University of Michigan
Varicella zoster virus (VZV) is a herpesvirus that causes chickenpox and shingles. The biological mechanisms underpinning the multi-decadal latency of VZV in the body and subsequent viral reactivation-which occurs in approximately 30% of individuals-are largely unknown. Because chickenpox and shingles are endemic worldwide, understanding the relationship between VZV transmission and reactivation is important for informing disease treatment and control. While chickenpox is a vaccine-preventable childhood disease with a rich legacy of research, shingles is not a notifiable disease in most countries. To date, population-level studies of shingles have had to rely on small-scale hospital or community-level datasets. Here, we examined chickenpox and shingles notifications from Thailand and found strong seasonal incidence in both diseases, with a 3-month lag between peak chickenpox transmission season and peak shingles reactivation. We tested and fit 14 mathematical models examining the biological driversof chickenpox and shingles over an 8-year period to estimate rates of VZV transmission, reactivation, and immunity boosting, wherein re-exposure to VZV boosts VZV-specific immunity to reinforce protection against shingles. The models suggested the seasonal cycles of chickenpox and shingles have different underlying mechanisms, with ultraviolet radiation (UV) being correlated with shingles reactivation.