ArticlePLoS pathogens2011
IFITM3 inhibits influenza A virus infection by preventing cytosolic entry.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 295 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
295 citing papers in PubMed, 1 synthesis or guideline pooled it, 395 citations in OpenAlex.
- Systematic review and meta-analysis of genome-wide pooled CRISPR screens to identify host factors involved in influenza A virus infection.Journal of virology · 2024Pooled it
- IFITM1 enhances anti-tumor function of unconventional TCRαβ double negative T cells by upregulating mitophagy.Science China. Life sciences · 2026Article
- IFITM1 and IFITM3 cooperate to restrict virus entry in endolysosomes.Journal of virology · 2026Article
- Interferon-induced transmembrane proteins in cancer and virus biology: a membrane perspective.mBio · 2026Review
- Viral subversion of megakaryopoiesis: reshaping the landscapes of immune regulation.Infection · 2026Review
- Nasal CD4+ tissue-resident memory T cells provide cross-protective immunity to influenza.The Journal of experimental medicine · 2026Article
- MYCT1-IFITM2/3 interaction links endothelial endolysosomal trafficking to white adipose tissue expansion.The Journal of experimental medicine · 2026Article
- Cyclosporine A rescues the influenza virus fusion with IFITM3-expressing cells by relocating the restriction factor to intraluminal vesicles of multivesicular bodies.Journal of virology · 2026Article
- IFITM3 at the viral fusion-pore checkpoint: membrane energetics and entry-route-dependent outcomes.Frontiers in immunology · 2026Review
- Interferon-induced transmembrane proteins: membrane gatekeepers of fusion and infection.Frontiers in cellular and infection microbiology · 2026Review
- Association of IFNL4 and IFITM3 Genetic Variants with Susceptibility to HCV-Related Liver Cirrhosis and Hepatocellular Carcinoma.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- STAT1-IFITM3 promotes autophagy in epithelial cells to controlLife science alliance · 2025Article
- Interferon-Induced Transmembrane Protein 3 (IFITM3) Restricts PRRSV Replication via Post-Entry Mechanisms.Microorganisms · 2025Article
- Genetic resilience or resistance in poultry against avian influenza virus: mirage or reality?Journal of virology · 2025Review
- SARS-CoV-2 infection enhancement by amphotericin B: implications for disease management.Journal of virology · 2025Article
- The HDL-transporting scavenger receptor B1 promotes viral infection through endolysosomal acidification.iScience · 2025Article
- IFITM1 and IFITM3 cooperate to restrict virus entry in endolysosomes.bioRxiv : the preprint server for biology · 2025Article
- Chicken interferon-induced transmembrane proteins inhibit Newcastle disease virus infection by affecting viral entry and W protein expression.Veterinary research · 2025Article
- Review
- HIV-1 inhibits IFITM3 expression to promote the infection of megakaryocytes.Journal of molecular cell biology · 2025Article
235 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
To replicate, viruses must gain access to the host cell's resources. Interferon (IFN) regulates the actions of a large complement of interferon effector genes (IEGs) that prevent viral replication. The interferon inducible transmembrane protein family members, IFITM1, 2 and 3, are IEGs required for inhibition of influenza A virus, dengue virus, and West Nile virus replication in vitro. Here we report that IFN prevents emergence of viral genomes from the endosomal pathway, and that IFITM3 is both necessary and sufficient for this function. Notably, viral pseudoparticles were inhibited from transferring their contents into the host cell cytosol by IFN, and IFITM3 was required and sufficient for this action. We further demonstrate that IFN expands Rab7 and LAMP1-containing structures, and that IFITM3 overexpression is sufficient for this phenotype. Moreover, IFITM3 partially resides in late endosomal and lysosomal structures, placing it in the path of invading viruses. Collectively our data are consistent with the prediction that viruses that fuse in the late endosomes or lysosomes are vulnerable to IFITM3's actions, while viruses that enter at the cell surface or in the early endosomes may avoid inhibition. Multiple viruses enter host cells through the late endocytic pathway, and many of these invaders are attenuated by IFN. Therefore these findings are likely to have significance for the intrinsic immune system's neutralization of a diverse array of threats.
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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.