Polyomaviruses

Over the last 10 years, the number of identified polyomaviruses has grown to more than 35 subtypes, including 13 in humans. The polyomaviruses have similar genetic makeup, including genes that encode viral capsid proteins VP1, 2, and 3 and large and small T region proteins. The T proteins play a role in viral replication and have been implicated in viral chromosomal integration and possible dysregulation of growth factor genes. In humans, the Merkel cell polyomavirus has been shown to be highly associated with integration and the development of Merkel cell cancers. The first two human polyomaviruses discovered, BKPyV and JCPyV, are the causative agents for transplant-related kidney disease, BK commonly and JC rarely. JC has also been strongly associated with the development of progressive multifocal leukoencephalopathy (PML), a rare but serious infection in untreated HIV-1-infected individuals and in other immunosuppressed patients including those treated with monoclonal antibody therapies for autoimmune diseases systemic lupus erythematosus, rheumatoid arthritis, or multiple sclerosis. The trichodysplasia spinulosa-associated polyomavirus (TSAPyV) may be the causative agent of the rare skin disease trichodysplasia spinulosa. The remaining nine polyomaviruses have not been strongly associated with clinical disease to date. Antiviral therapies for these infections are under development. Antibodies specific for each of the 13 human polyomaviruses have been identified in a high percentage of normal individuals, indicating a high rate of exposure to each of the polyomaviruses in the human population. PCR methods are now available for detection of these viruses in a variety of clinical samples.