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BK polyomavirus VP3 protein is a minor structural component of the BK polyomavirus (BKPyV) capsid, essential for the virus's ability to infect host cells and assemble new virions (UniProt P03091). It is encoded by the late region of the viral genome and is identical to the C-terminal portion of the VP2 protein, sharing a nuclear localization signal (NLS) that facilitates the transport of the viral genome into the nucleus (ViralZone). In clinical practice, BKPyV is a major cause of morbidity in immunocompromised patients, particularly kidney transplant recipients, where it leads to BK polyomavirus-associated nephropathy (BKVAN), and hematopoietic stem cell transplant recipients, where it causes hemorrhagic cystitis (NCBI TaxID: 1891762). While VP3 is a critical factor for viral infectivity, there are currently no FDA-approved drugs that specifically target this protein; instead, management relies on the reduction of immunosuppression and the use of broad-spectrum antivirals like cidofovir or brincidofovir (Rinaldo et al., 2013). Research into the structural biology of the BKPyV capsid suggests that VP3 could be a target for novel entry inhibitors or vaccine candidates designed to elicit neutralizing antibody responses (Bernhoff et al., 2008). Understanding the role of VP3 in the viral life cycle remains crucial for developing more effective and targeted therapies for polyomavirus-related diseases.
Inhibition of viral replication through DNA polymerase blockade or neutralization of viral particles to prevent entry.
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