Polyomavirus Infections of Humans

Abstract

Research on polyomaviruses began in 1953 when Ludwik Gross isolated a filterable agent that induced tumours in newborn mice. This agent became the archetypal member of the Polyomaviridae family. In 1971, JC virus and BK virus were reported and named after the patients’ initials. More than 30 years passed before the Karolinska Institute virus and Washington University virus were identified from respiratory samples in paediatric patients. The Merkel cell polyomavirus was identified in 2008 for its association with the aggressive Merkel cell carcinoma skin cancer. Recently, polyomaviruses 6, 7, 9 and the trichodysplasia spinulosa‐associated polyomavirus have been discovered. Along with simian virus 40, which has been associated with human disease, there are now 10 polyomaviruses relevant to humans. The range of diseases associated with these human polyomaviruses shows that they are significant causes of human infections. The accumulated knowledge gained from the study of each individual virus helps to understand each in their particular niche. Key Concepts: Polyomaviruses are DNA viruses. Polyomaviruses cause significant human infections, especially in the immunocompromised population. Human infection most likely occurs during childhood. Haemorrhagic cystitis and polyomavirus‐associated nephropathy are significant clinical entities caused by the BK virus in solid organ transplant recipients. Progressive multifocal encephalopathy is a fatal demyelinating disease caused by the JC virus. Merkel cell virus and SV40 are potential oncogenic agents. Treatment is supportive and an effective antiviral agent has not been identified so far.

The T Antigen Locus of Merkel Cell Polyomavirus Downregulates Human Toll-Like Receptor 9 Expression

“…Eleven different human polyomaviruses have been isolated so far (38). To determine whether TLR9 downregulation is common to most human polyomaviruses, we cloned early gene regions from four additional human polyomaviruses (BKPyV, JCPyV, WUPyV, and KIPyV) and simian virus 40 (SV40) into the retroviral vector pLXSN or into the pcDNA3 expression vector.…”