Anti-JCV VP1 Monoclonal antibody

The JC virus, also known as the JCV, is an enclosed double-stranded DNA virus that is a member of the polyomavirus family. It often infects people in childhood and continues to do so throughout life.About 5,130 base pairs make up the genome of JCV, which is separated into three sections: an early coding area, a late coding region, and a transcriptional regulatory region. The late coding region encodes the primary viral capsid proteins, such as VP1, VP2, and VP3, while the early coding area controls transcription and viral replication.The 72 VP1 pentamers that make up the JCV capsid are icosahedral in shape and comprise five VP1 proteins each. VP1 contains both VP2 and VP3. Normally, a JCV infection remains quiescent; however, in immunocompromised conditions, particularly in patients infected with HIV (human immunodeficiency virus), the virus reactivates, causing infection of oligodendrocytes in the central nervous system and starting the deadly demyelinating disease known as progressive multifocal leukoencephalopathy (PML).

Figure 1. Cysteine residues in JCV Vp1. (Source: Kobayashi S, et al., 2013)

The JC virus infection process is complex, since it enters the cell by adhering to a receptor on the host cell before releasing its DNA into the cytoplasm and beginning reproduction.The VP1 protein is important in infection because it serves as both a major component of the viral capsid and a modulator of viral binding to the host cell's receptor.The VP1 protein has a complicated three-dimensional structure that includes an N-terminal and a C-terminal extension. The N-terminal and C-terminal extensions are critical in pentamer formation and viral particle assembly. By attaching to host cell membrane receptors, VP1 helps the virus enter the cell. It then co-assembles with VP2 and VP3 in the nucleus to generate new viral particles. Mutations in VP1 can sometimes result in a decrease or elimination of the virus's ability to infect, endangering its stability and capacity to form pentamers in the host cell. Furthermore, VP1 plays a role in the development and release of viral particles.

The major complication of JCV infection is PML, a severe demyelinating disease of the central nervous system that usually occurs in individuals with suppressed immune systems, especially in AIDS patients. In addition, patients undergoing organ transplantation, chemotherapy for tumors, and the use of immunomodulatory drugs are also at risk for JCV reactivation.The main feature of PML is the lysogenic destruction of oligodendrocytes, leading to lesions in white matter regions of the brain, which ultimately lead to severe neurological impairment and fatal consequences. There are currently few choices for treating PML, and those that do exist mostly focus on boosting the patient's immune system, such as antiretroviral therapy for managing HIV infection. Nevertheless, for JCV infection brought on by immunosuppression, there isn't a reliable direct antiviral treatment. Studies against JCV VP1 have demonstrated in recent years that the VP1 protein can be used as a foundation for vaccine development and as a possible target for therapy. Recombinant VP1 has been extensively employed in the investigation of viral infection processes and vaccine development. It can self-assemble in the lab into virus-like particles (VLPs), which possess structural characteristics akin to those of wild viral particles.

Anti-JC virus VP1 antibody
Anti-JC Polyomavirus VP1 antibody
Anti-JC virus capsid protein 1 antibody