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. 2016 Dec;3(4):204-215.
doi: 10.1007/s40588-016-0044-4. Epub 2016 Sep 9.

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

Stefan L Oliver  1 , Edward Yang  1 , Ann M Arvin  1
Affiliations

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

Stefan L Oliver et al. Curr Clin Microbiol Rep. 2016 Dec.

Abstract

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.

Purpose of review: 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 remains poorly understood.

Summary: VZV glycoproteins are central to successful replication but their modus operandi during replication and pathogenesis remain elusive requiring further mechanistic based studies.

Keywords: Varicella zoster virus; fusion; glycoprotein; pathogenesis; receptor; replication.

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Conflict of interest statement

Conflict of Interest Edward Yang and Ann Arvin declare they have no conflicts of interest.

Figures

Figure 1
Figure 1
Model of the localization and trafficking of VZV glycoproteins during infection. VZV is presumed to use glycoproteins to bind cell surface receptors during attachment (1). The gB/gH-gL complex fuses the virion membrane with cell membranes either in endocytic vesicles or directly with the plasma membrane (2). The capsid is released into the cytoplasm and docks with a nuclear pore where the dsDNA genome is injected into the cell nucleus to initiate replication (3). Glycoproteins are synthesized in the endoplasmic reticulum (ER) and trafficked to the Golgi during maturation, exocytosed then endocytosed and trafficked to the trans-Golgi network (TGN) (4). Some glycoproteins, including gB, are trafficked to the nuclear envelope (inner nuclear membrane, INM; outer nuclear membrane, ONM) and might have roles in egress from the nucleus (5). Glycoproteins are trafficked from the TGN for incorporation into nascent virus particles (6). Adapted from [100].
See this image and copyright information in PMC

References

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