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Updated: Jun 12, 2026

An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
Palivizumab-resistant human respiratory syncytial virus infection in infancy
Ortwin Adams1, Linda Bonzel, Alexander Kovacevic
1Institute of Virology, University Children's Hospital, Heinrich-Heine University, Düsseldorf, Germany. ortwin.adams@uni-duesseldorf.de
Abstract:
Palivizumab-resistant respiratory syncytial virus was isolated from an infant treated with palivizumab. A stable mutation at codon 276 led to a nearly complete resistance to palivizumab. Additional studies revealed a second mutation at codon 272. Further passage of the virus led to a complete loss of binding of palivizumab.
Insights
Palivizumab-resistant respiratory syncytial virus (RSV) emerged in an infant receiving treatment. Mutations in the virus caused resistance to palivizumab, impacting its effectiveness.
Area of Science:
- Virology
- Immunology
- Antiviral Drug Development
Background:
- Respiratory Syncytial Virus (RSV) is a major cause of respiratory illness in infants.
- Palivizumab is a monoclonal antibody used for RSV prophylaxis.
- Viral resistance to therapeutic agents is a significant clinical concern.
Observation:
- RSV was isolated from an infant undergoing palivizumab therapy.
- The isolated virus exhibited reduced susceptibility to palivizumab.
- Viral evolution under selective pressure was observed.
Findings:
- A specific mutation at codon 276 conferred significant palivizumab resistance.
- A secondary mutation at codon 272 was identified.
- Extensive viral passage resulted in complete loss of palivizumab binding.
Implications:
- Emergence of palivizumab-resistant RSV poses a challenge to current prevention strategies.
- Understanding viral mutation pathways is crucial for developing next-generation antivirals.
- Monitoring viral resistance is essential for effective RSV treatment and control.
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