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Updated: Jun 2, 2026

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
13:41

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus

Published on: March 8, 2012

Human papillomavirus type-16 (HPV-16) major transforming proteins functionally interact with interferon signaling

S Perea1, O Lopezocejo, A Vongabain

  • 1UNIV VIENNA,DEPT CELL & MICROBIOL,INST MICROBIOL & GENET,A-1030 VIENNA,AUSTRIA.

International Journal of Oncology
|April 30, 2011
PubMed

Insights

Human papillomavirus (HPV) oncoproteins disrupt interferon (IFN) signaling pathways. This interference may contribute to HPV-induced cell transformation and resistance to IFN treatments.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • The interferon (IFN) system plays a crucial role in regulating cell growth and differentiation.
  • Human papillomavirus (HPV) infection is linked to cellular abnormalities and cancer development.

Purpose of the Study:

  • To investigate how HPV-16 E6 and E7 oncoproteins affect IFN signaling pathways.
  • To understand the molecular mechanisms underlying HPV's interaction with the IFN system.

Main Methods:

  • Cotransfection experiments were performed to assess the impact of HPV-16 oncoproteins on IFN signaling.
  • Reporter gene assays were used to measure the inducibility of IFN-beta and IFN-alpha promoters.
  • The function of STATs/IRFs and ISGF3 transcription factors was evaluated.

Main Results:

  • HPV-16 E6 and E7 oncoproteins differentially inhibited the inducibility of the IFN-beta promoter by Sendai virus.
  • Both viral oncoproteins significantly impaired the activation of a GBP ISRE reporter by IFN-gamma, indicating disruption of STATs/IRFs.
  • The inducibility of a 6-16 gene ISRE reporter by IFN-alpha was reduced, suggesting impaired ISGF3 function.

Conclusions:

  • HPV-16 oncoproteins negatively interact with cellular targets within the IFN system.
  • These interactions may play a role in HPV-mediated cellular transformation.
  • The disruption of IFN signaling by HPV-16 oncoproteins could explain the refractory response of HPV-infected cells to IFN treatment.

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