ArticleAutophagy2025
Bunyavirus SFTSV nucleoprotein exploits TUFM-mediated mitophagy to impair antiviral innate immunity.
Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Interplay between SFTSV and host innate immunity: Viral evasion mechanisms, pathogenesis, and therapeutic perspectives.iScience · 2026Review
- Mitophagy in pathogenesis and therapeutic implications for infection.Experimental & molecular medicine · 2026Review
- FAM134B Restricts African Swine Fever Virus Capsid Assembly via Reticulophagy and Its Antiviral Activity is Antagonized by the Viral Virulence-Associated Factor pMGF300-2R.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitophagy-mediated immune evasion: Shared strategies of pathogens.Redox biology · 2026Review
- Preparation and characterization of the affinity and neutralization abilities of human monoclonal antibodies against bunyavirus SFTSV glycoprotein C.Infectious medicine · 2026Article
- PINK1-Parkin pathway-mediated mitophagy in sepsis: friend or foe?Molecular biology reports · 2026Review
- Mitophagy interacts with mitochondrial dynamics and biogenesis, acting as a double-edged sword in digestive cancer.iScience · 2026Review
- Newcastle disease virus hijacks mitophagy to reprogram amino acid metabolism for enhanced replication.Autophagy · 2026Article
- Unraveling the complexities: A comprehensive review of severe fever with thrombocytopenia syndrome and its associated complications.iScience · 2026Review
- Targeting the lethal weakness of SFTSV: Latest advances in antiviral strategies and immune prevention.iScience · 2026Review
- TUFM: a central regulator in mitochondrial quality control and beyond.Cell death discovery · 2026Review
- DS96432529 enhances osteogenic differentiation and mitigates inflammatory damage in periodontal ligament stem cells involving mitophagy-related processes.Stem cell research & therapy · 2026Article
- A single mutation in nonstructural protein 1 is critical for the adaptive evolution of influenza B virus.Nature communications · 2026Article
- Crosstalk between mitophagy and breast cancer: mechanisms of action and clinical applications.Journal of cancer research and clinical oncology · 2026Review
- Multidimensional mechanisms of SFTSV-host interactions: viral protein functions, mFrontiers in cellular and infection microbiology · 2026Review
- Research progress on antiviral drugs and vaccines for severe fever with thrombocytopenia syndrome.Frontiers in immunology · 2026Review
- Mitochondrial quality control: a new mechanism for antiviral therapy.Frontiers in immunology · 2026Review
- ATG5 Plays a Role inTransboundary and emerging diseases · 2026Article
- Vitamin D disrupts NS1-TUFM interaction to suppress pathogenic mitophagy in RSV-induced mitochondrial injury of bronchial epithelial cells.Journal of microbiology (Seoul, Korea) · 2026Article
- Inhibition of STING-mediated antiviral innate immunity activation by CD97 via modulation of ER-phagy.Communications biology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe fever with thrombocytopenia syndrome is an emerging viral hemorrhagic fever caused by a tick-borne bunyavirus, severe fever with thrombocytopenia syndrome virus (SFTSV), with a high case fatality. We previously found that SFTSV nucleoprotein (NP) induces macroautophagy/autophagy to facilitate virus replication. However, the role of NP in antagonizing host innate immunity remains unclear. Mitophagy, a selected form of autophagy, eliminates damaged mitochondria to maintain mitochondrial homeostasis. Here, we demonstrate that SFTSV NP triggers mitophagy to degrade MAVS (mitochondrial antiviral signaling protein), thereby blocking MAVS-mediated antiviral signaling to escape the host immune response. Mechanistically, SFTSV NP translocates to mitochondria by interacting with TUFM (Tu translation elongation factor, mitochondrial), and mediates mitochondrial sequestration into phagophores through interacting with LC3, thus inducing mitophagy. Notably, the N-terminal LC3-interacting region (LIR) motif of NP is essential for mitophagy induction. Collectively, our results demonstrated that SFTSV NP serves as a novel virulence factor, inducing TUFM-mediated mitophagy to degrade MAVS and evade the host immune response.
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Registered trials
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 Socratic graph.