Abstract Rationale Obstructive sleep apnea (OSA) is a common pediatric disorder associated with impaired growth, behavioral difficulties, and cardiometabolic consequences. While adenotonsillar hypertrophy is the leading cause, its underlying drivers remain unclear. Respiratory syncytial virus (RSV) has been detected in tonsillar tissue of children with OSA, suggesting a possible link between early-life viral infection, chronic inflammation, and airway remodeling. The COVID-19 pandemic, which nearly eliminated RSV circulation during the winter of 2020, provided a natural experiment to assess whether reduced early-life RSV exposure influences later OSA risk. Objectives To compare the incidence of OSA among children born during March-June 2020 (low RSV exposure, L-RSV) with those born during the same months in 2014-2017 (high RSV exposure, H-RSV), up to 4 years of age. Methods A nationwide retrospective cohort study was conducted using data from Clalit Health Services, the largest healthcare provider in Israel, covering approximately 52% of the population (over 5 million members). Exclusion criteria included preterm birth, chromosomal abnormalities, congenital heart or lung malformations, cystic fibrosis, and immunodeficiencies.OSA was identified using surrogate markers: ICD-9 code 327.23, documented polysomnography, and records of adenotonsillectomy, individually or in combination. Statistical analyses included univariate and multivariable logistic regression. Results A total of 127,821 children met the inclusion criteria (H-RSV = 102,220; L-RSV = 25,601). Sex distribution was similar between groups (females = 48.36% vs. 48.31%, p = 0.4). Univariate analyses showed higher proportions of OSA surrogates in the L-RSV group versus the H-RSV group: OSA diagnoses (2.16% vs. 1.47%, p 0.001), adenotonsillectomy (3.93% vs. 3.51%, p 0.001), and polysomnography (2.4% vs. 1.78%, p 0.001). Adjusted multivariate analysis demonstrated similar trends (Figure). Conclusion Children with low RSV exposure during infancy exhibited higher rates of OSA-related surrogates, suggesting that early RSV infection may not be a primary driver of OSA. Alternatively, reduced viral exposure may delay immune maturation, leading to rebound lymphoid tissue growth later in childhood. This abstract is funded by: No funding
Goldbart et al. (Fri,) studied this question.