The kit is intended for professional use for the qualitative and semiquantitative detection of IgG antibodies against polyomavirus JC (JCV) in human serum. The kit is intended for laboratory research of diseases caused by or associated with JCV (e.g. progressive multifocal leukoencephalitis (PML) in immunodeficient patients).
Contents of Kit
1. ELISA break-away strips in the handling frame coated with the specific antigen, STRIPS Ag, 1 × 12 pcs 2. Negative control human serum, NC, (lyophilized), 1 vial 3. Positive control human serum, PC, (lyophilized), 1 vial 4. Calibrator (human serum), CAL, (lyophilized) 1 vial 5. 12 mL Anti-human IgG labelled with horseradish peroxidase (anti-IgG Px conjugate) r.t.u1. CONJ, 1 vial 6. 50 mL Wash buffer, 20× concentrated WASH, 1 vial 7. 50 mL Dilution buffer, r.t.u. DIL, 1 vial 8. 6 mL Chromogenic substrate TMB-O, r.t.u. TMB-O, 2 vial 9. 7 mL Stop solution, r.t.u. (0.5 sulfuric acid), STOP, 1 vial 1) r.t.u., ready to use Notice: Control sera may be colorless to yellowish or blue due to the use of different diluents.
Storage
1. Store the kit and the kit reagents at 2-10°C, in a dry place and protected from the light. Under these conditions, the expiration date is indicated at the ELISA kit label and at all reagent labels. 2. Store unused strips in the sealable pouch and keep the desiccant inside. 3. Store undiluted serum samples at 2-10°C up to one week. For longer period make aliquots and keep them at -18°C to -28°C. Avoid repeated thawing and freezing.
Performance Characteristics
The kit is intended for the qualitative and semi-quantitative detection of anti-JCV IgG antibodies in human serum and plasma. Suitable specimens are serum and plasma (heparinised) samples obtained by standard laboratory techniques. Validity of the test The absorbance value of the Dilution buffer (BLANK = reaction background) is stated in the Quality Control Certificate of the lot. The OD values of the standards / control sera and the ratio of the OD values of the standards PC / CAL should be within the ranges stated in the Quality Control Certificate of the lot. The Calibrator and Controls are human sera, and as such they may show inhomogeneity, if their value in the test is significantly different from the values stated in the Certificate of analysis (see CoA - lot characteristics), consult the results with the manufacturer.
Citations
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Background
JC polyomavirus is a type of human polyomavirus that was not isolated from glial cells in progressive multifocal leukoencephalopathy (PML) until 1971, when it was named JC virus (JCV) after the patient's initials. More recently, JCV has been named JC polyomavirus (JCPyV), but JCV is still the common name. Infection with the virus is asymptomatic in normal people, and the virus causes neuroinvasive and other diseases only in cases of immunosuppression or immunodeficiency. JCV is very common in the population, with seroprevalence rates ranging from 40-60%, and can be transmitted via the fecal-oral pathway. Primary infection usually occurs in childhood and establishes lifelong infection, when no clinical symptoms are manifested, and JCV-induced disease is usually the result of reactivation of the virus by persistent infection when the immune system is compromised.
Figure 1. Schematic diagram of the JCV genome (Source: Ferenczy MW, et al. 2012)
PML tends not to occur in immunologically healthy individuals; in immunosuppressed humans JCV invades oligodendrocytes and begins to replicate, followed by demyelination of the subcortical white matter of the CNS due to oligodendrocyte lysis. Clinical features of PML include motor weakness (monoparesis or hemiparesis), cognitive dysfunction, appendicular ataxia or gait ataxia, visual symptoms (hemianopia, diplopia), and language deficits. Imaging reveals brain lesions presenting as asymmetric multifocal areas of low density.
Brain biopsy by JCV DNA in situ hybridization or immunohistochemical staining, or detection of JCV DNA in cerebrospinal fluid confirms the diagnosis of PML. Although the detection of antibody levels of JCV in the blood can not be used as a means of diagnosis, it can also assist in clinical diagnosis and reflect the status and risk level of JCV infection. Creative Diagnostics provides you with Anti-polyomavirusJC (JCV) IgG ELISA kits for qualitative or quantitative detection of JCV IgG antibodies in human serum or plasma, suitable for laboratory studies of diseases caused by or related to JCV, such as PML.
1. Ferenczy MW, et al. Molecular biology, epidemiology, and pathogenesis of progressive multifocal leukoencephalopathy, the JC virus-induced demyelinating disease of the human brain. Clin Microbiol Rev. 2012 Jul;25(3):471-506.
2. Multani A, et al. JC Polyomavirus Infection Potentiated by Biologics. Infect Dis Clin North Am. 2020 Jun;34(2):359-388.
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References
JC Polyomavirus Infection Potentiated by Biologics
The risk of JC polyomavirus encephalopathy varies among biologic classes and among agents within the same class. Of currently used biologics, the highest risk is seen with natalizumab followed by rituximab. Multiple other agents have also been implicated. Drug-specific causality is difficult to establish because many patients receive multiple immunomodulatory medications concomitantly or sequentially, and have other immunocompromising factors related to their underlying disease. As use of biologic therapies continues to expand, further research is needed into pathogenesis, treatment, and prevention of JC polyomavirus encephalopathy such that risk for its development is better understood and mitigated, if not eliminated altogether.
JC polyomavirus: a short review of its biology, its association with progressive multifocal leukoencephalopathy, and the diagnostic value of different methods to manifest its activity or presence
Expert Rev Mol Diagn
Authors: Prezioso C, Pietropaolo V, Moens U, Ciotti M.
Introduction: JC polyomavirus is the causative agent of progressive multifocal leukoencephalopathy (PML), a demyelinating disease resulting from the lytic infection of oligodendrocytes that may develop in immunosuppressed individuals: HIV1 infected or individuals under immunosuppressive therapies. Understanding the biology of JCPyV is necessary for a proper patient management, the development of diagnostic tests, and risk stratification.
Areas covered: The review covers different areas of expertise including the genomic characterization of JCPyV strains detected in different body compartments (urine, plasma, and cerebrospinal fluid) of PML patients, viral mutations, molecular diagnostics, viral miRNAs, and disease.
Expert opinion: The implementation of molecular biology techniques improved our understanding of JCPyV biology. Deep sequencing analysis of viral genomes revealed the presence of viral quasispecies in the cerebrospinal fluid of PML patients characterized by noncoding control region rearrangements and VP1 mutations. These neurotropic JCPyV variants present enhanced replication and an altered cell tropism that contribute to PML development. Monitoring these variants may be relevant for the identification of patients at risk of PML. Multiplex realtime PCR targeting both the LTAg and the archetype NCCR could be used to identify them. Failure to amplify NCCR should indicate the presence of a JCPyV prototype speeding up the diagnostic process.
COA
Publication 
Figure 1. Schematic diagram of the JCV genome
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