Anti-viral activity of acetylsalicylic acid against human rhinovirus 14 infection involves suppression of VP3 expression and infection-dependent down-regulation of CD54

Abstract

Human rhinoviruses are known to cause mild upper respiratory tract infections. They are also now known to cause severe laryngotracheitis and play an important role in triggering asthma attacks. An anti-viral drug against rhinoviruses viruses would be helpful. Acetylsalicylic acid (ASA) might be such a candidate with proven activity against several RNA viruses in vitro and in vivo. ASA was initially mentioned as an anti-inflammatory compound. Viral infections are often accompanied by inflammatory processes. In this study, the anti-viral and anti-inflammatory activities of ASA were examined using the HeLa rhinovirus-infection model. Human rhinovirus (HRV14, major group) infection was quantified by flow cytometry using a monoclonal antibody against the major capsid protein HRV-VP3 in combination with analysis of surface expression of CD54, a key molecule involved in the initiation of an immune response. Our in vitro studies demonstrate on a single cell level HRV14 infection-dependent intra-cellular expression of the HRV-VP3 protein. This expression correlated with HRV14 infection severity and could be dose-dependently blocked with ASA. Further, infection-dependent VP3 expression correlated with a down-regulation of surface antigen expression of CD54. This CD54 down-regulation could also be dose-dependently blocked by ASA supporting the anti-viral efficacy of ASA.