Asthma has a striking temporal character, in which time-of-day, patient age, and season each influence disease activity. The extent to which rhythms in asthma activity reflect exposure to specific disease triggers remains unclear. In this study, we examined how virus mitigation strategies enacted during the COVID-19 pandemic (“lockdown measures”) affected rhythms in asthma clinical activity in children. To this end, we retrospectively analyzed asthma clinical presentations in children aged <18 years to our regional academic medical center, comparing 4 years of medical records prior to COVID-19 lockdown measures with the 12 months immediately after the institution of such measures. We correlated these data to positive viral test results, febrile seizures, and allergic clinical surrogates (allergic reaction visits and Emergency Department [ED] antihistamine prescriptions, respectively) over the same time frame. In the 12 months following the institution of the COVID-19 lockdown, positivity rates for common respiratory viruses dropped by 70.2% and ED visits for asthma among children dropped by 62% compared to pre-COVID years. Lockdown suppressed seasonal variation in positive viral tests and asthma ED visits, while diurnal rhythms in asthma visits were unchanged. Asthma seasonality correlated most strongly with rhinovirus positivity both before and after the institution of COVID lockdown measures. Altogether, our data support a causal role for viruses in driving seasonal variability in asthma exacerbations in children.

Asthma is a chronic disease of childhood, but for unknown reasons, disease activity sometimes subsides as children mature. In this study, we present clinical and animal model evidence suggesting that the age dependency of childhood asthma stems from an evolving host response to respiratory viral infection. Using clinical data, we show that societal suppression of respiratory virus transmission during coronavirus disease 2019 lockdown disrupted the traditional age gradient in pediatric asthma exacerbations, connecting the phenomenon of asthma remission to virus exposure. In mice, we show that asthmatic lung pathology triggered by Sendai virus (SeV) or influenza A virus is highly age-sensitive: robust in juvenile mice (4–6 wk old) but attenuated in mature mice (&gt;3 mo old). Interestingly, allergen induction of the same asthmatic traits was less dependent on chronological age than viruses. Age-specific responses to SeV included a juvenile bias toward type 2 airway inflammation that emerged early in infection, whereas mature mice exhibited a more restricted bronchiolar distribution of infection that produced a distinct type 2 low inflammatory cytokine profile. In the basal state, aging produced changes to lung leukocyte burden, including the number and transcriptional landscape of alveolar macrophages (AMs). Importantly, depleting AMs in mature mice restored post-SeV pathology to juvenile levels. Thus, aging influences chronic outcomes of respiratory viral infection through regulation of the AM compartment and type 2 inflammatory responses to viruses. Our data provide insight into how asthma remission might develop in children.

The United States is one of the few countries, and the only high-income country, that does not federally mandate protection of postpartum employment through paid postpartum maternity and family leave policies. At the onset of the COVID-19 pandemic in the U.S., stay-at-home orders were implemented nationally, creating a natural experiment in which to document the effects of de facto paid leave on infant feeding practices in the first postpartum year. The purpose of this cross-sectional, mixed-methods study was to describe infant and young child feeding intentions, practices, decision-making, and experiences during the first wave of the COVID-19 pandemic in the U.S. Quantitative and qualitative data were collected March 27–May 31, 2020 via online survey among a convenience sample of respondents, ages 18 years and older, who were currently feeding a child 2 years of age or younger, yielding 1,437 eligible responses. Nearly all (97%) respondents indicated an intention to feed their infant exclusively with human milk in the first 6 months. A majority of respondents who were breastfeeding (66%) reported no change in breastfeeding frequency after the implementation of COVID-19 stay-at-home orders. However, thirty-one percent indicated that they breastfed more frequently due to stay-at-home orders and delayed plans to wean their infant or young child. Key themes drawn from the qualitative data were: emerging knowledge and perceptions of the relationship between COVID-19 and breastfeeding, perceptions of immune factors in human milk, and the social construction of COVID-19 and infant and young child feeding perceptions and knowledge. There were immediate positive effects of stay-at-home policies on human milk feeding practices, even during a time of considerable uncertainty about the safety of breastfeeding and the transmissibility of SARS-CoV-2 via human milk, constrained access to health care services and COVID-19 testing, and no effective COVID-19 vaccines. Federally mandated paid postpartum and family leave are essential to achieving more equitable lactation outcomes.

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Asthma is a common chronic disease of childhood, but for unknown reasons disease activity sometimes subsides as children mature. To understand why, we exposed mice across a range of ages to viral and allergic triggers of asthma exacerbations and airway pathology. We found that pathology induced by Sendai virus (SeV) or influenza A virus (IAV) occurred selectively in juvenile mice in a microbiome-independent manner, while the same phenotypes induced by allergens were insensitive to age. Age-specific responses to SeV included a juvenile bias towards type-2 airway inflammation that emerged early in infection and was lost with maturation. With aging, we observed progressive transcriptional changes to alveolar macrophages (AMs) including the acquisition of high-level MHC-II expression. Importantly, depleting AMs canceled the protective effects of maturity on post-viral airway pathology. Thus, aging of the lung-immune microenvironment influences chronic outcomes of respiratory viral infection and may help to explain childhood asthma remission.