Abstract
Varicella Zoster Virus (VZV), a member of the herpes virus family, causes varicella (chicken pox) upon primary infection and later manifests as herpes zoster ([HZ] or shingles) upon reactivation. VZV-specific T-cell immunity acquired during primary infection aids recovery, with the virus lying latent in neuronal ganglia until it transports to the skin axonally during reactivation. It has been well-established that reduced T-cell recognition and proliferation, as well as immunosuppression more generally, contribute to VZV reactivation. It has also been discovered that seasonal variation, which is linked to ultraviolet radiation (UVR), correlates with increased HZ cases. This correlation may be explained by the direct immunosuppressant effects of UVR, with melanin offering photoprotective effects that decrease reactivation rates. However, an underexplored aspect of this correlation is the potential role of the skin microbiome in UVR-induced VZV reactivation. Vital for skin homeostasis and immune modulation, the skin microbiome has been found to influence various skin conditions. Preliminary evidence suggests that microbiome diversity may influence VZV reactivation rates, supported by antibiotic-induced effects on HZ incidence. Research also indicates the microbiome’s modulating effect on UVR-induced immune suppression, emphasizing its potential significance in VZV reactivation. The skin microbiome’s contribution may also help further explain sex and ethnicity-specific variations in VZV reactivation rates. Understanding the interplay between UVR, the skin microbiome, and VZV reactivation warrants further investigation and may help uncover preventive strategies for mitigating VZV reactivation.
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