Abstract
Since their discovery in 1971, the polyomaviruses JC (JCPyV) and BK (BKPyV), isolated from patients with progressive multifocal leukoencephalopathy and polyomavirus-associated nephropathy, respectively, remained for decades as the only known members of the Polyomaviridae family of viruses of human origin. Over the past five years, the application of new genomic amplification technologies has facilitated the discovery of several novel human polyomaviruses (HPyVs), bringing the present number to 10. These HPyVs share many fundamental features in common such as genome size and organization. Infection by all HPyVs is widespread in the human population, but they show important differences in their tissue tropism and association with disease. Much remains unknown about these new viruses. In this review, we discuss the problems associated with studying HPyVs, such as the lack of culture systems for the new viruses and the gaps in our basic understanding of their biology. We summarize what is known so far about their distribution, life cycle, tissue tropism, their associated pathologies (if any), and future research directions in the field.
Highlights
Polyomaviruses belong to a family of small, nonenveloped, DNA tumor viruses, which have small, circular, double-stranded DNA genomes encapsidated in icosahedral virions without a lipoprotein envelope [1]
Two human polyomaviruses (HPyVs) were discovered in 1971 and additional viruses in human were not detected until recent technologies such as digital transcriptome subtraction and rolling circle amplification allowed the identification of eight novel HPyVs over the last five years (Table 1)
The variety and number of polyomaviruses reflects their success in propagating themselves at low levels without causing disease while evading the immune system
Summary
Polyomaviruses belong to a family of small, nonenveloped, DNA tumor viruses, which have small, circular, double-stranded DNA genomes encapsidated in icosahedral virions without a lipoprotein envelope [1]. Polyomavirus JC (JCPyV), one of the first two HPyVs to be discovered, was first isolated from brain tissue of a patient with the CNS demyelinating disease, progressive multifocal leukoencephalopathy (PML) by Padgett et al in 1971 [4]. This neurotropic virus is established as the proven causative agent of PML. Polyomavirus BK (BKPyV) [6] was discovered around the same time as JCPyV in a patient with polyomavirus-associated nephropathy (PVAN) in a kidney transplant recipient. Like JCPyV, seroepidemiological studies indicate BKPyV infection is widespread but PVAN is relatively rare [7].
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