ArticleProceedings of the National Academy of Sciences of the United States of America2019
IFITM3 protects the heart during influenza virus infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 90 citations in OpenAlex.
- Delayed antiviral immune response in alveolar type 2 cells increases susceptibility to influenza virus in alveoli.Chinese medical journal · 2026Article
- Modeling the Exposome in Murine Cardiovascular Disease.JACC. Basic to translational science · 2026Review
- Research progress on the association between viruses and cardiac diseases.Journal of virology · 2026Review
- IFITM1 and IFITM3 cooperate to restrict virus entry in endolysosomes.Journal of virology · 2026Article
- Influenza hijacks myeloid cells to inflict type-I interferon-fueled damage in the heart.Immunity · 2026Article
- Gasdermin E is dispensable for H1N1 influenza virus pathogenesis in mice.Microbiology spectrum · 2026Article
- IFITM3 deficiency drives SARS-CoV-2 adaptation while preserving variant-specific traits.Nature communications · 2026Article
- MARCH E3 Ligases: Understudied Regulators of Pulmonary Immune Function.Journal of respiratory biology and translational medicine · 2026Article
- IFITM3-deficient mice as a model for testing influenza virus vaccines via the intramuscular route.Vaccine · 2025Article
- Cardioprotective effects of AMPK activation in H1N1 influenza virus infection.bioRxiv : the preprint server for biology · 2025Article
- O-GlcNAc transferase plays dual antiviral roles by integrating innate immunity and lipid metabolism.Nature communications · 2025Article
- Review
- Differential restriction of chikungunya virus in primary human cardiac endothelial cells occurs at multiple steps in the viral life cycle.PLoS neglected tropical diseases · 2025Article
- Three modes of viral adaption by the heart.Science advances · 2024Article
- Innate immune control of influenza virus interspecies adaptation via IFITM3.Nature communications · 2024Article
- FBXL19 in endothelial cells protects the heart from influenza A infection by enhancing antiviral immunity and reducing cellular senescence programs.American journal of physiology. Heart and circulatory physiology · 2024Article
- Rifaximin ameliorates influenza A virus infection-induced lung barrier damage by regulating gut microbiota.Applied microbiology and biotechnology · 2024Article
- Differential restriction of chikungunya virus in primary human cardiac endothelial cells occurs at multiple steps in the viral life cycle.bioRxiv : the preprint server for biology · 2024Article
- Correlates of disease severity in bluetongue as a model of acute arbovirus infection.PLoS pathogens · 2024Article
- The Antiviral Activity of Interferon-Induced Transmembrane Proteins and Virus Evasion Strategies.Viruses · 2024Review
8 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Influenza virus can disseminate from the lungs to the heart in severe infections and can induce cardiac pathology, but this has been difficult to study due to a lack of small animal models. In humans, polymorphisms in the gene encoding the antiviral restriction factor IFN-induced transmembrane protein 3 (IFITM3) are associated with susceptibility to severe influenza, but whether IFITM3 deficiencies contribute to cardiac dysfunction during infection is unclear. We show that IFITM3 deficiency in a new knockout (KO) mouse model increases weight loss and mortality following influenza virus infections. We investigated this enhanced pathogenesis with the A/PR/8/34 (H1N1) (PR8) influenza virus strain, which is lethal in KO mice even at low doses, and observed increased replication of virus in the lungs, spleens, and hearts of KO mice compared with wild-type (WT) mice. Infected IFITM3 KO mice developed aberrant cardiac electrical activity, including decreased heart rate and irregular, arrhythmic RR (interbeat) intervals, whereas WT mice exhibited a mild decrease in heart rate without irregular RR intervals. Cardiac electrical dysfunction in PR8-infected KO mice was accompanied by increased activation of fibrotic pathways and fibrotic lesions in the heart. Infection with a sublethal dose of a less virulent influenza virus strain (A/WSN/33 [H1N1]) resulted in a milder cardiac electrical dysfunction in KO mice that subsided as the mice recovered. Our findings reveal an essential role for IFITM3 in limiting influenza virus replication and pathogenesis in heart tissue and establish IFITM3 KO mice as a powerful model for studying mild and severe influenza virus-induced cardiac dysfunction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.