https://www.selleckchem.com/products/AZD0530.html
Strikingly, the RV response in PCLS was reflective of gene expression changes described in COPD and asthma patients. While RV-induced host immune responses were abrogated by rupintrivir, RV-triggered epithelial processes were largely refractory to antiviral treatment. Detailed analysis of RV-infected human PCLS and comparison with COPD and asthma patient gene signatures revealed that the human RV PCLS model represents disease relevant biological mechanisms that can be partially inhibited by a well-known antiviral compound and provide an
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