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Papillomaviruses and potential copathogens

J A DiPaolo1, N C Popescu, C D Woodworth

  • 1Laboratory of Biology, National Cancer Institute, Bethesda MD 20892, USA.

Toxicology Letters
|November 1, 1996
PubMed
Summary
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A new in vitro model using human papillomavirus (HPV) DNA and genital cells mimics cervical cancer development. This model shows that while carcinogens cause DNA damage, only specific oncogenes and viruses like herpes virus-2 induce malignancy.

Area of Science:

  • Oncology
  • Virology
  • Cell Biology

Background:

  • Cervical cancer is a significant global health concern.
  • Human papillomavirus (HPV) is the primary cause of cervical cancer.
  • Developing accurate in vitro models is crucial for studying cervical carcinogenesis.

Purpose of the Study:

  • To develop a multistage in vitro model of cervical cancer.
  • To investigate the role of HPV and co-factors in malignant transformation.
  • To assess the response of the model to carcinogens and other viral infections.

Main Methods:

  • Genital epithelial cells were immortalized using recombinant HPV-16 DNA.
  • The immortalized cells were exposed to chemical carcinogens, Ras oncogene, and various herpesviruses (HHV-2, HHV-6, HIV).

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  • Malignant transformation and HPV expression were monitored.

    • Main Results:

    • HPV-16 immortalized cells responded to genotoxic carcinogens but did not become malignant.
    • Introduction of Ras oncogene or human herpes virus-2 led to malignant conversion.
    • Human herpes virus-6 increased HPV expression, while HIV did not infect the cells.

    Conclusions:

    • The developed in vitro model effectively parallels in vivo cervical neoplastic progression.
    • Specific co-factors, such as Ras oncogene and HHV-2, are critical for HPV-induced malignant transformation.
    • The model provides a valuable tool for investigating cervical cancer etiology and prevention strategies.