<i>Pseudomonas aeruginosa</i> rhamnolipids stabilize human rhinovirus 14 virions

Many mammalian viruses encounter bacteria and bacterial molecules over the course of infection. Previous work has shown that the microbial ecology of the gut plays an integral role in poliovirus and coxsackievirus infection, where bacterial glycans can facilitate virus-receptor interactions, enhance viral replication, and stabilize viral particles. However, how airway bacteria alter respiratory viral infection is less understood. Therefore, we investigated whether a panel of airway bacteria affects rhinovirus stability. We found that <i>Pseudomonas aeruginosa,</i> an opportunistic airway pathogen, protects human rhinovirus 14 (HRV14) from acid or heat inactivation. Further investigation revealed that <i>P. aeruginosa</i> rhamnolipids, glycolipids with surfactant properties, are necessary and sufficient for stabilization of rhinovirus virions. However, airway bacteria did not stabilize HRV16, a distantly related rhinovirus with higher capsid stability. Taken together, this work demonstrates that specific molecules produced by an opportunistic airway pathogen can influence a respiratory virus.IMPORTANCEBacteria can enhance viral stability and infection for enteric members of the <i>Picornaviridae</i>, such as poliovirus and coxsackievirus; however, whether bacteria influence respiratory picornaviruses is unknown. In this study, we examined the impacts of airway bacteria on rhinovirus, a major etiological agent of the common cold. We found that <i>Pseudomonas aeruginosa</i> protects human rhinovirus 14 from both acid and heat inactivation through rhamnolipids. Overall, this work demonstrates bacterial effects on respiratory viruses through specific bacterial molecules.