JCV VP1 Specific Neutra™ Antibody Products

Creative Biolabs’ JCV VP1 antibodies are designed to provide researchers with reliable tools for a range of applications in JCV studies.

• Deliver specific and consistent results, enabling you to achieve your research goals efficiently.
• Engineered to offer high sensitivity and low background, which are critical for accurate and reproducible data in experiments.

Our solutions deliver the tools and expertise necessary to overcome the obstacles in rabies virus research. Contact our team to get an inquiry now!

Introduction of JC Virus

The John Cunningham virus, or JC virus (JCV), also called human polyomavirus 2, is the etiological agent of progressive multifocal leukoencephalopathy (PML), exhibits near-ubiquitous seroprevalence with most population exposure by adolescence. Though classified as human polyomavirus 2, this dsDNA virus maintains lifelong latency in immunocompetent hosts through renal urothelial persistence and bone marrow stromal cell colonization. Reactivation occurs exclusively in immunocompromised states, enabling CNS neurotropism through 5-HT2A receptor-mediated BBB penetration. While transmission vectors remain undefined, fecal-oral acquisition during childhood is hypothesized, with viral seeding to immune-privileged sites, including cerebral perivascular spaces and palatine tonsillar crypts.

Fig. 1 JC virus protein (stained brown) in a brain biopsyDistributed under CC BY-SA 2.0 DE, from Wiki, without modification

JCV is a virus without an envelope. The viral shell, roughly 40 nm across, is constructed from three structural proteins: VP1, VP2, and VP3. Five VP1 molecules combine to create a pentamer, and 72 such pentamers connect via extended C-terminal segments to form the complete viral shell. The virus attaches to target cells by interacting with a cell surface N-linked glycoprotein that has terminal alpha (2-6)-linked sialic acids. Following attachment, virions primarily enter through a ligand-inducible, clathrin-dependent mechanism, and are transported to the ER. Inside the endoplasmic reticulum, protein-folding enzymes modify the interpentamer disulfide bonds of the VP1 protein, which triggers the uncoating process. Following this, the virion likely uses the endoplasmic reticulum-associated degradation system to facilitate its translocation into the cytosol before progressing to the nucleus. The entry of the viral DNA into the nucleus occurs through the selective exposure and recognition of the VP2/VP3 nuclear localization signal by importins. During the late stage of infection, newly synthesized VP1 encloses replicated genomic DNA at nuclear regions known as promyelocytic leukemia (PML) bodies, and plays a role in rearranging nucleosomes surrounding the viral DNA.

Fig. 2 Structure of JC virus.¹

Antibodies against JCV

A recent investigation has elucidated disparities in JCV-specific T cell responses contingent upon natalizumab therapy and its associated sequela, PML. The study delineated that the magnitude and character of the JCV-specific T cell response in natalizumab-treated patients exhibited parity with healthy controls. Conversely, in natalizumab-associated PML, JCV-specific T cells were frequently undetectable, or, critically, skewed towards IL-10 production, a human cytokine synthesis inhibitor. These observations underscore the pivotal role of T cell responses in PML pathogenesis.

Remarkably, PML patients demonstrate elevated antibody titers against viral capsid proteins, both pre- and peri-disease. Intrathecal anti-JCV IgG synthesis has been documented, yet this fails to correlate with improved clinical outcomes. Furthermore, the virus appears adapted for replication and dissemination via B cells and their progenitors. Nevertheless, the advent of sophisticated methodologies for dissecting human antiviral immune responses against persistent and latent infections has revealed a complex landscape. Individual antibody clones exhibit heterogeneous neutralizing capacities; effective antibodies are rare, and certain partial responses may exert deleterious biological effects on the host. Consequently, a more granular investigation of this critical facet of virus-host interplay is warranted, specifically to define the contribution of select antibody clones capable of effective viral particle neutralization during peripheral reactivation.²

Why Choose Us?

Creative Biolabs try the best to delivering superior RABV antibodies and services, aiding your investigations and addressing your challenges. We provide several key advantages:

• High Specificity and Affinity: Our proprietary antibody development platform ensures the generation of antibodies with exceptional specificity for JCV VP1, minimizing cross-reactivity and ensuring reliable results.
• Customization Options: We offer a wide range of customization options, including different antibody isotypes, labeling with various tags (e.g., HRP, FITC), and tailored purification methods, to meet your specific research needs.
• Rigorous Quality Control: Every batch of our JCV VP1 antibodies undergoes stringent quality control testing to ensure consistent performance and reproducibility. Published Data supports the reliability of our quality control processes.
• Expert Technical Support: Our team of experienced scientists offers thorough technical support, including help with experimental design, troubleshooting, and data interpretation.

For more information about Creative Biolabs' JCV VP1 antibodies and services, please contact us.

REFERENCES

1. Barth, Heidi, et al. "In vitro and in vivo models for the study of human polyomavirus infection." Viruses 8.10 (2016): 292. Distributed under Open Access license CC BY 4.0, without modification.
2. Diotti, Roberta Antonia, et al. "JC polyomavirus (JCV) and monoclonal antibodies: friends or potential foes?." Journal of Immunology Research 2013.1 (2013): 967581. Distributed under Open Access license CC BY 3.0, without modification.