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Streptococcus pneumoniae is a leading cause of acute respiratory infection and invasive disease in all ages. Nasopharyngeal carriage is a necessary step preceding any pneumococcal disease. However, S pneumoniae is also a normal part of the microbiome of the upper respiratory tract in early childhood, and children constantly acquire and clear carriage, mostly without incident. This apparent paradox suggests that other factors beyond nasopharyngeal carriage play an important role in the pathogenesis of pneumococcal disease.1 Epidemiological, clinical, and experimental evidence suggests that certain respiratory viruses may have a substantial role in the burden of pneumococcal disease.1-4 However, most of the evidence for either coinfections or virus-induced pneumococcal secondary infections in children has been derived from observational epidemiological studies reporting association, which does not demonstrate a causative relationship. Interventions such as vaccination can unveil interactions between pathogens. A randomized clinical trial5 of a pneumococcal conjugate vaccine demonstrated reductions in pneumonia hospitalizations that were believed to be caused by viruses. Likewise, the widespread implementation of pneumococcal conjugate vaccines had considerable consequences for the rates of viral lower respiratory tract infections in infants and toddlers.1,4 Although these interventions against pneumococcus have revealed a role for the bacteria in viral pneumonia, there has not been an opportunity to observe the reverse consequences of an intervention against viruses with regard to the burden of pneumococcal disease. The respiratory viruses most commonly implicated in the burden of pneumococcal disease (namely respiratory syncytial virus [RSV], influenza, human metapneumovirus, and parainfluenza) typically share seasonality with pneumococcal disease, and vaccines that could substantially reduce the circulation of these viruses have not yet been introduced or widely administered. The COVID-19 pandemic that emerged in early 2020 disrupted the transmission of many respiratory pathogens and provided an opportunity to probe interactions. For several months, RSV, influenza, and human metapneumovirus largely disappeared around the world. At the same time, reduced rates of pneumococcal disease were reported in many countries, with patterns resembling those of the respiratory viruses.1,3,6-9 The unusual patterns of both viral and pneumococcal diseases were mostly associated with nonpharmaceutical interventions that were intended to limit the spread of SARS-CoV-2. Elsewhere in JAMA Network Open, Rybak and colleagues3 shed new light on the potential role of 2 respiratory viruses, RSV and influenza, in the pathogenesis of invasive pneumococcal disease (IPD) in children. The authors conducted an impressive multicenter study using several nationwide prospective surveillance programs in France, including a multiple-hospital IPD surveillance system, a national continuous surveillance program involving children in 70 metropolitan areas, a national continuous surveillance system of influenza-like illness (as a proxy for influenza cases, which can also capture the activity of other respiratory viruses), and a national laboratory surveillance program for RSV cases. The authors applied a quasi-experimental interrupted time series analysis to assess the changes in these outcomes after the implementation of nonpharmaceutical interventions. They then estimated the fraction of the change in IPD that was associated with RSV and influenza-like illness vs the fraction of change associated with pneumococcal carriage alone by fitting a quasi-Poisson regressive model. They observed a decrease of 63% (95% CI, −82% to −43%; P < .001) in IPD incidence but, notably, pneumococcal carriage rates were not significantly reduced (−12%; 95% CI, + Related article