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Presence of E6 and E7 mRNA from Human Papillomavirus Types 16, 18, 31, 33, and 45 in the Majority of Cervical Carcinomas

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Kraus, Irene, Molden, Tor, Holm, Ruth, Lie, A. Kathrine, Karlsen, Frank, Kristensen, Gunnar B., Skomedal, Hanne·2006·Journal of Clinical Microbiology
DOI 10.1128/jcm.44.4.1310-1317.2006PMC PMC1448674
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Abstract

The oncogenic potential of the human papillomavirus (HPV) early genes E6 and E7 is well established and a source of interest with regard to HPV testing for cervical carcinoma. Here we present a study performed with 204 histologically confirmed invasive cervical squamous cell carcinomas (SCCs) in which we evaluated the HPV E6 and E7 mRNA detection assay PreTect HPV-Proofer for detection of high-risk HPV types 16, 18, 31, 33, and 45. For further evaluation, detection of E6 and E7 mRNA from HPV types 35, 52, and 58 by real-time multiplex nucleic acid sequence-based amplification was also included. For comparison and to assess the overall prevalence of various HPV types, samples were also tested for HPV DNA by both consensus and type-specific PCR, reverse line blotting, sequencing, and in situ hybridization. The overall prevalence of HPV was 97%. HPV E6 and E7 transcripts were detected in 188 of 204 (92%) biopsy specimens, of which 181 contained one of the following HPV types: 16, 18, 31, 33, or 45. Consensus PCR and type-specific PCR detected HPV in 187 of 204 and 188 of 204 (92%) specimens, respectively. In conclusion, this study verifies the presence of HPV E6 and E7 mRNA in SCCs and demonstrates that HPV infections among Norwegian women with SCCs are limited mainly to the five high-risk types, 16, 18, 31, 33, and 45. This, together with the fact that PreTect HPV-Proofer detects the HPV oncogenic transcripts, suggests that the assay is a valuable approach in the field of HPV detection in cervical carcinoma.

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  • Nearly all cervical cancers harbour HPV DNA, particularly oncogenic sequences such as E6 and E7.

    “Nearly all cervical cancers harbour HPV DNA, particularly oncogenic sequences such as E6 and E7, emphasizing the causal role of persistent HPV infection in cervical carcinogenesis [5, 6].”

    From HPV Screening in Women Living with HIV (WLHIV) in Karnataka, India: Can it be Integrated into ART Centres? (2025) · cites this paper as [6]

    The Abstract reports 97% overall HPV prevalence in 204 invasive cervical squamous cell carcinomas, with HPV DNA detected by each PCR method in about 92% and E6/E7 transcripts detected in 92%. It also identifies E6 and E7 as oncogenic HPV genes. The claim extends these findings from squamous cell carcinomas to cervical cancers generally, which this study did not assess. (LLM, conf=0.84)

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  • Cervical HPV infection is common and typically clears or becomes latent within two years, but a subset of infections persists.

    “While cervical HPV infection is common and typically clears or becomes latent within two years, a subset of infections persists [6, 7].”

    From HPV Screening in Women Living with HIV (WLHIV) in Karnataka, India: Can it be Integrated into ART Centres? (2025) · cites this paper as [6]

    The Abstract says the lifetime risk of HPV infection is 80% and discusses identifying persistent infections; the Discussion says most cervical viral infections produce transient low-grade lesions. These passages support common infection, a typically transient course, and persistence in some cases. They do not say that infections clear or become latent within two years. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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Authors
Kraus, I., Molden, T., Holm, R., Lie, A. K., Karlsen, F., Kristensen, G. B., & Skomedal, H.
Affiliations
  • Institute of Pathology, National University Hospital, 0027 Oslo, Norway
  • Oslo University Hospital (NO)
  • Department of Pathology, Norwegian Radium Hospital, 0310 Oslo, Norway
  • NorChip (Norway) (NO)
  • Department of Gynaecologic Oncology, Norwegian Radium Hospital, 0310 Oslo, Norway
Corresponding author
Molden, Tor
ORCID
Venue
Journal of Clinical Microbiology
Publisher
American Society for Microbiology
Published
2006-04
Volume
44
Issue
4
Pages
1310-1317
ISSN
  • 0095-1137 (ISSN-L)
  • 1098-660X
DOI
10.1128/jcm.44.4.1310-1317.2006
PMC
PMC1448674
OpenAlex
W2163110120
Cited by
123
References
0
Citations by year
2026: 1 · 2025: 2 · 2024: 4 · 2023: 3 · 2022: 3 · 2021: 4 · 2019: 5 · 2018: 2 · 2017: 2 · 2016: 5 · 2015: 9 · 2014: 8 · 2013: 8 · 2012: 8
FWCI
9.07
Type
journal article
Language
en
Open access
Licence
journals.asm.org/non-commercial-tdm-license (tdm)
Locations
  • Journal of Clinical Microbiology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
Norges Forskningsråd (145316/213)
Topics
  • Health Sciences › Medicine › Epidemiology › Cervical Cancer and HPV Research
  • Health Sciences › Medicine › Otorhinolaryngology › Head and Neck Cancer Studies
  • Life Sciences › Immunology and Microbiology › Microbiology › Reproductive tract infections research
Keywords
human papillomavirus, cervical squamous cell carcinoma, high-risk HPV, HPV16, HPV 18, HPV 31, HPV 33, HPV45, HPV prevalence
MeSH terms
Carcinoma, Squamous Cell, Cell Line, Uterine Cervical Dysplasia, Uterine Cervical Neoplasms, DNA, Viral, Female, HeLa Cells, Humans, Oncogene Proteins, Viral, RNA, Messenger, RNA, Viral, Vaginal Smears, Papillomaviridae, Papillomavirus Infections

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