Human polyomaviruses and cancer: an overview

Detalhes bibliográficos
Autor(a) principal: Prado, José Carlos Mann
Data de Publicação: 2019
Outros Autores: Monezi, Telma Alves, Amorim, Aline Teixeira, Lino, Vanesca, Paladino, Andressa, Boccardo, Enrique
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/154816
Resumo: The name of the family Polyomaviridae, derives from the early observation that cells infected with murine polyomavirus induced multiple (poly) tumors (omas) in immunocompromised mice. Subsequent studies showed that many members of this family exhibit the capacity of mediating cell transformation and tumorigenesis in different experimental models. The transformation process mediated by these viruses is driven by viral pleiotropic regulatory proteins called T (tumor) antigens. Similar to other viral oncoproteins T antigens target cellular regulatory factors to favor cell proliferation, immune evasion and downregulation of apoptosis. The first two human polyomaviruses were isolated over 45 years ago. However, recent advances in the DNA sequencing technologies led to the rapid identification of additional twelve new polyomaviruses in different human samples. Many of these viruses establish chronic infections and have been associated with conditions in immunosuppressed individuals, particularly in organ transplant recipients. This has been associated to viral reactivation due to the immunosuppressant therapy applied to these patients. Four polyomaviruses namely, Merkel cell polyomavirus (MCPyV), Trichodysplasia spinulosa polyomavirus (TSPyV), John Cunningham Polyomavirus (JCPyV) and BK polyomavirus (BKPyV) have been associated with the development of specific malignant tumors. However, present evidence only supports the role of MCPyV as a carcinogen to humans. In the present review we present a summarized discussion on the current knowledge concerning the role of MCPyV, TSPyV, JCPyV and BKPyV in human cancers.
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spelling Human polyomaviruses and cancer: an overviewMCPyVBKPyVJCPyVTSPyVHuman cancerThe name of the family Polyomaviridae, derives from the early observation that cells infected with murine polyomavirus induced multiple (poly) tumors (omas) in immunocompromised mice. Subsequent studies showed that many members of this family exhibit the capacity of mediating cell transformation and tumorigenesis in different experimental models. The transformation process mediated by these viruses is driven by viral pleiotropic regulatory proteins called T (tumor) antigens. Similar to other viral oncoproteins T antigens target cellular regulatory factors to favor cell proliferation, immune evasion and downregulation of apoptosis. The first two human polyomaviruses were isolated over 45 years ago. However, recent advances in the DNA sequencing technologies led to the rapid identification of additional twelve new polyomaviruses in different human samples. Many of these viruses establish chronic infections and have been associated with conditions in immunosuppressed individuals, particularly in organ transplant recipients. This has been associated to viral reactivation due to the immunosuppressant therapy applied to these patients. Four polyomaviruses namely, Merkel cell polyomavirus (MCPyV), Trichodysplasia spinulosa polyomavirus (TSPyV), John Cunningham Polyomavirus (JCPyV) and BK polyomavirus (BKPyV) have been associated with the development of specific malignant tumors. However, present evidence only supports the role of MCPyV as a carcinogen to humans. In the present review we present a summarized discussion on the current knowledge concerning the role of MCPyV, TSPyV, JCPyV and BKPyV in human cancers.Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2019-02-15info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/15481610.6061/clinics/2018/e558sClinics; Vol. 73 No. Suppl. 1 (2018); e558sClinics; v. 73 n. Suppl. 1 (2018); e558sClinics; Vol. 73 Núm. Suppl. 1 (2018); e558s1980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/154816/150800Copyright (c) 2019 Clinicsinfo:eu-repo/semantics/openAccessPrado, José Carlos MannMonezi, Telma AlvesAmorim, Aline TeixeiraLino, VanescaPaladino, AndressaBoccardo, Enrique2019-05-14T11:48:25Zoai:revistas.usp.br:article/154816Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2019-05-14T11:48:25Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Human polyomaviruses and cancer: an overview
title Human polyomaviruses and cancer: an overview
spellingShingle Human polyomaviruses and cancer: an overview
Prado, José Carlos Mann
MCPyV
BKPyV
JCPyV
TSPyV
Human cancer
title_short Human polyomaviruses and cancer: an overview
title_full Human polyomaviruses and cancer: an overview
title_fullStr Human polyomaviruses and cancer: an overview
title_full_unstemmed Human polyomaviruses and cancer: an overview
title_sort Human polyomaviruses and cancer: an overview
author Prado, José Carlos Mann
author_facet Prado, José Carlos Mann
Monezi, Telma Alves
Amorim, Aline Teixeira
Lino, Vanesca
Paladino, Andressa
Boccardo, Enrique
author_role author
author2 Monezi, Telma Alves
Amorim, Aline Teixeira
Lino, Vanesca
Paladino, Andressa
Boccardo, Enrique
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Prado, José Carlos Mann
Monezi, Telma Alves
Amorim, Aline Teixeira
Lino, Vanesca
Paladino, Andressa
Boccardo, Enrique
dc.subject.por.fl_str_mv MCPyV
BKPyV
JCPyV
TSPyV
Human cancer
topic MCPyV
BKPyV
JCPyV
TSPyV
Human cancer
description The name of the family Polyomaviridae, derives from the early observation that cells infected with murine polyomavirus induced multiple (poly) tumors (omas) in immunocompromised mice. Subsequent studies showed that many members of this family exhibit the capacity of mediating cell transformation and tumorigenesis in different experimental models. The transformation process mediated by these viruses is driven by viral pleiotropic regulatory proteins called T (tumor) antigens. Similar to other viral oncoproteins T antigens target cellular regulatory factors to favor cell proliferation, immune evasion and downregulation of apoptosis. The first two human polyomaviruses were isolated over 45 years ago. However, recent advances in the DNA sequencing technologies led to the rapid identification of additional twelve new polyomaviruses in different human samples. Many of these viruses establish chronic infections and have been associated with conditions in immunosuppressed individuals, particularly in organ transplant recipients. This has been associated to viral reactivation due to the immunosuppressant therapy applied to these patients. Four polyomaviruses namely, Merkel cell polyomavirus (MCPyV), Trichodysplasia spinulosa polyomavirus (TSPyV), John Cunningham Polyomavirus (JCPyV) and BK polyomavirus (BKPyV) have been associated with the development of specific malignant tumors. However, present evidence only supports the role of MCPyV as a carcinogen to humans. In the present review we present a summarized discussion on the current knowledge concerning the role of MCPyV, TSPyV, JCPyV and BKPyV in human cancers.
publishDate 2019
dc.date.none.fl_str_mv 2019-02-15
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/154816
10.6061/clinics/2018/e558s
url https://www.revistas.usp.br/clinics/article/view/154816
identifier_str_mv 10.6061/clinics/2018/e558s
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/154816/150800
dc.rights.driver.fl_str_mv Copyright (c) 2019 Clinics
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2019 Clinics
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 73 No. Suppl. 1 (2018); e558s
Clinics; v. 73 n. Suppl. 1 (2018); e558s
Clinics; Vol. 73 Núm. Suppl. 1 (2018); e558s
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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