Varicella-Zoster Virus IgG ELISA Kit is quantitative and qualitative tests for detection of human antibodies in serum, plasma or cerebrospinal fluid against Varicella-Zoster Virus. For Research Use Only. Not for use in diagnostic procedures.
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General Description
Varicella-Zoster Viruses as well as Herpes-Simplex Viruses, CMV and EBV belong to the group of human Herpes viruses. This highly contagious virus is transmitted by droplet-infection (contaminated aerosols) or by smear-infection (vesicles with contaminated contents, or eschar). Varicella viruses are globally spread. Accumulating seasonal infections during winter and spring periods can be observed in temperate zones. Most pre-school children experience a primary infection, and 95% of adults show seropositivity. Contagion of infected patients starts 1-2 days before the onset of exanthema and ends towards the 7th day after the last efflorescence occurred. Pathogens persist in spinal ganglia and in cases of decreasing immunity they may be reactivated. The incubation period is 2-3 weeks. After a short prodromal period with non-specific symptoms, the primary manifestation of VZV-infection (chickenpox) appears. In general, the course of disease is benign except in cases of immunocompromised or elderly individuals and children younger than 1 year. Bacterial super infections, varicella pneumonia, various CNS-manifestations such as encephalitis, aseptic meningitis, Guillain-Barré-syndrome, Reye-syndrome, myocarditis, glomerulonephritis, inflammation of the gastro intestinal tract and hepatitis are some of the most severe complications resulting from VZV infections. In case of primary infections during pregnancy, diaplacental transmission may lead to congenital varicella syndrome. Infections occurring shortly before and after birth are a severe risk for the child. Reactivation of persisting viruses can lead to cases of herpes zoster (shingles). Most herpes zoster patients suffer from unilateral vesicular eruptions accompanied by severe pain. Post herpetic neuralgia may persist for a long period of time. Severe cases of zoster disease prevalently occur in cases of immunodeficiency. The method of choice for direct virus detection is VZV-polymerase-chain-reaction (PCR). Herpes Zoster may also be diagnosed serologically. For the detection of VZV specific IgG, ELISA is the method of choice. With the Varicella-Zoster Virus IgG ELISA Kit, evaluation of antibody activity is measured in international Units and, therefore, comparison of results from different tests is possible.
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Background
Varicella-zoster virus (VZV) causes primary infection (chickenpox) and subsequently establishes a latency period in the infected ganglion. Later under certain conditions the virus can be reactivated to cause herpes zoster, leading to severe morbidity but rarely death, although in immunocompromised hosts VZV can cause severe disseminated disease and occasionally death. Herpes zoster is characterized by a localized rash with unilateral skin distribution, usually accompanied by severe neuropathic pain. Risk factors for herpes zoster include older age, diabetes, genetic susceptibility, and recent psychological stress. The development of animal models that mimic VZV disease and the study of VZV pathogenesis is challenging due to the high restriction of VZV infection to humans, coupled with the high cellular relevance of the virus.
Figure 1. Model of the varicella zoster virus (VZV) life cycle (Source: Zerboni L, et al. 2014)
VZV belongs to the α-herpesvirus family along with herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), also known as human herpesvirus type 3 (HHV-3). The virus has a lipid-rich envelope with embedded viral glycoproteins, and the envelope contains a linear double-stranded DNA genome encoding approximately 71 open reading frames. Five evolutionary branches of VZV have been identified, but the most diverse branches also share 99.8% sequence conservation.
VZV virus particles enter host cells by direct fusion with the plasma membrane or by endocytosis, during which the viral envelope proteins interact with cell-surface molecules such as mannose-6-phosphate receptors or myelin-associated glycoproteins. VZV glycoproteins B (gB), gH, and gL function as core fusion complexes, but other envelope glycoproteins may function as accessory proteins. After entering the cell, the virus undergoes an exfoliation process where tegument proteins, including immediate-early protein 62 (IE62), are released. The nucleocapsid is anchored to the nuclear pore and the viral genome is injected into the cell nucleus. IE62 forms regulatory complexes with cytokines to transcriptionally activate the VZV gene.
Alternative Names
VZV IgG ELISA
References
1. Zerboni L, et al. Molecular mechanisms of varicella zoster virus pathogenesis. Nat Rev Microbiol. 2014 Mar;12(3):197-210.
2. Andrei G, et al. Advances and Perspectives in the Management of Varicella-Zoster Virus Infections. Molecules. 2021 Feb 20;26(4):1132.
Q: I'm looking for an ELISA KIT (QUANTITATIVE) to dose the human Ab a-VZV gE protein? I would like to know if you have this kind of kit.
A: The IgA/IgM plate is coated with: Varicella Zoster Virus preparation. The IgG plate is coated with: Affinity purified envelope glycoproteins mix from Varicella Zoster Virus. DEIA388: Varicella Zoster Virus IgA: Sensitivity 51.0 %* (98 %), Specificity > 99 % DEIA387: Varicella Zoster Virus IgG: Sensitivity 98.9 %, Specificity > 99 % DEIA389: Varicella Zoster Virus IgM: Sensitivity > 99 %, Specificity > 99 %. In addition, we do can provide a kit to detected IgG antibodies to gE. Please refer to DEIA-JY2141.
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References
Acute retinal necrosis secondary to Varicella Zoster Virus
A 54 year old female presented to the ophthalmology clinic with pain and decreased vision in her left eye. No past medical history other than primary varicella zoster infection, in her childhood. The eye exam revealed a macular region with scattered areas of retinal opacity along with patches of necrosis on the periphery. She was started on valganciclovir and referred to the infectious disease clinic. Cell Count, blood chemistry and HIV were negative. Serum was sent for polymerase chain reaction (PCR) for Varicella Zoster Virus (VZV), Herpes Simplex Virus (HSV) and Cytomegalovirus (CMV). The VZV PCR was positive. She had decreased vision on the right eye two days later, and exam revealed peripheral retinal whitening. She was admitted and started on intravenous acyclovir. VZV is one of the most common causes of ARN and has been described in both immunocompetent and immunocompromised persons. Visual changes are usually noted weeks to months after the antecedent herpes zoster. Retinal involvement is bilateral in over half of cases, suggesting that VZV reaches the central nervous system hematogenously. The retinal exam reveals multifocal necrotizing lesions, often initially involving the peripheral retina. Therapy includes intravenous acyclovir with consideration of intravitreal foscarnet and other antivirals for progressing disease. (C) 2019 Published by Elsevier Ltd.
Humoral immunity to varicella zoster virus is altered in patients with rheumatoid arthritis
CLINICAL RHEUMATOLOGY
Authors: Krasselt, Marco; Baerwald, Christoph; Liebert, Uwe G.; Seifert, Olga
Introduction The prevalence of herpes zoster (HZ) is high in patients with rheumatologic diseases. The incidence in patients with rheumatoid arthritis (RA) is at least twice as high as in healthy people. Nevertheless, little is known about humoral immunity against varicella zoster virus (VZV), in particular in patients with RA. We, therefore, aimed to retrospectively compare VZV antibody concentrations in a collective of patients with RA in a German outpatient clinic with age- and sex-matched controls without RA. Methods We included n = 247 patients with RA from one single university centre as well as n = 250 age- and sex-matched controls from the in-house routine in this retrospective analysis. The concentration of VZV IgG antibody concentration was either available from the records or was measured using an enzyme-linked immunosorbent assay (ELISA). Additionally, avidity for specific IgG was analysed for some of the samples. The antibody concentrations have been compared between the two groups. Moreover, a consecutive subgroup analysis after stratification by age was performed. Results A total of 68.4% (n = 169) of the included patients were treated with conventional synthetic DMARDs, either as monotherapy or in combination. Biological originator DMARDs were used in 45.8% (n = 113) of the patients, with the majority (85%, n = 96) of them being on tumour necrosis factor (TNF)-inhibiting agents. As the main result of this study, antibody titres for VZV were found to be significantly lower in RA patients compared with healthy controls (p < 0.0001). The observed difference was most pronounced for the older patients being in the sixth and seventh decade. Antibody avidity was high in both groups with a significantly higher avidity among the controls (p = 0.0006). Conclusions A possible explanation for the low VZV antibody concentration in RA patients might be premature immunosenescence, which most likely also effects the B cell compartment and humoral immunity. This thesis is emphasised by the significantly higher antibody avidity among the controls. The data also suggest that the increased HZ risk is a consequence of a poor humoral immunity. The available HZ vaccinations should contribute to decreasing the elevated HZ risk in RA patients.
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Figure 1. Model of the varicella zoster virus (VZV) life cycle
