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Polyomaviruses

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  • Author: Linda Cook1
  • Editors: Randall T. Hayden2, Donna M. Wolk3, Karen C. Carroll4, Yi-Wei Tang5
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: University of Washington, Laboratory Medicine, Seattle, WA 98102; 2: St. Jude’s Children’s Research Hospital, Memphis, TN; 3: Geisinger Clinic, Danville, PA; 4: Johns Hopkins University Hospital, Baltimore, MD; 5: Memorial Sloan-Kettering Institute, New York, NY
    • Source: microbiolspec July 2016 vol. 4 no. 4 doi:10.1128/microbiolspec.DMIH2-0010-2015
  • Received 13 April 2015 Accepted 02 March 2016 Published 22 July 2016
  • Linda Cook, [email protected]
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  • Abstract:

    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.

  • Citation: Cook L. 2016. Polyomaviruses. Microbiol Spectrum 4(4):DMIH2-0010-2015. doi:10.1128/microbiolspec.DMIH2-0010-2015.

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/content/journal/microbiolspec/10.1128/microbiolspec.DMIH2-0010-2015
2016-07-22
2021-01-24

Abstract:

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.

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Polyomaviruses
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Citation: Cook L. 2016. Polyomaviruses. microbiolspec 4(4): doi:10.1128/microbiolspec.DMIH2-0010-2015
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FIGURE 1
Phylogenetic tree created from an alignment of one whole genome sequence for each of the 13 human polyomavirus types.
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FIGURE 1

Phylogenetic tree created from an alignment of one whole genome sequence for each of the 13 human polyomavirus types.

Source: microbiolspec July 2016 vol. 4 no. 4 doi:10.1128/microbiolspec.DMIH2-0010-2015
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Polyomaviruses
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Citation: Cook L. 2016. Polyomaviruses. microbiolspec 4(4): doi:10.1128/microbiolspec.DMIH2-0010-2015
/content/microbiolspec/10.1128/microbiolspec.DMIH2-0010-2015.T1
TABLE 1
Human polyomavirus summary information
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TABLE 1

Human polyomavirus summary information

Source: microbiolspec July 2016 vol. 4 no. 4 doi:10.1128/microbiolspec.DMIH2-0010-2015
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TABLE 2
Available BK and JC reagents for PCR testing as of December 2015
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TABLE 2

Available BK and JC reagents for PCR testing as of December 2015

Source: microbiolspec July 2016 vol. 4 no. 4 doi:10.1128/microbiolspec.DMIH2-0010-2015
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TABLE 3
Therapeutic options for BK-related kidney disease
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TABLE 3

Therapeutic options for BK-related kidney disease

Source: microbiolspec July 2016 vol. 4 no. 4 doi:10.1128/microbiolspec.DMIH2-0010-2015

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