Two‐Faced Nature of BK‐Polyomavirus

In immunocompromised patients, reactivation of latent BK‐polyomavirus (BKPyV) can cause disease with lytic infections of kidneys and the lower urinary tract. Emerging evidence also links BKPyV to oncogenesis and high grade intra‐renal and transitional cell carcinomas. These neoplasms strongly express polyomavirus large‐T antigen as a defining feature, i.e. they are “large‐T positive carcinomas”. Such neoplasms arise in immunocompromised patients, typically in renal allograft recipients and preferentially in tissues harboring latent BKPyV. In recent papers in this journal it was shown that tumor cells harbor replication incompetent clonal BKPyV. The virus can be truncated and randomly integrated into the genome, and/or it can be mutated in an episomal state. Truncation and/or deletions in the BKPyV‐NCCR domain can hamper late viral gene expression, replication and cell lysis while facilitating overexpression of early genes including large‐T. Biologically active fusion proteins or alterations in human tumor suppressor or promoter function have not been described thus far, making uncontrolled large‐T gene expression in non‐lytically infected cells a prime suspect for neoplastic transformation.


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