Human papillomavirus infection: biology, epidemiology, and prevention

Authors

  • M.E. SCHEURER,

    1. Department of Epidemiology, University of Texas M. D. Anderson Cancer Center, Houston, Texas
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  • G. TORTOLERO-LUNA,

    Corresponding author
    1. Division of Environmental and Occupational Health, University of Texas School of Public Health at Houston, Houston, Texas, and Department of Gynecologic Oncology, University of Texas M. D. Anderson Cancer Center, Houston, Texas
      Address correspondence and reprint requests to: Guillermo Tortolero-Luna, MD, PhD, Associate Professor, Division of Environmental and Occupational Health, UT School of Public Health at Houston, UCT 2574, 7000 Fannin, Houston, TX 77030, USA. E-mail: Guillermo.Tortolero@uth.tmc.edu
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  • K. ADLER-STORTHZ

    1. Department of Diagnostic Sciences, University of Texas Dental Branch at Houston, Houston, Texas
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Address correspondence and reprint requests to: Guillermo Tortolero-Luna, MD, PhD, Associate Professor, Division of Environmental and Occupational Health, UT School of Public Health at Houston, UCT 2574, 7000 Fannin, Houston, TX 77030, USA. E-mail: Guillermo.Tortolero@uth.tmc.edu

Abstract

Abstract.  Scheurer ME, Tortolero-Luna G, Adler-Storthz K. Human papillomavirus infection: biology, epidemiology, and prevention. Int J Gynecol Cancer 2005;15:727–746.

Over the past several decades, knowledge of the biology and epidemiology of human papillomavirus (HPV) infection has increased tremendously. However, there are still many unanswered questions concerning the interaction of the virus with its host. The virus has been identified as a necessary causal agent for cervical squamous neoplasia and has been linked to the development of neoplasia in several other mucosal sites. The viral oncogenes E6 and E7 are the major players in the virus’ scheme to evade the immune system and use the host cell replication machinery to survive. Many risk factors for infection with HPV have been identified; however, the focus now centers on identifying risk factors for persistence of the infection as it is likely that transient infections play a very small role in the overall development of clinical disease. Prevention measures to date have centered around screening programs, mostly for cervical cancer, including the perfection of screening techniques and inclusion of molecular testing for HPV into screening regimens. The development of prophylactic and therapeutic vaccines has also increased as primary prevention measures appear to have the best hope for long-term effects on cancer incidence.

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