ArticleAutophagy2022
Bunyavirus SFTSV exploits autophagic flux for viral assembly and egress.
Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 45 citations in OpenAlex.
- Interplay between SFTSV and host innate immunity: Viral evasion mechanisms, pathogenesis, and therapeutic perspectives.iScience · 2026Review
- tRNA-derived small RNA, tsRNA-5017b, as a novel biomarker for predicting severity in severe fever with thrombocytopenia syndrome.Microbiology spectrum · 2026Article
- NIBV Induces Incomplete Autophagy via AMPK-TFEB, Causing Kidney Injury in Chicks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Genetic insights into dabie bandavirus from a clinical case of severe fever with thrombocytopenia syndrome in Longyou County, China.Virology journal · 2026Article
- Targeting the lethal weakness of SFTSV: Latest advances in antiviral strategies and immune prevention.iScience · 2026Review
- Unraveling the complexities: A comprehensive review of severe fever with thrombocytopenia syndrome and its associated complications.iScience · 2026Review
- SFTSV: a priority pathogen in need of a cure-reviewing the therapeutic.Archives of microbiology · 2026Review
- The molecular mechanisms of autophagy-virus interactions: from antiviral defense to viral counterstrategies.FEMS microbiology reviews · 2026Review
- Autophagy machinery as exploited by viruses.Autophagy reports · 2025Article
- Host-Microbe Interactions: Understanding the Mechanism of Autophagy in Viral Replication and Immune Evasion.Veterinary sciences · 2025Review
- Weakened invasion of severe fever with thrombocytopenia syndrome bunyavirus beneficial to its immune escape by multi-site mutation of glycoprotein.Molecular genetics and genomics : MGG · 2025Article
- Current status of severe fever with thrombocytopenia syndrome in China (Review).International journal of molecular medicine · 2025Review
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- Pair combinations of human monoclonal antibodies fully protected mice against bunyavirus SFTSV lethal challenge.PLoS pathogens · 2025Article
- Bunyavirus SFTSV nucleoprotein exploits TUFM-mediated mitophagy to impair antiviral innate immunity.Autophagy · 2025Article
- Alarming implications: severe fever with thrombocytopenia syndrome and its biological vectors in the context of climate change.Frontiers in microbiology · 2025Review
- A Focus on the Mechanisms of Alteration in Host Lymphocyte Level Following Severe Fever with Thrombocytopenia Syndrome Virus (SFTSV) Infection.Journal of inflammation research · 2025Review
- Pathogenesis and virulence of Heartland virus.Virulence · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging negatively stranded enveloped RNA bunyavirus that causes SFTS with a high case fatality rate of up to 30%. Macroautophagy/autophagy is an evolutionarily conserved process involved in the maintenance of host homeostasis, which exhibits anti-viral or pro-viral responses in reaction to different viral challenges. However, the interaction between the bunyavirus SFTSV and the autophagic process is still largely unclear. By establishing various autophagy-deficient cell lines, we found that SFTSV triggered RB1CC1/FIP200-BECN1-ATG5-dependent classical autophagy flux. SFTSV nucleoprotein induced BECN1-dependent autophagy by disrupting the BECN1-BCL2 association. Importantly, SFTSV utilized autophagy for the viral life cycle, which not only assembled in autophagosomes derived from the ERGIC and Golgi complex, but also utilized autophagic vesicles for exocytosis. Taken together, our results suggest a novel virus-autophagy interaction model in which bunyavirus SFTSV induces classical autophagy flux for viral assembly and egress processes, suggesting that autophagy inhibition may be a novel therapy for treating or releasing SFTS.
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What Socratic holds
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.