ABSTRACT
Polyomavirus infections are known to occur naturally in chickens, macaws, budgerigars, mice, hamsters, monkeys and humans [3]. The human infections were initially recognized as the clinically manifest syndromes of JCV and BKV. JCV causes the subacute, fatal central nervous system demyelinating disease progressive multifocal leukoencephalopathy (PML) due to a productive infection of oligodendrocytes. Although this syndrome was originally described in patients with systemic immunosuppression due to cancer and/or chemotherapy, it has subsequently been recognized as a consequence of human immunodeficiency virus (HIV-1) infection, accounting for a distinct rise in the incidence of PML in the AIDS population [4]. BKV most commonly causes a self-limited hemorrhagic
Figure 1 The polyomavirus genome. The genome of JCV is schematized as an exemplar. The circular genomes of all polyoma viruses are similar, with three general regions identified based on function. These comprise the regulatory (noncoding) region, the early coding region, and the late coding region.
