BK virus (BKV), a human polyomavirus, causes nephropathy (BKN) and allograft loss in renal transplant recipients. BK Virus VP1 forms an icosahedral capsid which is composed of 72 pentamers linked to each other by disulfide bonds and associated with VP2 or VP3 proteins. Interacts with gangliosides GT1b and GD1b containing terminal alpha2-8-linked sialic acids on the cell surface to provide virion attachment to target cell. This attachment induces virion internalization predominantly through caveolin-mediated endocytosis and traffics to the endoplasmic reticulum. Inside the endoplasmic reticulum, the protein folding machinery isomerizes VP1 interpentamer disulfide bonds, thereby triggering initial uncoating. Next, the virion uses the endoplasmic reticulum-associated degradation machinery to probably translocate in the cytosol before reaching the nucleus. Nuclear entry of the viral DNA involves the selective exposure and importin recognition of VP2/Vp3 nuclear localization signal. In late phase of infection, neo-synthesized VP1 encapsulates replicated genomic DNA in the nucleus, and participates in rearranging nucleosomes around the viral DNA.
Clone
6E10
Isotype
IgG1k
Host species
Mouse
Species Reactivity
BK Virus
Cellular Localization
nucleus
Positive Control
BK Virus infected tissues
Applications
IHC, ELISA, WB
Intended Use
Research Use Only