structural approaches to develop new therapeutic strategies against clinically relevant human polyomaviruses
Arwen Pearson, Eike Schulz and Nicole Fischer
Illustration: hegasy.de | © Infectophysics 2019
Human polyomaviruses (HPyV) are highly abundant, persist for life time and can induce severe, life threatening complications in elderly and immunosuppressed patients. In particular, Merkel cell polyomavirus (MCPyV) and BK virus (BKV) cause devastating diseases. MCPyV is the etiological agent of a rare but highly aggressive skin cancer, Merkel cell carcinoma (MCC). BK virus (BKV) causes polyomavirus associated nephropathy (PVAN) in up to 10% of kidney transplant patients and hemorrhagic cystitis (PVHC) in 5-15% of allogenic transplant patients. Due to the complete lack of specific anti-viral therapy, treatment options are mainly restricted to reconstitution of the immune system by alleviation of the immunosuppressive regimen, which in the case of BK associated diseases often results in graft rejection or an exacerbation of the underlying condition. For MCPyV and MCC the lack of a specific therapy results in a 5yr overall survival rate of less than 20%. Considering the clinical relevance of BKV and MCPyV the identification of efficient BKV and MCPyV inhibitors is highly desirable.