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Induction of Filopodia During Cytomegalovirus Entry Into Human Iris Stromal Cells

Kenneth Chang1, Hardik Majmudar1, Ritesh Tandon2

  • 1Department of Microbiology and Immunology, College of Graduate Studies, Chicago College of Osteopathic Medicine, and Chicago College of Pharmacy, Midwestern University, Downers Grove, IL, United States.

Frontiers in Microbiology
|April 22, 2022
PubMed

Insights

Human cytomegalovirus (HCMV) infection significantly increases filopodia, which are crucial for viral entry. The HCMV glycoprotein B (gB) and 3-O sulfated heparan sulfate (3-OS HS) receptor interact to promote this process.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Viruses frequently utilize cellular structures like filopodia for infection and spread.
  • Human cytomegalovirus (HCMV) is a significant pathogen with complex entry mechanisms.
  • Filopodia are dynamic actin-rich cell projections involved in cell adhesion and migration.

Purpose of the Study:

  • To investigate the role of filopodia in HCMV entry into human iris stromal (HIS) cells.
  • To elucidate the involvement of HCMV glycoprotein B (gB) and heparan sulfate (HS) in filopodia formation during infection.
  • To determine the specific contribution of 3-O sulfated HS (3-OS HS) in HCMV-induced filopodia.

Main Methods:

  • Primary culture of human iris stromal (HIS) cells.
  • Confocal microscopy to visualize virions and filopodia.
  • Actin filament depolymerization experiments.
  • Transient expression of HCMV gB and 3-O sulfotransferase-3 (3-OST-3) in cells.
  • Treatment with anti-3-OS HS peptide (G2) and heparinase-I.

Main Results:

  • HCMV infection significantly increased filopodia formation in HIS cells.
  • Virions were observed associated with filopodia prior to cell entry.
  • HCMV gB expression induced filopodia, with enhanced induction in cells expressing 3-OST-3 and wild-type HS.
  • Inhibition of actin polymerization and disruption of 3-OS HS signaling reduced HCMV entry and filopodia counts.

Conclusions:

  • HCMV actively modulates the actin cytoskeleton via filopodia for efficient cell entry into HIS cells.
  • HCMV glycoprotein B (gB) plays a key role in triggering filopodia formation.
  • The 3-O sulfated heparan sulfate (3-OS HS) receptor likely collaborates with gB to enhance HCMV infectivity through filopodia.
Keywords:
3-O sulfated heparan sulfateactin cytoskeletal networkheparan sulfatevirus cell to cell spreadvirus entry

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