202–217] found a 90% increase in shingles over 5 years (1999-2003).