Host response of rhinovirus infection among hospitalized adult patients

Abstract

Severe disease due to human rhinovirus (HRV) infection is most frequently caused by the exacerbation of underlying lung disease such as asthma and chronic obstructive pulmonary disease. Although most commonly detected in patients with community acquired pneumonia, HRV is less likely to cause direct virus-induced tissue damage than other respiratory viruses. In addition to pulmonary disease, HRV has been associated with severe extrapulmonary complications, such as the triggering of seizure and diabetic ketoacidosis. In order to better understand the pathogenesis of severe HRV infection, we compared the host response of HRV infection with influenza A virus (FluA) and influenza B virus (FluB) infection among hospitalized patients. We measured and analyzed the levels of 29 cytokines/chemokines on the plasma samples of 68 aged and sex-matched hospitalized adult patients using MILLIPLEX MAP Chemokine Magnetic Bead Panel Premixed 29 Plex (Merck Millipore, USA). The levels of IFN-2 (P = 0.028), IL-10 (P = 0.038), IL-5 (P = 0.025) and IP-10 (P < 0.001) were significantly different among the 3 groups (Figure 1). The levels of IP-10 were significantly lower for the HRV group than that of FluA group or FluB group. The levels of IFN-2 were significantly lower in the HRV group than those of the FluB group, while the levels of IL-5 were significantly higher in the HRV group than those of the FluB group. The levels of IL-10 were significantly lower in the HRV group than that of the FluA group. There were no significant differences in the levels of other cytokines/chemokines tested. Our results suggest that HRV infection triggers a unique cytokine/chemokine profile when compared with FluA or FluB infection.