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Peer-reviewedCC BYViruses

Respiratory Syncytial Virus Infection: Enhanced Reactive Oxygen Species Production and Weakened Antioxidant Defenses Worsen Disease Severity.

  • Oliviero Sacco1
  • Paola Borgia1
  • Giorgia M Rossi2
  • Angelo Florio1
  • Giovanni A Rossi1
  1. 1Pediatric Pulmonology and Respiratory Endoscopy Unit, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Istituto Giannina Gaslini, 16147 Genoa, Italy.
  2. 2Department of Internal Medicine, Università di Genova, 16132 Genova, Italy.
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Abstract

Respiratory syncytial virus (RSV) is a leading cause of severe respiratory infections in infants and young children globally. The severity of RSV-associated diseases is often ascribed to a dysregulated immune response, characterized by increased secretion of proinflammatory proteins and ineffective T helper type 2 (Th2) cell activity. The host's primary defense against RSV relies on a well-coordinated innate immune response initiated by resident airway epithelial cells, the first target of RSV infection. These cells respond to viral invasion by generating reactive oxygen species (ROS), activating the production of Type I and III interferons, and releasing proinflammatory cytokines and chemokines. Moderate levels of ROS act as key molecules that regulate antiviral signaling, enhancing the host's ability to recognize and eliminate invading pathogens. However, severe RSV infection disrupts cellular homeostasis triggering excessive ROS production, while simultaneously weakening the host's antioxidant defenses. This redox imbalance subverts the activity of key cellular defensive mechanisms, ultimately increasing viral replication, and worsening RSV infection severity. Modulation of oxidative stress may offer an innovative approach in managing the progression and outcome of RSV infection.

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Cite

BibTeXRIS
BibTeX
@article{sacco2026respiratory,
  title = {{Respiratory Syncytial Virus Infection: Enhanced Reactive Oxygen Species Production and Weakened Antioxidant Defenses Worsen Disease Severity.}},
  author = {Oliviero Sacco and Paola Borgia and Giorgia M Rossi and Angelo Florio and Giovanni A Rossi},
  journal = {Viruses},
  year = {2026},
  month = oct,
  doi = {10.3390/v18101146},
  url = {https://europepmc.org/article/MED/42944065},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Respiratory Syncytial Virus Infection: Enhanced Reactive Oxygen Species Production and Weakened Antioxidant Defenses Worsen Disease Severity.
AU  - Oliviero Sacco
AU  - Paola Borgia
AU  - Giorgia M Rossi
AU  - Angelo Florio
AU  - Giovanni A Rossi
PY  - 2026
DA  - 2026/10/15
JO  - Viruses
DO  - 10.3390/v18101146
UR  - https://europepmc.org/article/MED/42944065
AB  - Respiratory syncytial virus (RSV) is a leading cause of severe respiratory infections in infants and young children globally. The severity of RSV-associated diseases is often ascribed to a dysregulated immune response, characterized by increased secretion of proinflammatory proteins and ineffective T helper type 2 (Th2) cell activity. The host's primary defense against RSV relies on a well-coordinated innate immune response initiated by resident airway epithelial cells, the first target of RSV infection. These cells respond to viral invasion by generating reactive oxygen species (ROS), activating the production of Type I and III interferons, and releasing proinflammatory cytokines and chemokines. Moderate levels of ROS act as key molecules that regulate antiviral signaling, enhancing the host's ability to recognize and eliminate invading pathogens. However, severe RSV infection disrupts cellular homeostasis triggering excessive ROS production, while simultaneously weakening the host's antioxidant defenses. This redox imbalance subverts the activity of key cellular defensive mechanisms, ultimately increasing viral replication, and worsening RSV infection severity. Modulation of oxidative stress may offer an innovative approach in managing the progression and outcome of RSV infection.
SN  - 1999-4915
ER  -