HPV 16 infection and progression of cervical intra-epithelial neoplasia: analysis of HLA polymorphism and HPV 16 E6 sequence variants.

2.50
Hdl Handle:
http://hdl.handle.net/10541/93010
Title:
HPV 16 infection and progression of cervical intra-epithelial neoplasia: analysis of HLA polymorphism and HPV 16 E6 sequence variants.
Authors:
Bontkes, H J; Van Duin, M; De Gruijl, T D; Duggan-Keen, Margaret F; Walboomers, J M; Stukart, M J; Verheijen, R H; Helmerhorst, T J; Meijer, C J; Scheper, R J; Stevens, F R Adam; Dyer, P A; Sinnott, P; Stern, Peter L
Abstract:
High-risk human papillomavirus (HPV) infection plays an important role in cervical intra-epithelial neoplasia (CIN), but HPV infection alone is not sufficient for progression to cervical cancer. Several lines of evidence suggest that cellular immune surveillance is important in the control of HPV infection and the development of CIN. The presentation to T cells of target viral peptides in the context of HLA molecules is influenced by the genetic polymorphisms of both HPV and HLA and thereby influences the host immune response and clinical outcome of HPV infection. HLA class I and II polymorphism in susceptibility for HPV 16 infection, development and progression of CIN was analyzed in a group of 118 patients participating in a prospective study of women with initial abnormal cytology. Patients were stratified according to HPV status and course of the disease. HLA-B*44 frequency was increased in the small group of patients with a lesion that showed clinical progression during follow-up [OR = 9.0 (4.6-17.5), p = 0.007]. HLA-DRB1*07 frequency was increased among HPV 16-positive patients compared with patients who were negative for all HPV types [OR = 5.9 (3.0-11.3), p = 0.02]. Our results are consistent with the immunogenetic factors associated with disease progression being different from those associated with susceptibility to HPV 16 infection. Sequencing of the HPV 16 E6 and E7 open reading frames of a subset of these patients (n = 40) showed the frequency of HPV 16 variants to be similar to other studies. However, there was no significant correlation between variant incidence and disease progression or viral persistence and no significant correlation with any HLA allele. It appears that multiple HLA types can influence HPV 16-associated cervical dysplasia but the role of HPV 16 variants in disease progression and susceptibility in relation to HLA polymorphism remains unclear.
Affiliation:
Department of Pathology, Free University Hospital, Amsterdam, The Netherlands.
Citation:
HPV 16 infection and progression of cervical intra-epithelial neoplasia: analysis of HLA polymorphism and HPV 16 E6 sequence variants. 1998, 78 (2):166-71 Int. J. Cancer
Journal:
International Journal of Cancer
Issue Date:
5-Oct-1998
URI:
http://hdl.handle.net/10541/93010
PubMed ID:
9754647
Type:
Article
Language:
en
ISSN:
0020-7136
Appears in Collections:
All Paterson Institute for Cancer Research

Full metadata record

DC FieldValue Language
dc.contributor.authorBontkes, H Jen
dc.contributor.authorVan Duin, Men
dc.contributor.authorDe Gruijl, T Den
dc.contributor.authorDuggan-Keen, Margaret Fen
dc.contributor.authorWalboomers, J Men
dc.contributor.authorStukart, M Jen
dc.contributor.authorVerheijen, R Hen
dc.contributor.authorHelmerhorst, T Jen
dc.contributor.authorMeijer, C Jen
dc.contributor.authorScheper, R Jen
dc.contributor.authorStevens, F R Adamen
dc.contributor.authorDyer, P Aen
dc.contributor.authorSinnott, Pen
dc.contributor.authorStern, Peter Len
dc.date.accessioned2010-02-25T12:25:43Z-
dc.date.available2010-02-25T12:25:43Z-
dc.date.issued1998-10-05-
dc.identifier.citationHPV 16 infection and progression of cervical intra-epithelial neoplasia: analysis of HLA polymorphism and HPV 16 E6 sequence variants. 1998, 78 (2):166-71 Int. J. Canceren
dc.identifier.issn0020-7136-
dc.identifier.pmid9754647-
dc.identifier.urihttp://hdl.handle.net/10541/93010-
dc.description.abstractHigh-risk human papillomavirus (HPV) infection plays an important role in cervical intra-epithelial neoplasia (CIN), but HPV infection alone is not sufficient for progression to cervical cancer. Several lines of evidence suggest that cellular immune surveillance is important in the control of HPV infection and the development of CIN. The presentation to T cells of target viral peptides in the context of HLA molecules is influenced by the genetic polymorphisms of both HPV and HLA and thereby influences the host immune response and clinical outcome of HPV infection. HLA class I and II polymorphism in susceptibility for HPV 16 infection, development and progression of CIN was analyzed in a group of 118 patients participating in a prospective study of women with initial abnormal cytology. Patients were stratified according to HPV status and course of the disease. HLA-B*44 frequency was increased in the small group of patients with a lesion that showed clinical progression during follow-up [OR = 9.0 (4.6-17.5), p = 0.007]. HLA-DRB1*07 frequency was increased among HPV 16-positive patients compared with patients who were negative for all HPV types [OR = 5.9 (3.0-11.3), p = 0.02]. Our results are consistent with the immunogenetic factors associated with disease progression being different from those associated with susceptibility to HPV 16 infection. Sequencing of the HPV 16 E6 and E7 open reading frames of a subset of these patients (n = 40) showed the frequency of HPV 16 variants to be similar to other studies. However, there was no significant correlation between variant incidence and disease progression or viral persistence and no significant correlation with any HLA allele. It appears that multiple HLA types can influence HPV 16-associated cervical dysplasia but the role of HPV 16 variants in disease progression and susceptibility in relation to HLA polymorphism remains unclear.en
dc.language.isoenen
dc.subjectTumour Virus Infectionsen
dc.subjectUterine Cervical Canceren
dc.subject.meshAdult-
dc.subject.meshAlleles-
dc.subject.meshCervical Intraepithelial Neoplasia-
dc.subject.meshDisease Progression-
dc.subject.meshFemale-
dc.subject.meshGenetic Variation-
dc.subject.meshGenotype-
dc.subject.meshHistocompatibility Antigens Class I-
dc.subject.meshHistocompatibility Antigens Class II-
dc.subject.meshHumans-
dc.subject.meshMiddle Aged-
dc.subject.meshOncogene Proteins, Viral-
dc.subject.meshOpen Reading Frames-
dc.subject.meshPapillomaviridae-
dc.subject.meshPapillomavirus Infections-
dc.subject.meshPolymorphism, Genetic-
dc.subject.meshProspective Studies-
dc.subject.meshRepressor Proteins-
dc.subject.meshTumor Virus Infections-
dc.subject.meshUterine Cervical Neoplasms-
dc.titleHPV 16 infection and progression of cervical intra-epithelial neoplasia: analysis of HLA polymorphism and HPV 16 E6 sequence variants.en
dc.typeArticleen
dc.contributor.departmentDepartment of Pathology, Free University Hospital, Amsterdam, The Netherlands.en
dc.identifier.journalInternational Journal of Canceren

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