Abstract
Human rhinoviruses (HRVs), which are commonly associated with triggering asthma exacerbations, were reported to show persistent infection in asthmatic patients. While HRV-induced acute infection and the subsequent immune responses are well-studied, the mechanism of chronic HRV infection in contributing to chronic inflammation remains understudied. Therefore, we sought to investigate the virus loads at both the molecular level and the functional level during a prolong period of HRV infection in in vitro human nasal epithelial infection. By using a time-course study, the titer of both HRV RNA and infectious virus progeny, and the corresponding innate immune markers were quantified during a prolong infection period in the in vitro human nasal epithelial cells (hNECs) model. We found that the infectious virus progeny production only persisted up to 6dpi while HRV RNA were detected at high levels throughout the 14days infection period. While there was activation of antiviral IFNs (IFN-β1 and IFN-λ1) only during acute infection, upregulation of TLR3, key chemokines (RANTES, CXCL10, CXCL11) and anti-inflammatory cytokine IL10 were congruent with the production of infectious virus progeny up to 6dpi. On the other hand, the upregulation of TLR7, RIG-I and MDA5, and IRF7 persisted longer corresponding to HRV RNA persistence. Overall, our data showed the differential activation of immune signature following persistence of HRV infectious particles and RNA may be significant in differentiating active HRV chronic infections or persistence of HRV RNA in the upper airway.
Footnotes
Cite this article as: European Respiratory Journal 2019; 54: Suppl. 63, PA5439.
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- Copyright ©the authors 2019