Human papillomaviruses: basic mechanisms of pathogenesis and oncogenicity
Human papillomaviruses (HPVs) are small double‐stranded DNA viruses that infect the cutaneous and mucosal epithelium. Infection by specific HPV types has been linked to the development of cervical carcinoma. HPV infects epithelial cells that undergo terminal differentiation and so encode multiple me...
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| Veröffentlicht in: | Reviews in medical virology 2006-03, Vol.16 (2), p.83-97 |
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| description | Human papillomaviruses (HPVs) are small double‐stranded DNA viruses that infect the cutaneous and mucosal epithelium. Infection by specific HPV types has been linked to the development of cervical carcinoma. HPV infects epithelial cells that undergo terminal differentiation and so encode multiple mechanisms to override the normal regulation of differentiation to produce progeny virions. Two viral proteins, E6 and E7, alter cell cycle control and are the main arbitrators of HPV‐induced oncogenesis. Recent data suggest that E6 and E7 also play a major role in the inhibition of the host cell innate immune response to HPV. The E1 and E2 proteins, in combination with various cellular factors, mediate viral replication. In addition, E2 has been implicated in both viral and cellular transcriptional control. Despite decades of research, the function of other viral proteins still remains unclear. While prophylactic vaccines to block genital HPV infection will soon be available, the widespread nature of HPV infection requires greater understanding of both the HPV life cycle as well as the mechanisms underlying HPV‐induced carcinogenesis. Copyright © 2005 John Wiley & Sons, Ltd. |
| doi_str_mv | 10.1002/rmv.488 |
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Infection by specific HPV types has been linked to the development of cervical carcinoma. HPV infects epithelial cells that undergo terminal differentiation and so encode multiple mechanisms to override the normal regulation of differentiation to produce progeny virions. Two viral proteins, E6 and E7, alter cell cycle control and are the main arbitrators of HPV‐induced oncogenesis. Recent data suggest that E6 and E7 also play a major role in the inhibition of the host cell innate immune response to HPV. The E1 and E2 proteins, in combination with various cellular factors, mediate viral replication. In addition, E2 has been implicated in both viral and cellular transcriptional control. Despite decades of research, the function of other viral proteins still remains unclear. While prophylactic vaccines to block genital HPV infection will soon be available, the widespread nature of HPV infection requires greater understanding of both the HPV life cycle as well as the mechanisms underlying HPV‐induced carcinogenesis. 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Med. Virol</addtitle><description>Human papillomaviruses (HPVs) are small double‐stranded DNA viruses that infect the cutaneous and mucosal epithelium. Infection by specific HPV types has been linked to the development of cervical carcinoma. HPV infects epithelial cells that undergo terminal differentiation and so encode multiple mechanisms to override the normal regulation of differentiation to produce progeny virions. Two viral proteins, E6 and E7, alter cell cycle control and are the main arbitrators of HPV‐induced oncogenesis. Recent data suggest that E6 and E7 also play a major role in the inhibition of the host cell innate immune response to HPV. The E1 and E2 proteins, in combination with various cellular factors, mediate viral replication. In addition, E2 has been implicated in both viral and cellular transcriptional control. Despite decades of research, the function of other viral proteins still remains unclear. While prophylactic vaccines to block genital HPV infection will soon be available, the widespread nature of HPV infection requires greater understanding of both the HPV life cycle as well as the mechanisms underlying HPV‐induced carcinogenesis. Copyright © 2005 John Wiley & Sons, Ltd.</description><subject>Capsid Proteins - physiology</subject><subject>Female</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Neoplasms - virology</subject><subject>Oncogene Proteins, Viral - physiology</subject><subject>Papillomaviridae - genetics</subject><subject>Papillomaviridae - immunology</subject><subject>Papillomaviridae - metabolism</subject><subject>Papillomaviridae - physiology</subject><subject>Papillomavirus Infections - complications</subject><subject>Papillomavirus Infections - virology</subject><subject>Tumor Virus Infections - complications</subject><subject>Tumor Virus Infections - virology</subject><subject>Virus Replication</subject><issn>1052-9276</issn><issn>1099-1654</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp10MtKAzEUBuAgiq1VfAMZXOhCpiaZXGbcadG2WCsUL8uQziQ2dS416VT79qZMURAki5MDHz-HH4BjBLsIQnxpi1WXxPEOaCOYJCFilOxu_hSHCeasBQ6cm0OI_CP7oIUYjjmGpA2Gg7qQZbCQC5PnVSFXxtZOuatgKp1Jg0KlM1kaV7ig0l4tZ9WbKpUzLpBlFlRlutlNapbrQ7CnZe7U0XZ2wPPd7VNvEI4e-8Pe9ShMCedxSAkhUmfTTGlJOUOE6ZgRnCWUYsVIwinKYphpzViEYo6YxlRpzDVUEKZURh1w1uQubPVRK7cUhXGpynNZqqp2AnGME4ygh6d_4LyqbelvEyjhhEZxxDw6b1BqK-es0mJhTSHtWiAoNtUKX63w1Xp5so2rp4XKft22Sw8uGvBpcrX-L0dMHl6auLDRxi3V14-W9l0wHnEqXsd9cTNG_fvRZCRQ9A3OeZCn</recordid><startdate>200603</startdate><enddate>200603</enddate><creator>Hebner, Christy M.</creator><creator>Laimins, Laimonis A.</creator><general>John Wiley & Sons, Ltd</general><general>Wiley Periodicals Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope></search><sort><creationdate>200603</creationdate><title>Human papillomaviruses: basic mechanisms of pathogenesis and oncogenicity</title><author>Hebner, Christy M. ; 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| subjects | Capsid Proteins - physiology Female Human papillomavirus Humans Neoplasms - virology Oncogene Proteins, Viral - physiology Papillomaviridae - genetics Papillomaviridae - immunology Papillomaviridae - metabolism Papillomaviridae - physiology Papillomavirus Infections - complications Papillomavirus Infections - virology Tumor Virus Infections - complications Tumor Virus Infections - virology Virus Replication |
| title | Human papillomaviruses: basic mechanisms of pathogenesis and oncogenicity |
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