Work

VZV reactivation, immune remodeling, and dementia risk

Year: 2026
Type: review
Abstract: Varicella-Zoster Virus (VZV) is a highly dermatotropic and neurotropic α-herpesvirus that causes varicella (chickenpox) during primary infection, subsequently establishing lifelong latency, and reactivates to cause herpes zoster when host immunity declines or suppressed. Recent large-scale epidemiological studies consistently associate herpes zoster immunization, particularly with the recombinant zoster vaccine (RZV), with a significantly reduced risk of incident dementia. These findings have prompted a rigorous re-evaluation of the infectious etiology of progressive neurodegeneration. This review integrates the intersecting molecular mechanisms of VZV latency, localized ganglionic immunosenescence, and systemic inflammaging. We critically evaluate a synergistic VZV-HSV-1 amyloidogenic cascade, while explicitly addressing the biological limitations of extrapolating these transient interactions to human central nervous system (CNS) neuropathology. Furthermore, we propose the hypothesis that AS01B-induced trained immunity may contribute to neuroprotection. Therefore, this review provides insight for understanding the systemic consequences of chronic VZV infection and the impact of adjuvant-mediated immune remodeling in aging populations.
Language: English
Field: Medicine
Open Access status: gold
Estimated APC paid: $3,801
OpenAlex ID: W7221755180
FWCI:
Cites: 68
Cited by:
Related to: 10