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Host cell transcriptome modification upon exogenous HPV16 L2 protein expression.

Xinwei An1, Yuhan Hao2,3, Patricio I Meneses1

  • 1Department of Biological Sciences, Fordham University, Bronx, New York, United States of America.

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|December 7, 2017
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Summary
This summary is machine-generated.

Human papillomavirus type 16 L2 protein alters cell cycle progression and gene expression in keratinocytes. This suggests L2 may regulate host cell transcription during viral replication.

Keywords:
HPV16 L2Pathology SectionRNA sequencingRb & Cdc2cell cycletranscriptome modification

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Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Human papillomavirus type 16 (HPV16) minor capsid protein L2 aids viral genome entry and trafficking.
  • Previous studies indicate L2's role in early viral infection stages.

Purpose of the Study:

  • To investigate the cellular effects of HPV16 L2 protein expression in keratinocytes.
  • To identify host cell genes and pathways affected by L2.

Main Methods:

  • Expression of HPV16 L2 in HaCaT keratinocyte cell line.
  • Cell cycle analysis (flow cytometry).
  • Western blotting for retinoblastoma protein (Rb) and Cdc2 phosphorylation.
  • Genome-wide host cell mRNA sequencing.
  • Machine learning and protein network analysis.

Main Results:

  • L2 expression induced a shift from G0/G1 to mitotic S phase in HaCaTs.
  • Reduced retinoblastoma protein (Rb) levels and increased Cdc2 phosphorylation were observed.
  • 2586 differentially expressed genes were identified upon L2 expression.
  • Genes related to cellular differentiation and proliferation were significantly impacted.

Conclusions:

  • HPV16 L2 protein influences keratinocyte cell cycle progression and gene expression.
  • L2 may prevent cellular differentiation while supporting DNA replication during viral production.
  • A novel function of L2 as a regulator of cellular gene transcription is proposed.