Uncommon and Rare Human Papillomavirus Genotypes Relating to Cervical Carcinomas

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Abstract

Background

Human papillomavirus (HPV) is an oncogenic virus in cervical cancer and most invasive carcinomas (ICs) are caused by HPV16 and 18. However, the roles and contributions of other uncommon and rare genotypes remain uncertain.

Methods

HPV genotypes were retrospectively assessed using an HPV DNA chip that can specify up to 32 HPV genotypes. We arbitrarily regarded genotypes accounting for less than 6% of the total as uncommon and rare genotypes.

Results

A total of 3,164 HPV-positive cases were enrolled. In groups 2A, 2B, 3, and unclassified HPV genotypes, 2.4% of cases with uncommon HPV genotypes (68, 26, 34, 53, 66, 69, 70, 73, 40, 42, 43, 44, 54, 55, 61, 62, 6, and 11) showed high grade squamous intraepithelial lesions and ICs. There were no HPV32- and 57-infected cases.

Conclusions

We found that the uncommon and rare HPV genotypes may provide incremental etiologic contributions in cervical carcinogenesis, especially HPV68, 70, and 53. Further studies on these uncommon and rare HPV genotypes will be of importance in establishing the significance of genotypes in different regions, especially in planning a strategy for further vaccine development as well as follow-up on the effectiveness of the currently used vaccines.

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Most cited references 16

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Cross-protective efficacy of HPV-16/18 AS04-adjuvanted vaccine against cervical infection and precancer caused by non-vaccine oncogenic HPV types: 4-year end-of-study analysis of the randomised, double-blind PATRICIA trial.

Cosette M. Wheeler, Xavier Castellsagué, Suzanne Garland … (2012)

We evaluated the efficacy of the human papillomavirus HPV-16/18 AS04-adjuvanted vaccine against non-vaccine oncogenic HPV types in the end-of-study analysis after 4 years of follow-up in PATRICIA (PApilloma TRIal against Cancer In young Adults). Healthy women aged 15-25 years with no more than six lifetime sexual partners were included in PATRICIA irrespective of their baseline HPV DNA status, HPV-16 or HPV-18 serostatus, or cytology. Women were randomly assigned (1:1) to HPV-16/18 vaccine or a control hepatitis A vaccine, via an internet-based central randomisation system using a minimisation algorithm to account for age ranges and study sites. The study was double-blind. The primary endpoint of PATRICIA has been reported previously; the present analysis evaluates cross-protective vaccine efficacy against non-vaccine oncogenic HPV types in the end-of-study analysis. Analyses were done for three cohorts: the according-to-protocol cohort for efficacy (ATP-E; vaccine n=8067, control n=8047), total vaccinated HPV-naive cohort (TVC-naive; no evidence of infection with 14 oncogenic HPV types at baseline, approximating young adolescents before sexual debut; vaccine n=5824, control n=5820), and the total vaccinated cohort (TVC; all women who received at least one vaccine dose, approximating catch-up populations that include sexually active women; vaccine n=9319, control=9325). Vaccine efficacy was evaluated against 6-month persistent infection, cervical intraepithelial neoplasia grade 2 or greater (CIN2+) associated with 12 non-vaccine HPV types (individually or as composite endpoints), and CIN3+ associated with the composite of 12 non-vaccine HPV types. This study is registered with ClinicalTrials.gov, number NCT00122681. Consistent vaccine efficacy against persistent infection and CIN2+ (with or without HPV-16/18 co-infection) was seen across cohorts for HPV-33, HPV-31, HPV-45, and HPV-51. In the most conservative analysis of vaccine efficacy against CIN2+, where all cases co-infected with HPV-16/18 were removed, vaccine efficacy was noted for HPV-33 in all cohorts, and for HPV-31 in the ATP-E and TVC-naive. Vaccine efficacy against CIN2+ associated with the composite of 12 non-vaccine HPV types (31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68), with or without HPV-16/18 co-infection, was 46·8% (95% CI 30·7-59·4) in the ATP-E, 56·2% (37·2-69·9) in the TVC-naive, and 34·2% (20·4-45·8) in the TVC. Corresponding values for CIN3+ were 73·8% (48·3-87·9), 91·4% (65·0-99·0), and 47·5% (22·8-64·8). Data from the end-of-study analysis of PATRICIA show cross-protective efficacy of the HPV-16/18 vaccine against four oncogenic non-vaccine HPV types-HPV-33, HPV-31, HPV-45, and HPV-51-in different trial cohorts representing diverse groups of women. GlaxoSmithKline Biologicals. Copyright © 2012 Elsevier Ltd. All rights reserved.

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Human papilloma viruses

Denise Galloway (2012)

A group of approximately 13 human papillomaviruses (HPVs) are responsible for virtually all cervical cancers as well as the majority of vulvar, vaginal anal and penile cancers, as well as at least half of oropharyngeal cancers. Currently two prophylactic vaccines are highly efficacious in preventing HPV 16 and 18 associated disease, and the quadrivalent vaccine also prevents HPV 6 and 11 warts. Currently therapeutic vaccines targeting the viral E6 and E7 oncogenes are being developed. One topic that will be discussed is whether the prophylactic vaccine can have utility in any setting where individuals are already infected. Secondly, this review will discuss the basis of long-term immunity and whether it is afforded by both vaccination and natural infection. Finally, strategies to provide more broad based coverage to other HPV types will be discussed.

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Multiple HPV infection in cervical cancer screened by HPVDNAChip.

Sang Lee, Daehee Kang, Sang Seo … (2003)

This study determined the distribution of high-risk HPV type infection in cervical cancer using newly developed oligonucleotide chips (HPVDNAChips). The study subjects included 80 cases of cervical neoplasia and 746 controls with a normal Pap smear. For HPV genotyping, the commercially available HPVDNAChips was used. The risk of cervical cancer was increased in women with a family history of cervical cancer (adjusted OR=2.3, 95% CI: 0.92-6.17) and in smokers (adjusted OR=3.2, 95% CI: 1.45-7.06). There was also a trend of increased risk with the number of full term pregnancies (P(for trend)<0.001). There were only 7.2% (54 of 746) infected high-risk HPV types in the control, whereas 54.5% (six of 11) and 76.5% (52 of 68) were infected in the CIN and cervical cancer, respectively. Multiple HPV infection was observed in 0.5% (three of 592) of the control group but in 9.1% (seven of 77) of cases. Multivariate analysis revealed that subjects infected with multiple HPV types had a 31.8-fold (95% CI: 7.50-134.75) higher risk of cervical cancer, while the single HPV type had a 19.9-fold increased risk (95% CI: 10.90-36.18) (P(for trend)<0.001). These results show that the detection and typing of HPV infection by HPVDNAChip can be a useful in clinical applications because it provides information on multiple infections and the types of HPV in addition to HPV infection status.

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Author and article information

Journal

Journal ID (nlm-ta): Korean J Pathol

Journal ID (iso-abbrev): Korean J Pathol

Journal ID (publisher-id): KJP

Title: Korean Journal of Pathology

Publisher: The Korean Society of Pathologists and The Korean Society for Cytopathology

ISSN (Print): 1738-1843

ISSN (Electronic): 2092-8920

Publication date (Print): February 2014

Publication date (Electronic): 25 February 2014

Volume: 48

Issue: 1

Pages: 43-49

Affiliations

Department of Pathology, Gachon University Gil Medical Center, Incheon, Korea.

[1 ]Department of Pathology, Gachon University School of Medicine, Incheon, Korea.

[2 ]Department of Obstetrics and Gynecology, Gachon University Gil Medical Center, Incheon, Korea.

Author notes

Corresponding Author: Hyun Yee Cho, M.D. Department of Pathology, Gachon University Gil Medical Center, 21 Namdong-daero 774beon-gil, Namdong-gu, Incheon 405-760, Korea. Tel: +82-32-460-3865, Fax: +82-32-460-2394, hicho@ 123456gilhospital.com

^*Na Rae Kim and Myunghee Kang contributed equally to this work.

Article

DOI: 10.4132/KoreanJPathol.2014.48.1.43

PMC ID: 3950234

PubMed ID: 24627694

SO-VID: 0937fcdd-10c0-4916-9591-5bad4e771ac4

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 24 July 2013

Date revision received : 24 November 2013

Date accepted : 11 December 2013

Funding

Funded by: The Gachon University Research Fund of 2013

Award ID: GCU-2012-M104

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Uncommon and Rare Human Papillomavirus Genotypes Relating to Cervical Carcinomas

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Abstract

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Point-of-Care Testing for HIV

Most cited references 16

Cross-protective efficacy of HPV-16/18 AS04-adjuvanted vaccine against cervical infection and precancer caused by non-vaccine oncogenic HPV types: 4-year end-of-study analysis of the randomised, double-blind PATRICIA trial.

Human papilloma viruses

Multiple HPV infection in cervical cancer screened by HPVDNAChip.

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Cited by 6

Most referenced authors 618