Background: Both wild-type (WT) and vaccine strain (VS) varicella zoster virus (VZV) establish latency and can reactivate to cause herpes zoster (HZ), though HZ risks from VS-VZV seem lower. We assessed HZ incidence in birth cohorts born before and after introduction of varicella vaccine in 1995 to better understand these risks.
Methods: Medical claims data from MarketScan® commercial insurance databases were obtained for 1993-2013. We identified HZ based on first outpatient service with an HZ ICD-9 code (053.xx) and calculated unadjusted incidence by birth cohorts, sex and age.
Results: In the 1981-89 and 1990-2001 birth cohorts (born before and during introduction of varicella vaccine, respectively), HZ incidence increased with age; incidence was stable in the 2002-13 cohort (born after varicella vaccination was implemented) (Fig. 1). In adults, age-specific rates are higher in females than males (Fig. 2A), but in children, the divergence by sex has died out in recent years (Fig. 2B).
Conclusion: For children born in the pre-vaccine era, published data show that VZV seroprevalence increased from 86% to 93% between ages 10 and 20 years. The large rise in HZ incidence with age in the 1981-89 cohort is thus not due to increases in VZV-positivity (i.e., latency) with age. Unknown mechanisms seem to cause the increase during late teen and early adult years, before immunosenescence can be implicated. We have previously reported that females are at greater HZ risk than males, even in children for whom differential health seeking is unlikely. We now report that this difference has died out in recent years in children. Children born before availability of varicella vaccine were mostly infected with WT-VZV, but with each birth year after vaccine was introduced, prevalence of WT-VZV in children declines and that of VS-VZV increases. We posit that the cause of the sex disparity in HZ risk relates to WT-VZV and not VS-VZV.
M. Gambhir, None