Interferon response depends on viral transcription in human papillomavirus-containing lesions

Anticancer Res. Nov-Dec 1995;15(6B):2865-9.


Human papillomaviruses (HPVs) express various proteins which have been proven to interact with some cellular functions playing a role in cell cycle progression and differentiation. Therefore, these viral gene products might be candidates for interfering with IFN-mediated antiproliferative actions. Condyloma biopsies from patients subsequently demonstrated to be responsive or non-responsive to IFN treatment were investigated. mRNA levels of HPV genes and IFN-responsive genes were determined by RT-PCR and correlated with IFN responsiveness. Patients clinically nonresponsive to IFN demonstrated a characteristic HPV transcriptional activity differing from responder patients. Nonresponders expressed mostly early E7 mRNAs; responders demonstrated higher expression of the late L1 gene. This differential transcription of infecting HPV also correlated with the extent of IFN mediated antiproliferative effect. A hypothesis for further study is that HPV E7 may inhibit IFN responsiveness, while HPV L1 may promote IFN responsiveness.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antiviral Agents / pharmacology
  • Antiviral Agents / therapeutic use*
  • Condylomata Acuminata / therapy*
  • Condylomata Acuminata / virology
  • Drug Resistance
  • Gene Expression Regulation, Viral / drug effects*
  • Genes, Viral
  • Humans
  • Interferon alpha-2
  • Interferon-alpha / pharmacology
  • Interferon-alpha / therapeutic use*
  • Oncogene Proteins, Viral / biosynthesis
  • Oncogene Proteins, Viral / genetics*
  • Papillomaviridae / drug effects
  • Papillomaviridae / genetics*
  • Papillomaviridae / physiology
  • Papillomavirus Infections / therapy*
  • Papillomavirus Infections / virology
  • Polymerase Chain Reaction
  • RNA, Messenger / biosynthesis
  • RNA, Viral / biosynthesis
  • Recombinant Proteins
  • Transcription, Genetic*
  • Tumor Virus Infections / therapy*
  • Tumor Virus Infections / virology


  • Antiviral Agents
  • Interferon alpha-2
  • Interferon-alpha
  • Oncogene Proteins, Viral
  • RNA, Messenger
  • RNA, Viral
  • Recombinant Proteins