Papillomavirus E2 protein is regulated by specific fibroblast growth factor receptors

Marsha DeSmet1, Sriramana Kanginakudru1, Leny Jose1

  • 1Department of Dermatology, Indiana University School of Medicine, Indianapolis, IN, USA.

Virology
|June 10, 2018
PubMed

Insights

Fibroblast growth factor receptors (FGFRs) interact with papillomavirus (PV) E2 proteins, influencing viral replication. Different FGFRs associate with various PV types, suggesting a role in regulating viral activity in epithelial cells.

Area of Science:

  • Virology
  • Molecular Biology
  • Cellular Biology

Background:

  • The papillomavirus (PV) E2 protein is crucial for viral transcription and replication.
  • Phosphorylation of tyrosine 102 in bovine papillomavirus (BPV-1) E2 by fibroblast growth factor receptor-3 (FGFR3) inhibits these functions.
  • FGFR3's effect on viral replication suggested another kinase targets Y102.

Purpose of the Study:

  • To investigate the association of FGFR1, FGFR2, and FGFR4 with PV E2 proteins.
  • To determine if FGFR2-mediated suppression of viral replication depends on Y102 phosphorylation.
  • To explore interactions between human papillomavirus (HPV) E2 proteins and FGFRs.

Main Methods:

  • Co-immunoprecipitation assays to test protein interactions.
  • Replication assays to assess viral activity.
  • Analysis of interactions between different HPV types (HPV-16, HPV-31) and FGFRs.

Main Results:

  • FGFR2, but not FGFR1 or FGFR4, co-immunoprecipitated with BPV-1 E2.
  • FGFR2 suppressed BPV-1 replication independently of Y102 phosphorylation.
  • HPV-16 and HPV-31 E2 proteins interacted with FGFR1, FGFR2, and FGFR4.

Conclusions:

  • FGF receptors exhibit differential interactions with PV E2 proteins from various viral types.
  • FGFR2 can regulate PV replication through mechanisms not solely dependent on Y102 phosphorylation.
  • FGFR expression and activity in epithelial cells may control PV E2 function and viral replication.

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