Molecular variants of HPV‐16 associated with cervical cancer in Indian population
Human papilloma virus is a causative factor in the etiology of cervical cancer with HPV16 being the most prevalent genotype associated with it. Intratype variations in oncogenic E6/E7 and capsid L1 proteins of HPV 16 besides being of phylogenetic importance, are associated with risk of viral persist...
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| Veröffentlicht in: | International journal of cancer 2009-07, Vol.125 (1), p.91-103 |
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| creator | Pillai, M.R. Hariharan, R. Babu, Janki Mohan Lakshmi, S. Chiplunkar, S.V. Patkar, M. Tongaonkar, H. Dinshaw, K. Jayshree, R.S. Reddy, B.K.M. Siddiqui, M. Roychoudury, Soma Saha, Baisakhi Abraham, P. Gnanamony, M. Peedicayil, A. Subhashini, J. Ram, T.S. Dey, Bindu Sharma, C. Jain, S.K. Singh, N. |
| description | Human papilloma virus is a causative factor in the etiology of cervical cancer with HPV16 being the most prevalent genotype associated with it. Intratype variations in oncogenic E6/E7 and capsid L1 proteins of HPV 16 besides being of phylogenetic importance, are associated with risk of viral persistence and progression. The objective of this multicentric study was to identify HPV‐16 E6, E7 and L1 variants prevalent in India and their possible biological effects. Squamous cell cervical cancer biopsies were collected from 6 centres in India and examined for the presence of HPV 16. Variants of HPV‐16 were characterized by full length sequence analysis of L1, E6 and E7 genes in 412 samples. Similar distribution of the variants was seen from the different centres/regions, with the European variant E350G being the most prevalent (58%), followed by American Asian variant (11.4%). Fifty six changes were seen in E6 region, 31 being nonsynonymous. The most frequent being L83V (72.3%), Q14H (13.1%) and H78Y (12.1%). Twenty‐nine alterations were seen in E7 region, with 12 being nonsynonymous. The most frequent being F57V (9%). L1 region showed 204 changes, of which 67 were nonsynonymous. The most frequent being 448insS (100%), and 465delD (100%), H228D (94%), T292A (85%). The identified variants some new and some already reported can disrupt pentamer formation, transcriptional regulation of the virus, L1 protein interface interaction, B and T cell epitopes, p53 degradation, and thus their distribution is important for development of HPV diagnostics, vaccine, and for therapeutic purpose. © 2009 UICC |
| doi_str_mv | 10.1002/ijc.24322 |
| format | Article |
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Intratype variations in oncogenic E6/E7 and capsid L1 proteins of HPV 16 besides being of phylogenetic importance, are associated with risk of viral persistence and progression. The objective of this multicentric study was to identify HPV‐16 E6, E7 and L1 variants prevalent in India and their possible biological effects. Squamous cell cervical cancer biopsies were collected from 6 centres in India and examined for the presence of HPV 16. Variants of HPV‐16 were characterized by full length sequence analysis of L1, E6 and E7 genes in 412 samples. Similar distribution of the variants was seen from the different centres/regions, with the European variant E350G being the most prevalent (58%), followed by American Asian variant (11.4%). Fifty six changes were seen in E6 region, 31 being nonsynonymous. The most frequent being L83V (72.3%), Q14H (13.1%) and H78Y (12.1%). Twenty‐nine alterations were seen in E7 region, with 12 being nonsynonymous. The most frequent being F57V (9%). L1 region showed 204 changes, of which 67 were nonsynonymous. The most frequent being 448insS (100%), and 465delD (100%), H228D (94%), T292A (85%). The identified variants some new and some already reported can disrupt pentamer formation, transcriptional regulation of the virus, L1 protein interface interaction, B and T cell epitopes, p53 degradation, and thus their distribution is important for development of HPV diagnostics, vaccine, and for therapeutic purpose. © 2009 UICC</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.24322</identifier><identifier>PMID: 19358280</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Capsid Proteins - genetics ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - virology ; cervical cancer ; Female ; Female genital diseases ; Genetic Variation ; Gynecology. Andrology. Obstetrics ; human papilloma virus 16 ; Human papillomavirus 16 ; Human papillomavirus 16 - classification ; Human papillomavirus 16 - genetics ; Humans ; India ; Medical sciences ; Middle Aged ; Oncogene Proteins, Viral - genetics ; Papillomavirus E7 Proteins ; Papillomavirus Infections - epidemiology ; Papillomavirus Infections - genetics ; Papillomavirus Infections - virology ; Repressor Proteins - genetics ; Tropical medicine ; Tumors ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - virology ; variants</subject><ispartof>International journal of cancer, 2009-07, Vol.125 (1), p.91-103</ispartof><rights>Copyright © 2009 UICC</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4192-9dbb538c1788901a09db3bf616778933399db6ab6be5a0b79ebbdb46f3e1e1ee3</citedby><cites>FETCH-LOGICAL-c4192-9dbb538c1788901a09db3bf616778933399db6ab6be5a0b79ebbdb46f3e1e1ee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fijc.24322$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fijc.24322$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21440010$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19358280$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pillai, M.R.</creatorcontrib><creatorcontrib>Hariharan, R.</creatorcontrib><creatorcontrib>Babu, Janki Mohan</creatorcontrib><creatorcontrib>Lakshmi, S.</creatorcontrib><creatorcontrib>Chiplunkar, S.V.</creatorcontrib><creatorcontrib>Patkar, M.</creatorcontrib><creatorcontrib>Tongaonkar, H.</creatorcontrib><creatorcontrib>Dinshaw, K.</creatorcontrib><creatorcontrib>Jayshree, R.S.</creatorcontrib><creatorcontrib>Reddy, B.K.M.</creatorcontrib><creatorcontrib>Siddiqui, M.</creatorcontrib><creatorcontrib>Roychoudury, Soma</creatorcontrib><creatorcontrib>Saha, Baisakhi</creatorcontrib><creatorcontrib>Abraham, P.</creatorcontrib><creatorcontrib>Gnanamony, M.</creatorcontrib><creatorcontrib>Peedicayil, A.</creatorcontrib><creatorcontrib>Subhashini, J.</creatorcontrib><creatorcontrib>Ram, T.S.</creatorcontrib><creatorcontrib>Dey, Bindu</creatorcontrib><creatorcontrib>Sharma, C.</creatorcontrib><creatorcontrib>Jain, S.K.</creatorcontrib><creatorcontrib>Singh, N.</creatorcontrib><title>Molecular variants of HPV‐16 associated with cervical cancer in Indian population</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>Human papilloma virus is a causative factor in the etiology of cervical cancer with HPV16 being the most prevalent genotype associated with it. Intratype variations in oncogenic E6/E7 and capsid L1 proteins of HPV 16 besides being of phylogenetic importance, are associated with risk of viral persistence and progression. The objective of this multicentric study was to identify HPV‐16 E6, E7 and L1 variants prevalent in India and their possible biological effects. Squamous cell cervical cancer biopsies were collected from 6 centres in India and examined for the presence of HPV 16. Variants of HPV‐16 were characterized by full length sequence analysis of L1, E6 and E7 genes in 412 samples. Similar distribution of the variants was seen from the different centres/regions, with the European variant E350G being the most prevalent (58%), followed by American Asian variant (11.4%). Fifty six changes were seen in E6 region, 31 being nonsynonymous. The most frequent being L83V (72.3%), Q14H (13.1%) and H78Y (12.1%). Twenty‐nine alterations were seen in E7 region, with 12 being nonsynonymous. The most frequent being F57V (9%). L1 region showed 204 changes, of which 67 were nonsynonymous. The most frequent being 448insS (100%), and 465delD (100%), H228D (94%), T292A (85%). The identified variants some new and some already reported can disrupt pentamer formation, transcriptional regulation of the virus, L1 protein interface interaction, B and T cell epitopes, p53 degradation, and thus their distribution is important for development of HPV diagnostics, vaccine, and for therapeutic purpose. © 2009 UICC</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Capsid Proteins - genetics</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - virology</subject><subject>cervical cancer</subject><subject>Female</subject><subject>Female genital diseases</subject><subject>Genetic Variation</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>human papilloma virus 16</subject><subject>Human papillomavirus 16</subject><subject>Human papillomavirus 16 - classification</subject><subject>Human papillomavirus 16 - genetics</subject><subject>Humans</subject><subject>India</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Oncogene Proteins, Viral - genetics</subject><subject>Papillomavirus E7 Proteins</subject><subject>Papillomavirus Infections - epidemiology</subject><subject>Papillomavirus Infections - genetics</subject><subject>Papillomavirus Infections - virology</subject><subject>Repressor Proteins - genetics</subject><subject>Tropical medicine</subject><subject>Tumors</subject><subject>Uterine Cervical Neoplasms - genetics</subject><subject>Uterine Cervical Neoplasms - virology</subject><subject>variants</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkd9KwzAUh4Mobk4vfAHJjYIXnSdJm7aXMtRNJgr-uS1JmmJG19ak29idj-Az-iRmruiVSC5OOOfL78AXhI4JDAkAvTAzNaQho3QH9QmkcQCURLuo72cQxITxHjpwbgZASAThPuqRlEUJTaCPHu_qUqtFKSxeCmtE1TpcF3j88PL5_kE4Fs7VyohW53hl2lestF0aJUqsROXv2FR4UuX-HW7qxse0pq4O0V4hSqePujpAz9dXT6NxML2_mYwup4EKSUqDNJcyYokicZKkQAT4BpMFJzyOk5QxlvoGF5JLHQmQcaqlzGXIC6aJP5oN0Nk2t7H120K7Npsbp3RZikrXC5fxmEKUROxfkAJnkEDkwfMtqGztnNVF1lgzF3adEcg2qjOvOvtW7dmTLnQh5zr_JTu3HjjtAOG8scJ6Y8b9cJSEof-RDXex5Vam1Ou_N2aT29F29RecHpUg</recordid><startdate>20090701</startdate><enddate>20090701</enddate><creator>Pillai, M.R.</creator><creator>Hariharan, R.</creator><creator>Babu, Janki Mohan</creator><creator>Lakshmi, S.</creator><creator>Chiplunkar, S.V.</creator><creator>Patkar, M.</creator><creator>Tongaonkar, H.</creator><creator>Dinshaw, K.</creator><creator>Jayshree, R.S.</creator><creator>Reddy, B.K.M.</creator><creator>Siddiqui, M.</creator><creator>Roychoudury, Soma</creator><creator>Saha, Baisakhi</creator><creator>Abraham, P.</creator><creator>Gnanamony, M.</creator><creator>Peedicayil, A.</creator><creator>Subhashini, J.</creator><creator>Ram, T.S.</creator><creator>Dey, Bindu</creator><creator>Sharma, C.</creator><creator>Jain, S.K.</creator><creator>Singh, N.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Blackwell</general><scope>IQODW</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>7TO</scope><scope>7U1</scope><scope>7U2</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20090701</creationdate><title>Molecular variants of HPV‐16 associated with cervical cancer in Indian population</title><author>Pillai, M.R. ; Hariharan, R. ; Babu, Janki Mohan ; Lakshmi, S. ; Chiplunkar, S.V. ; Patkar, M. ; Tongaonkar, H. ; Dinshaw, K. ; Jayshree, R.S. ; Reddy, B.K.M. ; Siddiqui, M. ; Roychoudury, Soma ; Saha, Baisakhi ; Abraham, P. ; Gnanamony, M. ; Peedicayil, A. ; Subhashini, J. ; Ram, T.S. ; Dey, Bindu ; Sharma, C. ; Jain, S.K. ; Singh, N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4192-9dbb538c1788901a09db3bf616778933399db6ab6be5a0b79ebbdb46f3e1e1ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Capsid Proteins - genetics</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - virology</topic><topic>cervical cancer</topic><topic>Female</topic><topic>Female genital diseases</topic><topic>Genetic Variation</topic><topic>Gynecology. 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Intratype variations in oncogenic E6/E7 and capsid L1 proteins of HPV 16 besides being of phylogenetic importance, are associated with risk of viral persistence and progression. The objective of this multicentric study was to identify HPV‐16 E6, E7 and L1 variants prevalent in India and their possible biological effects. Squamous cell cervical cancer biopsies were collected from 6 centres in India and examined for the presence of HPV 16. Variants of HPV‐16 were characterized by full length sequence analysis of L1, E6 and E7 genes in 412 samples. Similar distribution of the variants was seen from the different centres/regions, with the European variant E350G being the most prevalent (58%), followed by American Asian variant (11.4%). Fifty six changes were seen in E6 region, 31 being nonsynonymous. The most frequent being L83V (72.3%), Q14H (13.1%) and H78Y (12.1%). Twenty‐nine alterations were seen in E7 region, with 12 being nonsynonymous. The most frequent being F57V (9%). L1 region showed 204 changes, of which 67 were nonsynonymous. The most frequent being 448insS (100%), and 465delD (100%), H228D (94%), T292A (85%). The identified variants some new and some already reported can disrupt pentamer formation, transcriptional regulation of the virus, L1 protein interface interaction, B and T cell epitopes, p53 degradation, and thus their distribution is important for development of HPV diagnostics, vaccine, and for therapeutic purpose. © 2009 UICC</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>19358280</pmid><doi>10.1002/ijc.24322</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of cancer, 2009-07, Vol.125 (1), p.91-103 |
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| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley Online Library All Journals |
| subjects | Adult Aged Aged, 80 and over Biological and medical sciences Capsid Proteins - genetics Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - virology cervical cancer Female Female genital diseases Genetic Variation Gynecology. Andrology. Obstetrics human papilloma virus 16 Human papillomavirus 16 Human papillomavirus 16 - classification Human papillomavirus 16 - genetics Humans India Medical sciences Middle Aged Oncogene Proteins, Viral - genetics Papillomavirus E7 Proteins Papillomavirus Infections - epidemiology Papillomavirus Infections - genetics Papillomavirus Infections - virology Repressor Proteins - genetics Tropical medicine Tumors Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - virology variants |
| title | Molecular variants of HPV‐16 associated with cervical cancer in Indian population |
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