Rhinovirus infection preferentially increases lower airway responsiveness in allergic subjects.

Abstract

Rhinovirus (RV) infections are important triggers of acute asthma symptoms in susceptible persons. To determine whether the presence of allergy is a risk factor for enhanced lower airway effects during RV infection, we experimentally infected (RV16) 18 volunteers with allergic rhinitis and 13 normal control subjects and measured the effects on the response of the lower airways to histamine. All subjects were successfully infected, as indicated by increased upper respiratory symptoms and RV16 cultured from nasal secretions. The change in histamine PD20(deltaPD20) caused by RV infection was significantly different in allergic subjects from that in nonallergic control subjects (deltaPD20 = -0.40 versus -0.03 log units, p = 0.04). This relationship was strengthened after adjusting for initial PD20 and FEV1 (mean deltaPD20 = -0.43 versus 0.01 log units, p < 0.01). The virus-induced deltaPD20 was also influenced by baseline lung function: there was a positive correlation between initial FEV1 and deltaPD20, and a weak but significant negative correlation between baseline PD20 and deltaPD20. These findings indicate that host factors such as allergy, baseline FEV1, and baseline PD20 influence the changes in lower airway physiology caused by RV infection and raise the possibility that these factors contribute to the increased lower airway effects of RV infection in subjects with asthma.

Infantile respiratory syncytial virus and human rhinovirus infections: respective role in inception and persistence of wheezing

“…Only 2 days after HRV serotype 16 inoculation, the authors demonstrated increased airway hyperresponsiveness that augmented at days 7 and 15, and correlated with worsening of the asthma symptom score [129]. Experimental inoculation of HRV serotype 16 in volunteers with respiratory allergy also increases airway hyperresponsiveness to inhaled histamine [130] and, similar to the observation for methacholine, the change in histamine response caused by rhinovirus infection seems to be more significant in allergic subjects compared with non-allergic control subjects [131]. These data further support the concept that the presence of atopy may contribute to increased lower airway effects of rhinovirus infection.…”

Thymic Stromal Lymphopoietin Gene Promoter Polymorphisms Are Associated with Susceptibility to Bronchial Asthma

“…A synergistic relationship is evident between viral infection and allergen sensitization and exposure in provoking exacerbations, and the major trigger for exacerbations in both children and adults is viral infection (27)(28)(29). Clinical studies suggest that patients with asthma are more susceptible to rhinovirus infections than normal individuals, and sustain a longer duration of lower respiratory tract symptoms when infected with rhinoviruses (30)(31)(32). TSLP appears to be involved in the development of bronchial asthma through functional genetic polymorphisms that may contribute to Th2-polarized immunity through higher TSLP production by bronchial epithelial cells in response to viral respiratory infections.…”

A Case‐Control Study of the Role of Cold Symptoms and other Historical Triggering Factors in Asthma Exacerbations

“…In adults, they have been shown to increase airway responsiveness, even in subjects without clinical asthma (5), especially in allergic subjects (6); in mice, viral infections can enhance airway sensitization to allergen (7). Some, but not all studies have shown an association with acute asthma exacerbations (8)(9)(10)(11), especially when newer, sensitive virological detection methods are used (8).…”