Related Experiment Video
Updated: Jul 7, 2025

Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses
Published on: April 4, 2019
RSV Induces Activation of Intracellular EGFR on the Mitochondrial Membrane for Virus Propagation
Se Sil Noh1,2,3, Hye Jin Shin1,2,4
1Department of Microbiology, School of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Abstract:
Respiratory syncytial virus (RSV) infects people of all ages and is one of the most common causative agents of lower respiratory tract infections, such as pneumonia, especially in infants under one year of age. However, no direct treatment has been developed for RSV infections. Maintenance of mitochondrial homeostasis and epidermal growth factor receptor (EGFR) activity is important for human cell growth. This study reported that RSV infection maintained the total cellular ATP levels and promoted the intracellular activity of EGFR to replicate RSV. RSV activates the intracellular EGFR-mediated cell survival signaling cascade and maintains mitochondrial EGFR expression for viral production during early events after infection. The approved EGFR inhibitor, vandetanib, markedly reduces RSV propagation, suggesting that EGFR is an attractive host target for RSV therapeutics. Our results suggest that RSV infection maintains cellular ATP levels and promotes the activation of intracellular EGFR in the mitochondrial membrane, significantly contributing to robust RSV propagation.
Insights
Respiratory syncytial virus (RSV) promotes its replication by activating epidermal growth factor receptor (EGFR) signaling and maintaining cellular ATP levels. Targeting EGFR with drugs like vandetanib may offer new treatments for RSV infections.
Area of Science:
- Virology
- Cellular Biology
- Molecular Medicine
Background:
- Respiratory syncytial virus (RSV) is a major cause of lower respiratory tract infections, particularly in infants.
- Currently, no specific antiviral treatment exists for RSV infections.
- Cellular homeostasis, including mitochondrial function and epidermal growth factor receptor (EGFR) activity, is crucial for cell survival and growth.
Purpose of the Study:
- To investigate the role of EGFR signaling and cellular energy metabolism in RSV replication.
- To identify potential host-targeting strategies for developing RSV therapeutics.
Main Methods:
- The study analyzed cellular ATP levels and EGFR activity in RSV-infected cells.
- The effect of the EGFR inhibitor vandetanib on RSV propagation was assessed.
- Mitochondrial EGFR expression and its role in viral production were examined.
Main Results:
- RSV infection was found to maintain cellular ATP levels.
- RSV actively promotes intracellular EGFR activity, particularly within mitochondria, to facilitate viral replication.
- The EGFR inhibitor vandetanib significantly inhibited RSV propagation in vitro.
- EGFR activation appears to be a key component of the cell survival signaling cascade initiated by RSV.
Conclusions:
- RSV hijacks host cell machinery, specifically EGFR signaling and ATP maintenance, for its own propagation.
- EGFR represents a promising host-directed therapeutic target for combating RSV infections.
- Targeting host factors like EGFR offers a potential strategy to develop novel antiviral therapies against RSV.
More Related Videos
Related Concept Videos
Rous Sarcoma Virus (RSV) and Cancer
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
MAPK Signaling Cascades
Mechanisms of Retrovirus-induced Cancers
Retrovirus Life Cycles
The Ras Gene
Ras is a...
Rab Proteins
Rab proteins switch between a cytosolic, GDP-bound inactive state and a membrane-anchored, GTP-bound active state. By themselves, Rabs show slow rates of GDP/GTP exchange and GTP hydrolysis. Thus, Rab proteins are considered...

