Beyond RSV: why the bronchiolitis burden in infants will not simply disappear.

Nirsevimab and maternal respiratory syncytial virus (RSV) vaccination are delivering real-world important reductions in RSV-bronchiolitis hospitalisations, a landmark achievement in paediatric preventive medicine. We argue, however, that these successes should not be mistaken for the resolution of severe bronchiolitis as a clinical and public health problem. First, RSV's epidemiological dominance may partly reflect its transmission efficiency rather than a unique pathogenic superiority: rhinovirus, human metapneumovirus, adenovirus, and bocavirus already cause substantial disease, and genetic variants in CDHR3, GSDMB, and innate immune genes indicate that host susceptibility, not pathogen identity, is a key driver of severity. Second, although current evidence does not support viral replacement, the possibility that other respiratory viruses could expand into the ecological niche vacated by suppressed RSV transmission warrants close monitoring, alongside the theoretical, fitness-limited risk of nirsevimab-resistant RSV escape variants. Third, important gaps remain in long-term virological surveillance, cost-effectiveness evaluation, and equitable global access, particularly for the low- and middle-income countries that bear over 97% of RSV-attributable mortality. Conclusion: We contend that bronchiolitis should be understood as a syndrome reflecting the infant airway's stereotyped response to viral injury, rather than a disease defined by a single pathogen. Sustained broad-spectrum surveillance, transparent cost-effectiveness monitoring, and continued investment in a pan-respiratory mucosal vaccine pipeline are needed to ensure that early success against RSV translates into a durable reduction of the overall infant bronchiolitis burden. What is Known: • Nirsevimab and maternal RSV vaccination are producing substantial real-world reductions in RSV-bronchiolitis hospitalisations, a major success in paediatric preventive medicine. What is New: • We argue that the control of RSV does not equate to the control of severe infant bronchiolitis. Other respiratory viruses-rhinovirus, human metapneumovirus, adenovirus and bocavirus-already cause substantial disease and could expand into the ecological niche left by suppressed RSV transmission, while host genetic susceptibility, not pathogen identity, remains a key driver of severity. We call for sustained broad spectrum viral surveillance to ensure that success against RSV translates into a durable reduction of the overall bronchiolitis burden, rather than its replacement by other pathogens.