Viral Contributions to Asthma Exacerbations

Asthma exacerbations are frequently precipitated by respiratory viral infections, with rhinoviruses and respiratory syncytial virus representing the most common agents. Viral challenge of the airway epithelium disrupts barrier integrity and provokes an exaggerated inflammatory response in susceptible individuals. Deficient production of type I and III interferons by airway epithelial cells leads to delayed viral clearance and persistent inflammation, while activation of innate immune complexes such as the RIG-I inflammasome further amplifies cytokine release. Genetic predispositions—including risk variants in epithelial cell genes—interact with viral triggers to drive childhood-onset disease. Environmental cofactors, such as allergen exposure, can prime epithelial inflammasomes and suppress early antiviral defences, creating a feed-forward loop of airway hyperresponsiveness. Understanding these virus–host interactions is critical for the development of therapies that restore antiviral immunity, limit airway inflammation and reduce the global burden of virus-induced asthma crises.

Research from Nature Portfolio

Recent studies have demonstrated that rhinovirus infection in asthma patients activates the epithelial RIG-I inflammasome to such an extent that it hinders access of type I/III interferon pathways, resulting in prolonged viral persistence and unresolved inflammation. Pre-exposure to common aeroallergens intensifies this effect by priming the inflammasome and further suppressing early interferon responses. Co-infection sequences, for example rhinovirus followed by SARS-CoV-2, bolster RIG-I-driven epithelial inflammation. Selective inhibition of the RIG-I inflammasome in airway models has been shown to accelerate viral clearance and attenuate inflammation, offering a promising strategy for managing virus-induced asthma exacerbations.

Viral Contributions to Asthma Exacerbations publication trend

The graph below shows the total number of articles in viral contributions to asthma exacerbations across all publications each year (not limited to Nature Index journals).

Technical terms

Rhinovirus: A non-enveloped RNA virus that is the predominant cause of common colds and asthma exacerbations.

RIG-I inflammasome: A cytosolic sensor complex that recognises viral RNA and initiates inflammatory cytokine release.

Interferons (Type I/III): Families of cytokines critical for antiviral defence, upregulating genes that inhibit viral replication.

Pattern recognition receptor: Innate immune receptor that detects pathogen-associated molecular patterns to trigger host defences.

Airway epithelial cells: The lining cells of the respiratory tract that act as a physical barrier and immune sentinel against inhaled pathogens.

References

1. Rhinovirus-induced epithelial RIG-I inflammasome suppresses antiviral immunity and promotes inflammation in asthma and COVID-19. Nature Communications (2023).
2. Rhinovirus infection of airway epithelial cells uncovers the non-ciliated subset as a likely driver of genetic risk to childhood-onset asthma. Cell Genomics (2024).
3. Emerging role for interferons in respiratory viral infections and childhood asthma. Frontiers in Immunology (2023).
4. Role of viruses in asthma. Seminars in Immunopathology (2020).