Related Experiment Video

Updated: May 12, 2026

Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses
11:48

Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses

Published on: April 4, 2019

Dual inhibition of intercellular adhesion molecule-1 and nucleolin reduces RSV infection efficiency in human

Abeer Keshta1, Rina Hashimoto2, Yuki Kitai3

  • 1Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan.

Molecular Therapy. Nucleic Acids
|May 11, 2026
PubMed

Insights

Respiratory syncytial virus (RSV) infection in infants and older adults is a major concern. This study reveals that intercellular adhesion molecule-1 (ICAM-1) and nucleolin (NCL) are key host factors facilitating RSV infection.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Respiratory syncytial virus (RSV) causes significant lower respiratory tract infections, especially in vulnerable populations.
  • Host factors mediating RSV infection are not well understood.
  • Four host surface proteins (ICAM-1, EGFR, NCL, IGF1R) are hypothesized to interact with the RSV fusion (F) protein.

Purpose of the Study:

  • To investigate the roles of ICAM-1, EGFR, NCL, and IGF1R in RSV infection using a human iPSC-derived respiratory organoid model.
  • To determine the impact of suppressing these host factors on viral replication and protein expression.

Main Methods:

  • Utilized human induced pluripotent stem cell (iPSC)-derived respiratory organoids as a model for RSV infection.
  • Genetically depleted ICAM-1 and EGFR using CRISPR-Cas9.
  • Inhibited NCL and IGF1R using neutralizing antibodies.

Main Results:

  • Suppression of ICAM-1 or NCL significantly reduced RSV nucleoprotein gene expression.
  • Inhibition of EGFR or IGF1R showed no significant effect on viral gene expression.
  • Combined suppression of ICAM-1 and NCL led to a greater reduction in infectious viral titers and RSV F protein expression compared to single-protein inhibition.

Conclusions:

  • ICAM-1 and NCL are identified as important host factors in RSV infection within the studied organoid model.
  • Targeting ICAM-1 and NCL may offer a potential therapeutic strategy for RSV.
  • The iPSC-derived respiratory organoid model provides a relevant platform for studying RSV-host interactions.
Keywords:
CRISPR-Cas9ICAM-1MT: RNA/DNA editingNCLembryonic stem cellsinduced pluripotent stem cellsorganoidsrespiratory syncytial virus

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