2025 Volume 9 Issue 1 Pages 1-10
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.
In addition to its role in vesicle formation, damage to VEG facilitates immune cell infiltration and intensifies local inflammation, contributing to pain and prolonged symptoms. Moreover, systemic VEG damage in conditions such as disseminated HZ and primary varicella leads to widespread vesicular eruptions and potential complications, including organ involvement.
Preventive and therapeutic strategies aimed at preserving VEG integrity are crucial for mitigating the severity of HZ. These include lifestyle interventions, such as glycemic and blood pressure control, smoking cessation, and regular moderate exercise. Nutritional support and prompt antiviral therapy protect the glycocalyx. Vaccination against VZV has demonstrated efficacy in reducing the incidence and severity of HZ with potential cardiovascular benefits.
Understanding the mechanisms of VEG damage and its role in HZ pathophysiology highlights the need for targeted interventions. Research focusing on VEG protection may offer innovative approaches for preventing severe HZ and improving clinical outcomes.
