Varicella-Zoster Virus Glycoproteins: Entry, Replication, and Pathogenesis

Purpose of Review Varicella-zoster virus (VZV), an alphaherpesvirus that causes chicken pox (varicella) and shingles (herpes zoster), is a medically important pathogen that causes considerable morbidity and, on occasion, mortality in immunocompromised patients. Herpes zoster can afflict the elderly with a debilitating condition, postherpetic neuralgia, triggering severe, untreatable pain for months or years. The lipid envelope of VZV, similar to all herpesviruses, contains numerous glycoproteins required for replication and pathogenesis. This study aims to summarize the current knowledge about VZV glycoproteins and their roles in cell entry, replication, and pathogenesis. Recent Findings The functions for some VZV glycoproteins are known, such as gB, gH, and gL, in membrane fusion, cell-cell fusion regulation, and receptor binding properties. However, the molecular mechanisms that trigger or mediate VZV glycoproteins remain poorly understood. Summary VZV glycoproteins are central to successful replication but their modus operandi during replication and pathogenesis remains elusive requiring further mechanistic-based studies.