ArticlePLoS pathogens2020
Virus subtype-specific suppression of MAVS aggregation and activation by PB1-F2 protein of influenza A (H7N9) virus.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- C-terminal tail of MAVS dictates organelle targeting and innate immune response.Cell communication and signaling : CCS · 2026Article
- FMDV 3A cooperates with PDCD10 to promote FMDV replication by inhibiting VISA-mediated innate immunity.Journal of virology · 2025Article
- Mpox virus poxin-schlafen fusion protein suppresses innate antiviral response by sequestering STAT2.Emerging microbes & infections · 2025Article
- Cgref1 is a CREB-H-regulated hepatokine that promotes hepaticInternational journal of biological sciences · 2025Article
- Palmitoylation acts as a checkpoint for MAVS aggregation to promote antiviral innate immune responses.The Journal of clinical investigation · 2024Article
- Identification of a short sequence motif in the influenza A virus pathogenicity factor PB1-F2 required for inhibition of human NLRP3.Journal of virology · 2024Article
- Exploring TRIM proteins' role in antiviral defense against influenza A virus and respiratory coronaviruses.Frontiers in cellular and infection microbiology · 2024Review
- Pathogenicity and virulence of influenza.Virulence · 2023Review
- Aggregated Hendra virus C-protein activates the NLRP3 inflammasome to induce inflammation.Journal of inflammation (London, England) · 2023Article
- Suppression of cGAS- and RIG-I-mediated innate immune signaling by Epstein-Barr virus deubiquitinase BPLF1.PLoS pathogens · 2023Article
- Avian Influenza NS1 Proteins Inhibit Human, but Not Duck, RIG-I Ubiquitination and Interferon Signaling.Journal of virology · 2022Article
- Cytoplasmic RNA sensors and their interplay with RNA-binding partners in innate antiviral response: theme and variations.RNA (New York, N.Y.) · 2022Review
- MicroRNA-200c-targeted contactin 1 facilitates the replication of influenza A virus by accelerating the degradation of MAVS.PLoS pathogens · 2022Article
- TRIM31: A molecule with a dual role in cancer.Frontiers in oncology · 2022Review
- Advances on Innate Immune Evasion by Avian Immunosuppressive Viruses.Frontiers in immunology · 2022Review
- Functions of Viroporins in the Viral Life Cycle and Their Regulation of Host Cell Responses.Frontiers in immunology · 2022Review
- Suppression of JAK-STAT Signaling by Epstein-Barr Virus Tegument Protein BGLF2 through Recruitment of SHP1 Phosphatase and Promotion of STAT2 Degradation.Journal of virology · 2021Article
- Review
- Role of Mitochondria in Viral Infections.Life (Basel, Switzerland) · 2021Review
- Regulation of RIG-I-like receptor-mediated signaling: interaction between host and viral factors.Cellular & molecular immunology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human infection with avian influenza A (H5N1) and (H7N9) viruses causes severe respiratory diseases. PB1-F2 protein is a critical virulence factor that suppresses early type I interferon response, but the mechanism of its action in relation to high pathogenicity is not well understood. Here we show that PB1-F2 protein of H7N9 virus is a particularly potent suppressor of antiviral signaling through formation of protein aggregates on mitochondria and inhibition of TRIM31-MAVS interaction, leading to prevention of K63-polyubiquitination and aggregation of MAVS. Unaggregated MAVS accumulated on fragmented mitochondria is prone to degradation by both proteasomal and lysosomal pathways. These properties are proprietary to PB1-F2 of H7N9 virus but not shared by its counterpart in WSN virus. A recombinant virus deficient of PB1-F2 of H7N9 induces more interferon β in infected cells. Our findings reveal a subtype-specific mechanism for destabilization of MAVS and suppression of interferon response by PB1-F2 of H7N9 virus.
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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.