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Host cell restriction factors that limit transcription and replication of human papillomavirus

Samuel S Porter1, Wesley H Stepp2, James D Stamos2

  • 1Laboratory of Viral Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, 33 North Drive, MSC3209, Bethesda, MD 20892, USA; Biological Sciences Graduate Program, University of Maryland, University of Maryland, 4066 Campus Drive, College Park, MD 20742, USA.

Virus Research
|November 20, 2016
PubMed

Insights

Human papillomaviruses (HPV) life cycles depend on keratinocyte differentiation. Cellular restriction factors combat HPV, but viral proteins can overcome them, leading to persistent infections.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Human papillomaviruses (HPV) infect keratinocytes, with their life cycle linked to host cell differentiation.
  • Cellular restriction factors are crucial in limiting viral gene expression and replication.
  • HPV has evolved mechanisms to counteract these cellular defenses.

Purpose of the Study:

  • To review the role of nuclear restriction factors in the human papillomavirus infectious cycle.
  • To elucidate the interplay between HPV and cellular restriction factors.

Main Methods:

  • This review synthesizes existing research on nuclear restriction factors and HPV.
  • Analysis of literature detailing the molecular mechanisms of restriction factor interaction with HPV.

Main Results:

  • Nuclear restriction factors directly inhibit HPV gene expression and replication.
  • HPV oncoproteins actively target and neutralize restriction factors.
  • The balance between HPV and restriction factors can paradoxically promote persistent infection.

Conclusions:

  • Nuclear restriction factors are key regulators of the HPV infectious cycle.
  • Understanding this host-pathogen interaction is vital for developing antiviral strategies.
  • Targeting the interplay between HPV and restriction factors may offer therapeutic avenues.
Keywords:
HPVIFI16IFIT1Intrinsic immunityRestriction factorSp100

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