Varicella zoster virus and cardiovascular diseases

Abstract

Varicella zoster virus (VZV) is a Herpesviridae family double-stranded DNA virus that only affects humans. The first clinical manifestation appears to be varicella, typical of childhood. VZV, on the other hand, becomes latent in ganglion neurons throughout the neuroaxis after primary infection. The VZV reactivates and travels along peripheral nerve fibers in the elderly and immunocompromised individuals, resulting in Zoster. It can, however, spread centrally and infect cerebral and extracranial arteries, resulting in vasculopathy, which can lead to transient ischemic attacks, strokes, aneurysms, cavernous sinus thrombosis, giant cell arteritis, and granulomatous aortitis. Although the mechanisms of virus-induced pathological vascular remodeling are not fully understood, recent research indicates that inflammation and dysregulation of ligand-1 programmed death play a significant role. Few studies, on the other hand, have looked into the role of VZV in cardiovascular disease. As a result, the purpose of this review is to examine the relationship between VZV and cardiovascular disease, the efficacy of the vaccine as a protective mechanism, and the target population of heart disease patients who could benefit from vaccination.