ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Childhood tolerance of severe influenza: a mortality analysis in mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Virological, innate, and adaptive immune profiles shaped by variation in route and age of host in murine cytomegalovirus infection.Journal of virology · 2024Article
- Immune dynamics throughout life in relation to sex hormones and perspectives gained from gender-affirming hormone therapy.Frontiers in immunology · 2024Review
- The Identification Distinct Antiviral Factors Regulated Influenza Pandemic H1N1 Infection.International journal of microbiology · 2024Article
- Treating COVID-19: Targeting the Host Response, Not the Virus.Life (Basel, Switzerland) · 2023Review
- Influenza in High-Risk Hosts-Lessons Learned from Animal Models.Cold Spring Harbor perspectives in medicine · 2020Review
- Androgen receptor signaling in the lungs mitigates inflammation and improves the outcome of influenza in mice.PLoS pathogens · 2020Article
- The relative resistance of children to sepsis mortality: from pathways to drug candidates.Molecular systems biology · 2018Article
- Clinician-initiated research on treating the host response to pandemic influenza.Human vaccines & immunotherapeutics · 2018Article
- Influenza, evolution, and the next pandemic.Evolution, medicine, and public health · 2018Review
- Characterising Pre-pubertal Resistance to Death from Endotoxemia.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
During the 1918 influenza pandemic, children experienced substantially lower mortality than adults, a striking but unexplained finding. Whether this was due to enhanced resistance (reduced virus load) or better tolerance (reduced impact of infection) has not been defined. We found that prepubertal mice infected with H1N1 influenza virus also showed greater survival than infected pubertal mice, despite similar virus loads. Transcriptome profiling of infected lungs identified estrogen as a regulator of susceptibility in both sexes and also linked better survival to late expression of IL-1β. Blocking puberty with gonadectomy or a gonadotropin-releasing hormone antagonist improved survival. Estrogen or testosterone (which can be converted to estrogen) restored susceptibility of gonadectomized pubertal mice to influenza mortality, but dihydrotestosterone (which cannot be converted to estrogen) did not. Estrogen receptor blockade with fulvestrant in both male and female pubertal mice resulted in improved survival, even when given 3 days after infection. Moreover, late, but not early, IL-1β neutralization after infection was also protective. These findings indicate that pubertal increases in estrogen in both sexes are associated with increased mortality during influenza. This helps explain the reduced mortality of children seen with influenza in 1918 and might also be relevant to childhood tolerance to many other infectious diseases.
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