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Human polyomavirus 1, commonly known as BK polyomavirus (BKV), is a double-stranded DNA virus that establishes lifelong latency in the renal tubular cells and urothelium of a majority of the global population (PubMed: 29437630). In immunocompromised individuals, particularly kidney transplant recipients and hematopoietic stem cell transplant patients, BKV can reactivate and cause severe conditions such as BK virus-associated nephropathy (BKVAN) and hemorrhagic cystitis (PubMed: 30811461). The virus hijacks the host's cellular machinery to replicate, often utilizing the Large T-antigen to drive the cell into the S-phase of the cell cycle (UniProt: P03072). Therapeutic strategies include the off-label use of antivirals like cidofovir, which inhibits viral DNA synthesis, and emerging adoptive immunotherapies like virus-specific T-cells (VSTs) that target infected cells expressing viral antigens (PubMed: 34162817). Managing BKV infection often involves a delicate balance between reducing immunosuppressive drugs to allow for natural immune clearance and avoiding the risk of organ transplant rejection.
Drugs targeting BK virus-infected cells primarily act by inhibiting viral DNA polymerase to stop replication (e.g., Cidofovir), or by utilizing virus-specific T-cells (VSTs) to recognize viral antigens like the Large T-antigen and VP1 protein on the surface of infected cells, leading to targeted cell lysis (e.g., Posoleucel).
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