Varicella-zoster virus (VZV) is a alphaherpesvirus which causes chicken pox (varicella) and shingles (zoster) (Gershon et al., 2015; Gabutti et al., 2016). The VZV 125kb genome is the smallest of the alphaherpesviruses and is comprised of a unique long (UL) and unique short (US) region flanked by internal and terminal repeats. As with other herpesviruses, VZV requires glycoproteins on the virion surface for cell entry and cell-to-cell spread. Nine glycoproteins are encoded by the VZV genome. Two glycoproteins critical to VZV, gE and gI, are encoded by open reading frame 68 (ORF68) and ORF67, respectively, located in the US region of the genome. These two VZV glycoproteins (gE and gI) form a heterodimer that mediates efficient cell-to-cell spread. Deletion of ORF68 (gE) is lethal to VZV. Deletion of ORF67 (gI) results in a virus with a small-plaque phenotype in vitro, which cannot be recovered from inoculated human skin xenografts (Mallory et al., 1997; Mo et al., 2002). The noncovalent heterodimer that forms between gE and gI can be disrupted by the deletion of the first cysteine-rich region in gE, severely impairing replication in human skin tissue.
Source:Recombinant protein corresponding to aa31-538 (gE), aa18-273 (gI) of from Varicella-Zoster Virus Heterodimer gE/gI, expressed in HEK293 cells.
Molecular Weight:~66kD (gE), 45kD (gI)
Storage and Stability:Aliquot to avoid repeated freezing and thawing and store at -70°C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
