Polyomaviruses of Humans

Abstract

Both JC virus (JCV) and BK virus (BKV) were first isolated in 1971 from the brain tissue of a patient suffering from progressive multifocal encephalopathy (PML) and from the urine of a kidney allograft recipient with chronic pyelonephritis respectively. Both viruses are members of the polyomavirus family and are non-enveloped DNA viruses with icosahedral capsids containing a small, circular, double-stranded DNA genome. JCV is the etiologic agent of PML, whereas BKV is involved in polyomavirus-associated nephropathy (PVAN) in patients receiving kidney transplants. The genomic organization of both viruses is very similar to that of simian vacuolating virus 40 (SV40) in that regulatory and coding regions make-up of the genome of each virus. The regulatory region of each virus consists of the origin of DNA replication and promoter/enhancer elements and is responsible for the regulation of the viral early and late gene expression; and the viral DNA replication. Both viral genomes are oncogenic in experimental animals and can transform cells in tissue culture system. In addition, both genomes have been detected in a variety of human tumors. Despite the extensive structural and genomic similarities, JCV and BKV display a distinct biology with respect to the infection of the specific tissues in human host. There has been a rapid expansion in the number of the additional human polyomaviruses in recent years, due to new discoveries, bringing the present number to 13. Those include Merkel cell carcinoma-associated polyomavirus (MCPyV) and Trichodysplasia Spinulosa-associated polyomavirus (TSPyV), Karolinska Institute polyomavirus (KIPyV), Washington University polyomavirus (WUPyV), human polyomavirus-6 (HPyV6), human polyomavirus-7 (HPyV7), human polyomavirus-9 (HPyV9), human polyomavirus-10 (HPyV10), Malawi human polyomavirus (MWPyV), Mexico X human polyomavirus (MXPyV), human polyomavirus-12 (HPyV12) and New Jersey polyomavirus (NJPyV). Among those recently discovered human polyomaviruses, only MCPyV and TSPyV appear to be associated with a human disease; the rest has yet to be definitively linked to with a particular human disease. In this review, a particular attention was devoted to the description of the biology of JCV, BKV, MCPyV, and TSPyV.