Rhinovirus (RV) is the main cause of asthma exacerbations in children. Some studies demonstrate that persons with asthma have attenuated interferon (IFN) responses to experimental RV infection compared to healthy individuals. However, responses to community-acquired RV infections in control and asthmatic children have not been compared.
To evaluate nasal cytokine responses following natural RV infections in asthmatic and healthy children.
We compared nasal cytokine expression among control and asthmatic children during healthy virus-negative surveillance weeks and self-reported RV-positive sick weeks. Fourteen control and 21 asthmatic subjects were studied. Asthma disease severity was based on symptoms and medication use. Viral genome was detected by multiplex PCR. Nasal cytokine protein levels were determined by multiplex assays.
Two out of 47 surveillance weeks tested positive for RV, showing an asymptomatic infection rate of 5%. Thirty-eight of 47 sick weeks (81%) tested positive for respiratory virus. Of these, 33 (87%) were positive for RV. During well weeks, nasal CXCL8, IL-12 and IL-1β levels were significantly higher in children with asthma than controls. Compared to healthy virus-negative surveillance weeks, CXCL8, IL-13 and IFN-β increased during colds only in asthmatic subjects. In both control and asthmatic children, nasal levels of IFN-γ, IFN-λ1, IL-1β, IL-8 and IL-10 significantly increased during RV-positive sick weeks. During RV infection, IL-8, IL-1β and TNF-α levels were strongly correlated.
In both controls and asthmatics, natural RV infection results in robust type II and III interferon responses.