Human polyoma viruses and disease with emphasis on clinical BK and JC

Abstract

Polyoma viruses are ubiquitous infecting many different mammalian species including humans. There are five known human polyoma viruses. JC virus and BK virus are two polyoma viruses identified nearly three decades ago. Recently WU, KI and Merkel cell polyoma viruses have been isolated from humans. The exact role of these three newly discovered viruses in human disease is not known. Most human polyoma disease is caused by BK and JC viruses which are usually acquired in childhood. Approximately 50-80% of humans have seropositivity to these viruses. Clinically apparent diseases in immunocompetent hosts are extremely rare. These viruses remain latent possibly in the lymphoid organs, neuronal tissue, and kidney and under the circumstances of severe immunosuppression both these viruses reactivate. Neurotropic JC virus reaches the brain and causes progressive multifocal leukoencephalopathy, a demyelinating disease of the central nervous system with a high mortality rate. BK virus is urotheliotropic and its reactivation causes a form of interstitial nephritis, known as BK or polyoma virus associated nephropathy which is associated with high graft loss if not recognized early. There are no known effective antiviral agents for any of the polyoma viruses.

Figure 1. Neighbor-joining trees for the polyoma viruses with the putative MCV based on small T proteins

The four previously known human polyomaviruses (BKV, JCV, KIV and WUV) cluster together in the SV40 subgroup (blue) while MCV is most closely related to MuPyV subgroup viruses (red). Both subgroups are distinct from the avian polyomavirus subgroup (orange). Adapted from Feng H et al., Science 2008; 319:1096 with permission.