VZV reactivation, immune remodeling, and dementia risk
- 1Beijing ABZYMO Biosciences Co., Ltd.
- 2Jiangsu Recbio Technology Co.
- 3State Key Laboratory of Drug Regulatory Science (SKLDRS), National Institutes for Drug Control
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.
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BibTeX
@article{zhang2026reactivation,
title = {{VZV reactivation, immune remodeling, and dementia risk}},
author = {Lijun Zhang and Shuang Wu and Yaru Quan and Wenrong Yao},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1953013},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1953013/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - VZV reactivation, immune remodeling, and dementia risk
AU - Lijun Zhang
AU - Shuang Wu
AU - Yaru Quan
AU - Wenrong Yao
PY - 2026
DA - 2026/10/14
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1953013
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1953013/full
AB - 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.
SN - 1664-3224
ER -