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Background
Varicella-zoster virus (VZV) is a lymphotropic and neurotropic virus that causes chickenpox and herpes zoster and can cause primary infection in the mucosal epithelium through respiratory droplets or vesicular fluid in infected individuals. Initial infection with VZV results in chickenpox, neurons in the skin connected to sensory ganglia are subsequently infected, and the VZV genome resides in the host's dorsal root ganglia or cranial ganglia for life. Decreased immunity to VZV can reactivate the virus, causing herpes zoster. A subset of patients develops postherpetic neuralgia (PHN), which is difficult to treat and manifests as severe pain that can last from days to months.
VZV glycoprotein E (gE) is encoded by the open reading frame ORF68, located in a short unique region of the VZV genome. It is the most abundant glycoprotein in infected cells and a major component of the viral particle envelope. Extensively phosphorylated gE usually forms stable heterodimers with gI, which are synthesized and post-translationally modified in cells using typical cellular processes. gE is synthesized in the endoplasmic reticulum (ER) and then shuttled to the Golgi where it is transported to the cell surface by vesicles. gE has an endocytosis motif and a trans-Golgi network (TGN) signaling motif that recycles cell membrane gE, allowing cell surface glycoproteins to be endocytosed and transported to the TGN. Glycoproteins in the TGN are ultimately transported to nascent viral particles. The maturation process of gE also requires the involvement of gI. It was found that in induced cell lines lacking gI, gE co-localizes with TGN markers at perinuclear sites but is not transported to the plasma membrane.
Figure 1. Model of the localization and trafficking of VZV glycoproteins during infection (Source: Oliver SL, et al. 2016)
Viral surface glycoproteins are often thought to be involved in the interactions between viral and cell surface proteins that allow VZV to attach to, ingest, and enter the cell, thereby initiating the replication cycle. Initially, researchers thought that the insulin degrading enzyme (IDE) was an important factor influencing VZV entry into cells, as VZV replication was significantly reduced in IDE knockout cells. In addition, the mannose-6-phosphate receptor encoded by IGFR2 was also implicated in VZV entry. Subsequent studies showed that IDE binds to the gE precursor found in the ER and that IGFR2 plays a role in lysosomal biogenesis. This also suggests that their effect on VZV is not related to viral attachment and entry into the cell, but rather that they act during the replication cycle after VZV entry.
Alternative Names
Anti-VZV Glycoprotein E Monoclonal antibody VZV gE mAb
References
1. Oliver SL, et al. Varicella-Zoster Virus Glycoproteins: Entry, Replication, and Pathogenesis. Curr Clin Microbiol Rep. 2016 Dec;3(4):204-215.
2. Heineman TC, et al. Understanding the immunology of Shingrix, a recombinant glycoprotein E adjuvanted herpes zoster vaccine. Curr Opin Immunol. 2019 Aug;59:42-48.
3. Arvin AM, et al. Analysis of the functions of glycoproteins E and I and their promoters during VZV replication in vitro and in skin and T-cell xenografts in the SCID mouse model of VZV pathogenesis. Curr Top Microbiol Immunol. 2010;342:129-46.
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References
LNP-CpG ODN-adjuvanted varicella-zoster virus glycoprotein E induced comparable levels of immunity with Shingrix™ in VZV-primed mice
Latent varicella-zoster virus (VZV) may be reactivated to cause herpes zoster, which affects one in three people during their lifetime. The currently available subunit vaccine Shingrix? is superior to the attenuated vaccine Zostavax? in terms of both safety and efficacy, but the supply of its key adjuvant component QS21 is limited. With ionizable lipid nanoparticles (LNPs) that were recently approved by the FDA for COVID-19 mRNA vaccines as carriers, and oligodeoxynucleotides containing CpG motifs (CpG ODNs) approved by the FDA for a subunit hepatitis B vaccine as immunostimulators, we developed a LNP vaccine encapsulating VZV-glycoprotein E (gE) and CpG ODN, and compared its immunogenicity with Shingrix? in C57BL/6J mice. The results showed that the LNP vaccine induced comparable levels of gE-specific IgG antibodies to Shingrix? as determined by enzyme-linked immunosorbent assay (ELISA). Most importantly, the LNP vaccine induced comparable levels of cell-mediated immunity (CMI) that plays decisive roles in the efficacy of zoster vaccines to Shingrix? in a VZV-primed mouse model that was adopted for preclinical studies of Shingrix?. Number of IL-2 and IFN-γ secreting splenocytes and proportion of T helper 1 (Th1) cytokine-expressing CD4+ T cells in LNP-CpG-adjuvanted VZV-gE vaccinated mice were similar to that of Shingrix? boosted mice. All of the components in this LNP vaccine can be artificially and economically synthesized in large quantities, indicating the potential of LNP-CpG-adjuvanted VZV-gE as a more cost-effective zoster vaccine.
Detection of Circulating VZV-Glycoprotein E-Specific Antibodies by Chemiluminescent Immunoassay (CLIA) for Varicella-Zoster Diagnosis
Pathogens
Authors: Kombe Kombe AJ, Xie J, Zahid A, Ma H, Xu G, Deng Y, Nsole Biteghe FA, Mohammed A, Dan Z, Yang Y, Feng C, Zeng W, Chang R, Zhu K, Zhang S, Jin T.
Varicella and herpes zoster are mild symptoms-associated diseases caused by varicella-zoster virus (VZV). They often cause severe complications (disseminated zoster), leading to death when diagnoses and treatment are delayed. However, most commercial VZV diagnostic tests have low sensitivity, and the most sensitive tests are unevenly available worldwide. Here, we developed and validated a highly sensitive VZV diagnostic kit based on the chemiluminescent immunoassay (CLIA) approach. VZV-glycoprotein E (gE) was used to develop a CLIA diagnostic approach for detecting VZV-specific IgA, IgG, and IgM. The kit was tested with 62 blood samples from 29 VZV-patients classified by standard ELISA into true-positive and equivocal groups and 453 blood samples from VZV-negative individuals. The diagnostic accuracy of the CLIA kit was evaluated by receiver-operating characteristic (ROC) analysis. The relationships of immunoglobulin-isotype levels between the two groups and with patient age ranges were analyzed. Overall, the developed CLIA-based diagnostic kit demonstrated the detection of VZV-specific immunoglobulin titers depending on sample dilution. From the ELISA-based true-positive patient samples, the diagnostic approach showed sensitivities of 95.2%, 95.2%, and 97.6% and specificities of 98.0%, 100%, and 98.9% for the detection of VZV-gE-specific IgA, IgG, and IgM, respectively. Combining IgM to IgG and IgA detection improved diagnostic accuracy. Comparative analyses on diagnosing patients with equivocal results displaying very low immunoglobulin titers revealed that the CLIA-based diagnostic approach is overall more sensitive than ELISA. In the presence of typical VZV symptoms, CLIA-based detection of high titer of IgM and low titer of IgA/IgG suggested the equivocal patients experienced primary VZV infection. Furthermore, while no difference in IgA/IgG level was found regarding patient age, IgM level was significantly higher in young adults. The CLIA approach-based detection kit for diagnosing VZV-gE-specific IgA, IgG, and IgM is simple, suitable for high-throughput routine analysis situations, and provides enhanced specificity compared to ELISA.
COA
Publication 
Figure 1. Model of the localization and trafficking of VZV glycoproteins during infection
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