Varicella zoster virus and the central nervous system

Scritto il 24/02/2026
da Benson Ogunjimi

Nat Rev Microbiol. 2026 Feb 24. doi: 10.1038/s41579-026-01289-9. Online ahead of print.

ABSTRACT

Varicella zoster virus (VZV) causes varicella, also known as chickenpox, after which VZV remains latent in neural ganglia. VZV reactivation can result in herpes zoster, also known as shingles. In addition to its well-known effects on the peripheral nervous system, reports increasingly suggest that VZV can have potentially devastating effects on the central nervous system (CNS). Several epidemiological studies indicate that VZV reactivation is associated with stroke and interest is growing in potential associations of VZV with dementia. In the past 5-6 years, vaccination against herpes zoster has been reported to reduce the risk of developing cardiovascular events (including stroke) and dementia in observational studies, although interpretation of their findings is hindered by complex methodological challenges. This Review considers the relationship between VZV and the CNS from a multidisciplinary perspective that focuses on VZV physiology and immunity. The strengths and weaknesses of published studies are discussed, and areas for future investigation that remain to be addressed before the links between VZV and CNS conditions can be considered definitive and medically actionable are highlighted. Finally, these insights are integrated into an overarching conclusion that addresses potential consequences of the connection between VZV and the CNS for both public health and healthy ageing.

PMID:41735628 | DOI:10.1038/s41579-026-01289-9