Viral coinfections account for ~10-30% of all respiratory viral infections. They are particularly prevalent in children and are thought to play a critical role in influencing susceptibility, disease severity and transmission. In previous studies, we showed that coinfection of a human-derived respiratory cell line with laboratory-adapted strains of influenza A virus (IAV) and respiratory syncytial virus (RSV) generated hybrid viral particles (HVPs). These HVPs exhibited structural changes that affected both antigenicity and receptor tropism, suggesting an important role in virus fitness. To determine if HVPs could be formed under more physiologically relevant conditions, we infected A549s and differentiated human bronchial epithelial cells (hBECs) with a prototype strain of RSV A2 and a clinical isolate of IAV H3N2, as well as with clinical isolates of RSV and IAV H1N1. Using confocal microscopy, we observed that A549s coinfected by both virus combinations displayed filamentous structures resembling HVPs. In separate experiments, we confirmed the presence of coinfected cells in hBECs, suggesting opportunities for the formation of HVPs in the human respiratory epithelium. Further, IAV H1N1 replicated at higher levels in the presence of RSV in both systems, likely as a result of syncytia formation. Our findings suggest that HVPs can be formed during natural coinfections, with potential implications for virus pathogenesis due to increased IAV replication. Understanding the impact of viral coinfections and specifically how RSV might be responsible for the enhancement of infectivity of other respiratory viruses could help improve diagnosis, treatment, and infection control, especially in children, in whom coinfections are common.