Varicella zoster virus IgG ELISA Kit (DEIA4425)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
cerebrospinal fluid, serum
Species Reactivity
Human
Intended Use
Varicella zoster virus IgG ELISA assay is intended for research use of VZV associated diseases, namely varicella and herpes zoster, including their neurological complications, i.e. encephalitis, meningitis, cerebellitis, vacsulitis, myelitis or inflammatory neuropathies.
Contents of Kit
1. ELISA break-away strips (blue)
2. Anti-human IgG antibodies
3. Wash buffer
4. Dilution buffer (DB)
5. Chromogenic substrate (TMB substrate)
6. Stop solution
Storage
Store the kit and the kit reagents at 2-10°C, in a dry place and protected from the light. Store unused strips in the sealable pouch and keep the desiccant inside. For more detailed information, please download the following document on our website.
Sensitivity
The diagnostic sensitivity of the test is 96.6%.

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References


Understanding the immunology of Shingrix, a recombinant glycoprotein E adjuvanted herpes zoster vaccine

CURRENT OPINION IN IMMUNOLOGY

Authors: Heineman, Thomas C.; Cunningham, Anthony; Levin, Myron

Herpes zoster is common in older and immune suppressed persons due to diminished VZV-specific cellular immunity. A recombinant herpes zoster vaccine (RZV) consisting of a single VZV glycoprotein and an adjuvant system stimulates robust and persistent VZV-specific antibody and CD4+ T cell responses in these high-risk populations. VZV-specific immune responses induced by RZV, including the generation of polyfunctional T cells, are driven by the synergistic actions of the components of the vaccine adjuvant system. RZV provides unprecedented protection against herpes zoster in older adults regardless of age at vaccination and is efficacious in immune suppressed populations. Adjuvanted subunit antigens may represent a general strategy for vaccines in the elderly and other individuals typically considered immunologically resistant to vaccination.

Infection and Functional Modulation of Human Monocytes and Macrophages by Varicella-Zoster Virus

JOURNAL OF VIROLOGY

Authors: Kennedy, Jarrod J.; Steain, Megan; Slobedman, Barry; Abendroth, Allison

Varicella-zoster virus (VZV) is associated with viremia during primary infection that is presumed to stem from infection of circulating immune cells. While VZV has been shown to be capable of infecting a number of different subsets of circulating immune cells, such as T cells, dendritic cells, and NK cells, less is known about the interaction between VZV and monocytes. Here, we demonstrate that blood-derived human monocytes are permissive to VZV replication in vitro. VZV-infected monocytes exhibited each temporal class of VZV gene expression, as evidenced by immunofluorescent staining. VZV virions were observed on the cell surface and viral nucleocapsids were observed in the nucleus of VZV-infected monocytes by scanning electron microscopy. In addition, VZV-infected monocytes were able to transfer infectious virus to human fibroblasts. Infected monocytes displayed impaired dextran-mediated endocytosis, and cell surface immunophenotyping revealed the downregulation of CD14, HLA-DR, CD11b, and the macrophage colony-stimulating factor (M-CSF) receptor. Analysis of the impact of VZV infection on M-CSF-stimulated monocyte-to-macrophage differentiation demonstrated the loss of cell viability, indicating that VZV-infected monocytes were unable to differentiate into viable macrophages. In contrast, macrophages differentiated from monocytes prior to exposure to VZV were highly permissive to infection. This study defines the permissiveness of these myeloid cell types to productive VZV infection and identifies the functional impairment of VZV-infected monocytes. IMPORTANCE Primary VZV infection results in the widespread dissemination of the virus throughout the host. Viral transportation is known to be directly influenced by susceptible immune cells in the circulation. Moreover, infection of immune cells by VZV results in attenuation of the antiviral mechanisms used to control infection and limit spread. Here, we provide evidence that human monocytes, which are highly abundant in the circulation, are permissive to productive VZV infection. Furthermore, monocyte-derived macrophages were also highly permissive to VZV infection, although VZV-infected monocytes were unable to differentiate into macrophages. Exploring the relationships between VZV and permissive immune cells, such as human monocytes and macrophages, elucidates novel immune evasion strategies and provides further insight into the control that VZV has over the immune system.

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