This finding underscores HPIV3 as another key inducer of bacterial co-infections, corroborating clinical observations by Johnson et al. (2008) (Johnson et al., 2008), RSV and HPIV3 facilitated bacterial adhesion primarily through overexpression of ICAM-1 and PAFr, while CEACAM-1 played a minor role in Hib binding and was irrelevant for S. pneumoniae adherence. Here, ICAM1 is linked to coinfection.