ArticleFrontiers in microbiology2021
Enterovirus 71 Antagonizes Antiviral Effects of Type III Interferon and Evades the Clearance of Intestinal Intraepithelial Lymphocytes.
Article in Frontiers in microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Prohibitins: emerging host targets of bacteria and viruses at the plasma membrane, mitochondria, and cytoplasm.Microbial cell (Graz, Austria) · 2026Article
- Mucosal Immunity: The Key to Combating Enteroviruses and Beyond.Journal of immunology research · 2026Review
- Review
- Review
- Insights into the mechanisms of apoptosis and pathogenesis in enterovirus 71 infections: A review.Medicine · 2025Review
- Antiviral Activity of Marine BacteriumInternational journal of molecular sciences · 2025Article
- Emerging Therapeutics in the Fight Against EV-D68: A Review of Current Strategies.Influenza and other respiratory viruses · 2024Review
- Update on enteroviral protease 2A: Structure, function, and host factor interaction.Biosafety and health · 2023Review
- Research progress on pathogenic and therapeutic mechanisms of Enterovirus A71.Archives of virology · 2023Review
- Current status of hand-foot-and-mouth disease.Journal of biomedical science · 2023Review
- Roles of Interleukin-6-mediated immunometabolic reprogramming in COVID-19 and other viral infection-associated diseases.International immunopharmacology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV71) is the major pathogen causing severe neurological complications and hand, foot, and mouth disease. The intestinal mucosal immune system has a complete immune response and immune regulation mechanism, consisting of densely arranged monolayer intestinal epithelial cells (IECs) and intestinal intraepithelial lymphocytes (iIELs) distributed among the IECs, which constitute the first line of intestinal mucosa against infection of foreign pathogens. As an enterovirus, EV71 is transmitted by the intestinal tract; however, the mechanisms it uses to evade the immunosurveillance of the intestinal mucosal immune system are still incompletely clarified. The present study investigated how EV71 evades from recognizing and eliminating IECs, iIELs, and iNK cells. We found that EV71 infection induced a higher level of type III interferons (IFN-λ) than type I interferons (IFN-β) in IECs, and the addition of IFN-λ markedly restricted EV71 replication in IECs. These results indicate that IFN-λ plays a more important role in anti-EV71 intestinal infection. However, EV71 infection could markedly attenuate the antiviral responses of IFN-λ. Mechanistically, 2A protease (2Apro) and 3C protease (3Cpro) of EV71 inhibited the IFN-λ production and IFN-λ receptor expression and further decreased the response of IECs to IFN-λ. In addition, we found that EV71-infected IECs were less susceptible to the lysis of intestinal NK (iNK) cells and CD3
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