Understanding the asthmatic response to rhinovirus and the effects of blocking IgE
Published online: February 1, 2020
Rhinovirus, the “common cold” virus, is associated with the majority of asthma exacerbations among children and young adults. Most of these exacerbations occur in asthmatics who are allergic during seasons of allergen exposure. Understanding how the interaction between allergen exposure and rhinovirus infections causes airway inflammation and restriction to air flow holds promise to guide the development of new treatments.
In clinical trials recently published in The Journal of Allergy and Clinical Immunology (JACI), Heymann and colleagues compared the response to rhinovirus in allergic asthmatics and healthy controls during an experimental infection. In a parallel study, the authors evaluated the effects of administering the anti-IgE biologic medication (omalizumab) to examine the effects of blocking IgE-mediated pathways. This intervention was of interest because of the known effectiveness of this treatment for preventing asthma attacks caused by naturally occurring rhinovirus infections in those with moderate to severe asthma. Participants in both clinical trials were carefully monitored for 3 weeks after virus inoculation with frequent assessments of upper and lower respiratory tract symptoms, lung function, blood counts, and virus load.
Early in the infection, rapid changes in lower respiratory tract symptoms, lung function, and blood eosinophil counts were observed. These changes were most prominent among asthmatics who were highly allergic and began before cold symptoms peaked. Administering the anti-IgE medication proved to be to most effective during the early phase of the infection. Additionally, the highly allergic asthmatics experienced significantly increased upper and lower respiratory tract symptoms, reduced lung function, and higher blood eosinophil counts three weeks after virus inoculation. Whether these late changes impart an increased risk for subsequent exacerbations and/or lead to further deterioration in lung function if left untreated warrants further investigation.
Results from these trials highlight that understanding the allergic status of asthmatic children and adults is critical for understanding the etiology of their symptoms caused by rhinovirus. In another recent article, Muehling, Woodfolk and colleagues report the comprehensive analysis of circulating rhinovirus-specific Th1 and allergen-specific Th2 cells from the subjects participating in these trials (Reference: JACI-D-19-01687). Their results highlight the capacity of rhinovirus to stimulate a robust virus-specific Th1 response that is likely to contribute to the pathogenesis of exacerbations and the persistence of chronic inflammation in the airway of those with allergic asthma.
The Journal of Allergy and Clinical Immunology (JACI) is an official scientific journal of the AAAAI, and is the most-cited journal in the field of allergy and clinical immunology.
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