ArticleCell death & disease2018
Rhinovirus 3C protease suppresses apoptosis and triggers caspase-independent cell death.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 59 citations in OpenAlex.
- Unmasking programmed cell death in rhinovirus-driven asthma pathology.Biochemical Society transactions · 2026Review
- Programmed Cell Death in Chronic Rhinosinusitis.Clinical and translational allergy · 2026Review
- Quercetin-3-Methyl Ether Induces Early Apoptosis to Overcome HRV1B Immune Evasion, Suppress Viral Replication, and Mitigate Inflammatory Pathogenesis.Biomolecules & therapeutics · 2025Article
- The Interplay Between Viral Infection and Cell Death: A Ping-Pong Effect.Advances in virology · 2025Review
- Development of a necroptosis-related gene signature and the immune landscape in ovarian cancer.Journal of ovarian research · 2023Article
- T-helper 2 mechanisms involved in human rhinovirus infections and asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2022Review
- High-content, arrayed compound screens with rhinovirus, influenza A virus and herpes simplex virus infections.Scientific data · 2022Article
- Article
- Crosstalk Between Pyroptosis and Apoptosis in Hepatitis C Virus-induced Cell Death.Frontiers in immunology · 2022Article
- The evolution of regulated cell death pathways in animals and their evasion by pathogens.Physiological reviews · 2022Review
- Article
- RIPK1 Is Cleaved by 3C Protease of Rhinovirus A and B Strains and Minor and Major Groups.Viruses · 2021Article
- Embryotoxic activity of 3C protease of human hepatitis A virus in developing Danio rerio embryos.Scientific reports · 2021Article
- The endoplasmic reticulum unfolded protein response - homeostasis, cell death and evolution in virus infections.FEMS microbiology reviews · 2021Review
- Airway epithelial cell necroptosis contributes to asthma exacerbation in a mouse model of house dust mite-induced allergic inflammation.Mucosal immunology · 2021Article
- Individual Expression of Hepatitis A Virus 3C Protease Induces Ferroptosis in Human Cells In Vitro.International journal of molecular sciences · 2021Article
- Microscopy deep learning predicts virus infections and reveals mechanics of lytic-infected cells.iScience · 2021Article
- Rhinovirus and Cell Death.Viruses · 2021Review
- From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways.Computational and structural biotechnology journal · 2021Review
- Different Culture Conditions Affect Drug Transporter Gene Expression, Ultrastructure, and Permeability of Primary Human Nasal Epithelial Cells.Pharmaceutical research · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis and programmed necrosis (necroptosis) determine cell fate, and antagonize infection. Execution of these complementary death pathways involves the formation of receptor-interacting protein kinase 1 (RIPK1) containing complexes. RIPK1 binds to adaptor proteins, such as TRIF (Toll-IL-1 receptor-domain-containing-adaptor-inducing interferon-beta factor), FADD (Fas-associated-protein with death domain), NEMO (NF-κB regulatory subunit IKKγ), SQSTM1 (sequestosome 1/p62), or RIPK3 (receptor-interacting protein kinase 3), which are involved in RNA sensing, NF-κB signaling, autophagosome formation, apoptosis, and necroptosis. We report that a range of rhinoviruses impair apoptosis and necroptosis in epithelial cells late in infection. Unlike the double-strand (ds) RNA mimetic poly I:C (polyinosinic:polycytidylic acid), the exposure of dsRNA to toll-like receptor 3 (TLR3) in rhinovirus-infected cells did not lead to apoptosis execution. Accordingly, necroptosis and the production of ROS (reactive oxygen species) were not observed late in infection, when RIPK3 was absent. Instead, a virus-induced alternative necrotic cell death pathway proceeded, which led to membrane rupture, indicated by propidium iodide staining. The impairment of dsRNA-induced apoptosis late in infection was controlled by the viral 3C-protease (3Cpro), which disrupted RIPK1-TRIF/FADD /SQSTM1 immune-complexes. 3Cpro and 3C precursors were found to coimmuno-precipitate with RIPK1, cleaving the RIPK1 death-domain, and generating N-terminal RIPK1 fragments. The depletion of RIPK1 or chemical inhibition of its kinase at the N-terminus did not interfere with virus progeny formation or cell fate. The data show that rhinoviruses suppress apoptosis and necroptosis, and release progeny by an alternative cell death pathway, which is controlled by viral proteases modifying innate immune complexes.
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