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Human papillomavirus 16 E6 oncoprotein binds to interferon regulatory factor-3 and inhibits its transcriptional

L V Ronco1, A Y Karpova, M Vidal

  • 1Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115 USA.

Genes & Development
|July 3, 1998
PubMed

Insights

Human papillomavirus type 16 E6 protein inhibits interferon regulatory factor-3 (IRF-3) activation. This interaction may help HPV16 evade the host

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Interferon regulatory factor-3 (IRF-3) is a key transcription factor in the innate immune response.
  • IRF-3 activation is crucial for antiviral defense, particularly against RNA viruses.
  • Human papillomavirus type 16 (HPV16) is a common oncogenic virus.

Purpose of the Study:

  • To investigate the interaction between HPV16 E6 and IRF-3.
  • To determine the functional consequences of this interaction on IRF-3 activity and antiviral response.

Main Methods:

  • Yeast two-hybrid screening to identify protein interactions.
  • Reporter assays to assess transcriptional activation.
  • Analysis of IFNbeta mRNA induction in primary human keratinocytes.

Main Results:

  • HPV16 E6 specifically interacts with IRF-3.
  • HPV16 E6 inhibits the transactivation function of IRF-3.
  • HPV16 E6 expression in keratinocytes suppresses Sendai virus-induced IFNbeta mRNA production.
  • The interaction does not lead to IRF-3 ubiquitination or degradation.

Conclusions:

  • HPV16 E6 antagonizes the antiviral activity of IRF-3.
  • This inhibition likely contributes to HPV16's immune evasion strategy in infected cells.

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