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Asthma and Viral Infections


Asthma is a chronic inflammatory respiratory disease characterized by airway hyperresponsiveness, inflammation, and remodeling. It is one of the most common chronic diseases, with a global prevalence of over 300 million. While asthma exacerbations can be triggered by various factors, viral infections, particularly respiratory viruses, are among the most common precipitants (Adeli M, et al. 2019). The relationship between viral infections and asthma exacerbations is complex and multifaceted, involving interactions between the immune system, airway epithelium, and viral pathogens. 

Viral Infections and Asthma Exacerbations:

Numerous respiratory viruses, including rhinovirus and influenza virus, are frequently implicated in asthma exacerbations. These viruses infect the respiratory epithelium, triggering an immune response characterized by the release of pro-inflammatory cytokines, chemokines, and other mediators. In individuals with asthma, this immune response is often exaggerated, leading to airway inflammation, bronchoconstriction, and increased mucus production (N. G. Hansbro et al., 2007).

Mechanisms of Virus-Induced Exacerbations:

Several mechanisms contribute to the exacerbation of asthma following viral infections. Firstly, viruses can directly infect airway epithelial cells, leading to cell damage and disruption of barrier function. This allows for increased penetration of allergens and other environmental triggers, exacerbating airway inflammation. Additionally, viral replication within epithelial cells stimulates the release of inflammatory cytokines, such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interferons, which further contribute to airway inflammation and hyperreactivity (C. Hammond, et al. 2015).

Furthermore, viral infections can dysregulate the host immune response, leading to an imbalance between pro-inflammatory and anti-inflammatory pathways. For example, viruses may inhibit the production of type I interferons, which are crucial for antiviral defense, while promoting the release of Th2 cytokines, such as interleukin-4 (IL-4) and interleukin-13 (IL-13), which are associated with asthma pathogenesis. This dysregulated immune response exacerbates airway inflammation and hyperresponsiveness in individuals with asthma (N. G. Hansbro et al., 2007).

Moreover, viral infections can disrupt the epithelial barrier and enhance the expression of adhesion molecules, such as intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), facilitating the recruitment of inflammatory cells, including eosinophils and neutrophils, to the airways. These inflammatory cells release cytotoxic mediators and proteases, causing further damage to the airway epithelium and exacerbating asthma symptoms (C. Hammond, et al. 2015).

Clinical Implications and Management:

Understanding the role of viral infections in asthma exacerbations has important clinical implications for the management of asthma. Firstly, recognizing the signs and symptoms of viral respiratory infections in individuals with asthma is crucial for early intervention and prevention of exacerbations. Symptoms such as increased cough, wheezing, shortness of breath, and fever may indicate a viral exacerbation of asthma and should prompt prompt evaluation and treatment (Adeli M, et al. 2019).

Treatment strategies for virus-induced exacerbations of asthma typically involve a combination of bronchodilators, such as short-acting beta-agonists (SABAs), and corticosteroids to reduce airway inflammation. In severe cases, systemic corticosteroids may be necessary to control symptoms and prevent further exacerbations. Additionally, antiviral medications, such as neuraminidase inhibitors (e.g., omalizumab), may be considered in certain cases, particularly to prevent fall asthma exacerbations (S. J. Teach et al, 2015).

Preventive measures, such as influenza vaccination and good hand hygiene, are also important for reducing the risk of viral exacerbations in individuals with asthma. Annual influenza vaccination is recommended for all individuals with asthma, as viral infections can significantly increase the risk of exacerbations during the influenza season. Moreover, practising good hand hygiene, avoiding close contact with individuals who are sick, and minimizing exposure to respiratory viruses can help reduce the risk of viral infections and subsequent exacerbations of asthma.


Viral infections play a significant role in exacerbating asthma symptoms and increasing the risk of asthma exacerbations. The complex interplay between respiratory viruses, the immune system, and the airway epithelium contributes to the pathogenesis of virus-induced exacerbations. Understanding these mechanisms is essential for developing effective strategies for the diagnosis, treatment, and prevention of viral exacerbations in individuals with asthma. By targeting the underlying mechanisms of virus-induced exacerbations, clinicians can optimize the management of asthma and improve outcomes for patients.


Article prepared by: Melisa Wong, MBIOS R&D Associate 23/24

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  1. Adeli M, El-Shareif T, Hendaus MA. Asthma exacerbation related to viral infections: An up to date summary. J Family Med Prim Care. 2019 Sep 30;8(9):2753-2759. doi: 10.4103/jfmpc.jfmpc_86_19. PMID: 31681638; PMCID: PMC6820381.

  2. Hammond, C., Kurten, M. & Kennedy, J.L. (2015) Rhinovirus and Asthma: a Storied History of Incompatibility. Current Allergy and Asthma Reports. [Online] 15 (2). Available from: doi:10.1007/s11882-014-0502-0.

  3. Hansbro, N.G., Horvat, J.C., Wark, P.A. & Hansbro, P.M. (2008) Understanding the mechanisms of viral induced asthma: New therapeutic directions. Pharmacology & Therapeutics. [Online] 117 (3), 313–353. Available from: doi:10.1016/j.pharmthera.2007.11.002.

  4. Teach, S.J., Gill, M.A., Togias, A., Sorkness, C.A., et al. (2015) Preseasonal treatment with either omalizumab or an inhaled corticosteroid boost to prevent fall asthma exacerbations. Journal of Allergy and Clinical Immunology. [Online] 136 (6), 1476–1485. Available from: doi:10.1016/j.jaci.2015.09.008.


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