The human papillomavirus 16 E5 gene potentiates MmuPV1-Dependent pathogenesis
The papillomavirus E5 gene contributes to transformation and tumorigenesis; however, its exact function in these processes and viral pathogenesis is unclear. While E5 is present in high-risk mucosotropic HPVs that cause anogenital and head and neck cancers, it is absent in cutaneous HPVs and the rec...
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description | The papillomavirus E5 gene contributes to transformation and tumorigenesis; however, its exact function in these processes and viral pathogenesis is unclear. While E5 is present in high-risk mucosotropic HPVs that cause anogenital and head and neck cancers, it is absent in cutaneous HPVs and the recently discovered mouse papillomavirus (MmuPV1), which causes papillomas and squamous cell carcinomas of the skin and mucosal epithelia in laboratory mice. We infected K14E5 transgenic mice, which express the high-risk mucosotropic HPV16 E5 gene in stratified epithelia, with MmuPV1 to investigate the effects of E5 on papillomavirus-induced pathogenesis. Skin lesions in MmuPV1-infected K14E5 mice had earlier onset, higher incidence, and reduced frequency of spontaneous regression compared to those in non-transgenic mice. K14E5 mice were also more susceptible to cervicovaginal cancers when infected with MmuPV1 and treated with estrogen compared to non-transgenic mice. Our studies support the hypothesis that E5 contributes to papillomavirus-induced pathogenesis. |
doi_str_mv | 10.1016/j.virol.2019.12.002 |
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While E5 is present in high-risk mucosotropic HPVs that cause anogenital and head and neck cancers, it is absent in cutaneous HPVs and the recently discovered mouse papillomavirus (MmuPV1), which causes papillomas and squamous cell carcinomas of the skin and mucosal epithelia in laboratory mice. We infected K14E5 transgenic mice, which express the high-risk mucosotropic HPV16 E5 gene in stratified epithelia, with MmuPV1 to investigate the effects of E5 on papillomavirus-induced pathogenesis. Skin lesions in MmuPV1-infected K14E5 mice had earlier onset, higher incidence, and reduced frequency of spontaneous regression compared to those in non-transgenic mice. K14E5 mice were also more susceptible to cervicovaginal cancers when infected with MmuPV1 and treated with estrogen compared to non-transgenic mice. 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While E5 is present in high-risk mucosotropic HPVs that cause anogenital and head and neck cancers, it is absent in cutaneous HPVs and the recently discovered mouse papillomavirus (MmuPV1), which causes papillomas and squamous cell carcinomas of the skin and mucosal epithelia in laboratory mice. We infected K14E5 transgenic mice, which express the high-risk mucosotropic HPV16 E5 gene in stratified epithelia, with MmuPV1 to investigate the effects of E5 on papillomavirus-induced pathogenesis. Skin lesions in MmuPV1-infected K14E5 mice had earlier onset, higher incidence, and reduced frequency of spontaneous regression compared to those in non-transgenic mice. K14E5 mice were also more susceptible to cervicovaginal cancers when infected with MmuPV1 and treated with estrogen compared to non-transgenic mice. Our studies support the hypothesis that E5 contributes to papillomavirus-induced pathogenesis.</description><subject>Animals</subject><subject>Carcinoma, Squamous Cell - etiology</subject><subject>Carcinoma, Squamous Cell - virology</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Life Sciences & Biomedicine</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Mouse papillomavirus</subject><subject>Oncogene</subject><subject>Oncogene Proteins, Viral - genetics</subject><subject>Oncogene Proteins, Viral - physiology</subject><subject>Papillomavirus Infections - etiology</subject><subject>Pathogenesis</subject><subject>Science & Technology</subject><subject>Skin Neoplasms - etiology</subject><subject>Skin Neoplasms - virology</subject><subject>Virology</subject><issn>0042-6822</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><sourceid>EIF</sourceid><recordid>eNqNkV-L1DAUxYMo7rj6CQTpoyAdb27Spn1QkHH9A7vow-pryKS3OxnapjbpiN_e1BkHfRGfQpLfOTk3h7GnHNYcePlyvz64yXdrBF6vOa4B8B5bcajLHITk99kKQGJeVogX7FEIe0h7peAhuxC8wrKSfMVubneU7ebeDNloRtd1vjfJdg4ZL7OrIrujgbLRRxqiM5FCdtPPn7_y_C2NNDTpNMnizi9YcOExe9CaLtCT03rJvry7ut18yK8_vf-4eXOdW1nUMRdqWxuLBTeqbluSogJUqkBOaQbVYllCTaJslAUFha2BGymVQdUINIBCXLLXR99x3vbU2JRjMp0eJ9eb6Yf2xum_bwa303f-oBWgTN-QDJ6fDCb_baYQde-Cpa4zA_k5aBRYYF1JtaDiiNrJhzBRe36Gg16K0Hv9qwi9FKE56jREUj37M-FZ8_vnE_DiCHynrW-DdTRYOmMpY8El8npJCwtd_T-9cdFE54eNn4eYpK-OUkqFHBxN-iRv3EQ26sa7f07yE0RZur0</recordid><startdate>20200201</startdate><enddate>20200201</enddate><creator>Torres, Alexandra D.</creator><creator>Spurgeon, Megan E.</creator><creator>Bilger, Andrea</creator><creator>Blaine-Sauer, Simon</creator><creator>Uberoi, Aayushi</creator><creator>Buehler, Darya</creator><creator>McGregor, Stephanie M.</creator><creator>Ward-Shaw, Ella</creator><creator>Lambert, Paul F.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6027-1409</orcidid><orcidid>https://orcid.org/0000-0002-2389-5957</orcidid></search><sort><creationdate>20200201</creationdate><title>The human papillomavirus 16 E5 gene potentiates MmuPV1-Dependent pathogenesis</title><author>Torres, Alexandra D. ; Spurgeon, Megan E. ; Bilger, Andrea ; Blaine-Sauer, Simon ; Uberoi, Aayushi ; Buehler, Darya ; McGregor, Stephanie M. ; Ward-Shaw, Ella ; Lambert, Paul F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-37b9ac251a79ffe4380277521e0027f26609e36d7c0705c901a447a27d32a0233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Carcinoma, Squamous Cell - etiology</topic><topic>Carcinoma, Squamous Cell - virology</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>Life Sciences & Biomedicine</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Mouse papillomavirus</topic><topic>Oncogene</topic><topic>Oncogene Proteins, Viral - genetics</topic><topic>Oncogene Proteins, Viral - physiology</topic><topic>Papillomavirus Infections - etiology</topic><topic>Pathogenesis</topic><topic>Science & Technology</topic><topic>Skin Neoplasms - etiology</topic><topic>Skin Neoplasms - virology</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Torres, Alexandra D.</creatorcontrib><creatorcontrib>Spurgeon, Megan E.</creatorcontrib><creatorcontrib>Bilger, Andrea</creatorcontrib><creatorcontrib>Blaine-Sauer, Simon</creatorcontrib><creatorcontrib>Uberoi, Aayushi</creatorcontrib><creatorcontrib>Buehler, Darya</creatorcontrib><creatorcontrib>McGregor, Stephanie M.</creatorcontrib><creatorcontrib>Ward-Shaw, Ella</creatorcontrib><creatorcontrib>Lambert, Paul F.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Virology (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Torres, Alexandra D.</au><au>Spurgeon, Megan E.</au><au>Bilger, Andrea</au><au>Blaine-Sauer, Simon</au><au>Uberoi, Aayushi</au><au>Buehler, Darya</au><au>McGregor, Stephanie M.</au><au>Ward-Shaw, Ella</au><au>Lambert, Paul F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The human papillomavirus 16 E5 gene potentiates MmuPV1-Dependent pathogenesis</atitle><jtitle>Virology (New York, N.Y.)</jtitle><stitle>VIROLOGY</stitle><addtitle>Virology</addtitle><date>2020-02-01</date><risdate>2020</risdate><volume>541</volume><spage>1</spage><epage>12</epage><pages>1-12</pages><issn>0042-6822</issn><eissn>1096-0341</eissn><abstract>The papillomavirus E5 gene contributes to transformation and tumorigenesis; however, its exact function in these processes and viral pathogenesis is unclear. While E5 is present in high-risk mucosotropic HPVs that cause anogenital and head and neck cancers, it is absent in cutaneous HPVs and the recently discovered mouse papillomavirus (MmuPV1), which causes papillomas and squamous cell carcinomas of the skin and mucosal epithelia in laboratory mice. We infected K14E5 transgenic mice, which express the high-risk mucosotropic HPV16 E5 gene in stratified epithelia, with MmuPV1 to investigate the effects of E5 on papillomavirus-induced pathogenesis. Skin lesions in MmuPV1-infected K14E5 mice had earlier onset, higher incidence, and reduced frequency of spontaneous regression compared to those in non-transgenic mice. K14E5 mice were also more susceptible to cervicovaginal cancers when infected with MmuPV1 and treated with estrogen compared to non-transgenic mice. 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subjects | Animals Carcinoma, Squamous Cell - etiology Carcinoma, Squamous Cell - virology Human papillomavirus Humans Life Sciences & Biomedicine Mice Mice, Transgenic Mouse papillomavirus Oncogene Oncogene Proteins, Viral - genetics Oncogene Proteins, Viral - physiology Papillomavirus Infections - etiology Pathogenesis Science & Technology Skin Neoplasms - etiology Skin Neoplasms - virology Virology |
title | The human papillomavirus 16 E5 gene potentiates MmuPV1-Dependent pathogenesis |
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