ArticleProceedings of the National Academy of Sciences of the United States of America2016
Two interferon-independent double-stranded RNA-induced host defense strategies suppress the common cold virus at warm temperature.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- TRPV4-mediated calcium influx contributes temperature-dependent SARS-CoV-2 replication.PLoS pathogens · 2026Article
- Temperature and developmental stage govern intestinal susceptibility to human coronavirus 229E.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Rental housing may contribute to racial and ethnic disparities in upper respiratory infections.medRxiv : the preprint server for health sciences · 2026Article
- Seasonal Trends of Major Respiratory, Gastrointestinal, and Other Viral Infections in Korea: An Analysis Before, During, and After the Coronavirus Disease 2019 Pandemic.Annals of laboratory medicine · 2026Review
- Dose-dependent activation of the Hippo pathway by Type I and Type III interferons suppresses tissue repair by human bronchial epithelial cells.PLoS biology · 2026Article
- Clinical Significance of Rhinoviruses and Progress Toward Vaccination.Allergy, asthma & immunology research · 2025Review
- Mathematical Modeling of Influenza Dynamics: Integrating Seasonality and Gradual Waning Immunity.Bulletin of mathematical biology · 2025Article
- Human respiratory organoids sustained reproducible propagation of human rhinovirus C and elucidation of virus-host interaction.Nature communications · 2024Article
- Parabacteroides distasonis regulates the infectivity and pathogenicity of SVCV at different water temperatures.Microbiome · 2024Article
- Interferon signaling in the nasal epithelium distinguishes among lethal and common cold coronaviruses and mediates viral clearance.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Evolution of enhanced innate immune suppression by SARS-CoV-2 Omicron subvariants.Nature microbiology · 2024Article
- Impact of SARS-CoV-2 vaccination and of seasonal variations on the innate immune inflammatory response.Frontiers in immunology · 2024Article
- Interferon signaling in the nasal epithelium distinguishes among lethal and common cold respiratory viruses and is critical for viral clearance.bioRxiv : the preprint server for biology · 2023Article
- Quantifying individual-level heterogeneity in infectiousness and susceptibility through household studies.Epidemics · 2023Article
- High body temperature increases gut microbiota-dependent host resistance to influenza A virus and SARS-CoV-2 infection.Nature communications · 2023Article
- Anionic Pulmonary Surfactant Lipid Treatment Inhibits Rhinovirus A Infection of the Human Airway Epithelium.Viruses · 2023Article
- Warmer ambient air temperatures reduce nasal turbinate and brain infection, but increase lung inflammation in the K18-hACE2 mouse model of COVID-19.The Science of the total environment · 2023Article
- Cold exposure impairs extracellular vesicle swarm-mediated nasal antiviral immunity.The Journal of allergy and clinical immunology · 2023Article
- Quantifying individual-level heterogeneity in infectiousness and susceptibility through household studies.medRxiv : the preprint server for health sciences · 2022Article
- Review
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5 authors.
Funding
Abstract
Most strains of rhinovirus (RV), the common cold virus, replicate better at cool temperatures found in the nasal cavity (33-35 °C) than at lung temperature (37 °C). Recent studies found that although 37 °C temperature suppressed RV growth largely by engaging the type 1 IFN response in infected epithelial cells, a significant temperature dependence to viral replication remained in cells devoid of IFN induction or signaling. To gain insight into IFN-independent mechanisms limiting RV replication at 37 °C, we studied RV infection in human bronchial epithelial cells and H1-HeLa cells. During the single replication cycle, RV exhibited temperature-dependent replication in both cell types in the absence of IFN induction. At 37 °C, earlier signs of apoptosis in RV-infected cells were accompanied by reduced virus production. Furthermore, apoptosis of epithelial cells was enhanced at 37 °C in response to diverse stimuli. Dynamic mathematical modeling and B cell lymphoma 2 (BCL2) overexpression revealed that temperature-dependent host cell death could partially account for the temperature-dependent growth observed during RV amplification, but also suggested additional mechanisms of virus control. In search of a redundant antiviral pathway, we identified a role for the RNA-degrading enzyme RNAseL. Simultaneous antagonism of apoptosis and RNAseL increased viral replication and dramatically reduced temperature dependence. These findings reveal two IFN-independent mechanisms active in innate defense against RV, and demonstrate that even in the absence of IFNs, temperature-dependent RV amplification is largely a result of host cell antiviral restriction mechanisms operating more effectively at 37 °C than at 33 °C.
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