Herpes Zoster and Cardiovascular Health: Preventing Glycocalyx Damage-induced Vascular Failure

Herpes zoster (HZ), caused by reactivation of the varicella-zoster virus (VZV), presents with painful vesicular rashes localized to specific dermatomes. The formation of these vesicles is closely linked to damage of the vascular endothelial glycocalyx (VEG). After establishing latency in the sensory ganglia, VZV reactivates under conditions such as immunosuppression and spreads along nerve pathways to the skin. Local viral replication and inflammatory responses lead to VEG disruption, increased vascular permeability, and vesicle formation. The extent of glycocalyx damage influences the severity of HZ, with more pronounced damage observed in immunocompromised individuals and those with preexisting vascular conditions.