Human polyomaviruses and cancer: an overview
Autor(a) principal: | |
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Data de Publicação: | 2019 |
Outros Autores: | , , , , |
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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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 |
_version_ |
1800222764071649280 |