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Original citation: J Clin Invest. 2019;129(10):4523-4538. https://doi.org/10.1172/JCI128865. Citation for this erratum: J Clin Invest. 2022;132(11):e161565. https://doi.org/10.1172/JCI161565. During the preparation of this manuscript, the labels for Figure 5, A and D, [...]

BACKGROUND. Although recent epidemiological data suggest that pneumococci may contribute to the risk of SARS-CoV-2 disease, cases of coinfection with Streptococcus pneumoniae in patients with coronavirus disease 2019 (COVID-19) during hospitalization have been reported infrequently. This apparent contradiction may be explained by interactions of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and pneumococci in the upper airway, resulting in the escape of SARS-CoV-2 from protective host immune responses. METHODS. Here, we investigated the relationship of these 2 respiratory pathogens in 2 distinct cohorts of health care workers with asymptomatic or mildly symptomatic SARS-CoV-2 infection identified by systematic screening and patients with moderate to severe disease who presented to the hospital. We assessed the effect of coinfection on host antibody, cellular, and inflammatory responses to the virus. RESULTS. In both cohorts, pneumococcal colonization was associated with diminished antiviral immune responses, which primarily affected mucosal IgA levels among individuals with mild or asymptomatic infection and cellular memory responses in infected patients. CONCLUSION. Our findings suggest that S. pneumoniae impair host immunity to SARS-CoV-2 and raise the question of whether pneumococcal carriage also enables immune escape of other respiratory viruses and facilitates reinfection. TRIAL REGISTRATION. ISRCTN89159899 (FASTER study) and ClinicalTrials.gov NCT03502291 (LAIV study)., Introduction Despite the widespread global effects of the coronavirus disease 2019 (COVID-19) pandemic, few reports have assessed potential interactions between upper airway bacterial colonization and severe acute respiratory syndrome coronavirus [...]

Streptococcus pneumoniae (Spn) is a common cause of respiratory infection, but also frequently colonizes the nasopharynx in the absence of disease. We used mass cytometry to study immune cells from nasal biopsy samples collected following experimental human pneumococcal challenge in order to identify immunological mechanisms of control of Spn colonization. Using 37 markers, we characterized 293 nasal immune cell clusters, of which 7 were associated with Spn colonization. B cell and [CD161.sup.+][CD8.sup.+] T cell clusters were significantly lower in colonized than in noncolonized subjects. By following a second cohort before and after pneumococcal challenge we observed that B cells were depleted from the nasal mucosa upon Spn colonization. This associated with an expansion of Spn polysaccharide- specific and total plasmablasts in blood. Moreover, increased responses of blood mucosa-associated invariant T (MAIT) cells against in vitro stimulation with pneumococcus prior to challenge associated with protection against establishment of Spn colonization and with increased mucosal MAIT cell populations. These results implicate MAIT cells in the protection against pneumococcal colonization and demonstrate that colonization affects mucosal and circulating B cell populations., Introduction Streptococcus pneumoniae (Spn) is a major cause of morbidity and mortality worldwide (1, 2). It is the most common bacterial cause of otitis media, pneumonia, and meningitis in children [...]