ArticleThe Journal of biological chemistry2016
Synaptogyrin-2 Promotes Replication of a Novel Tick-borne Bunyavirus through Interacting with Viral Nonstructural Protein NSs.
Article in The Journal of biological chemistry, 2016. 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, 30 citations in OpenAlex.
- Causal variants in animal genomes: approaches to identification, phenotypic impact, and implications for selective breeding.BMC genomics · 2026Review
- Cellugyrin (Synaptogyrin-2) Regulates Macrophage Phagocytosis ofPathogens (Basel, Switzerland) · 2026Article
- In vitro investigation of host Synaptogyrin-2 role in BVDV-1 replication.Journal of animal science · 2026Article
- Host cell glycosylation selects for infection with CCR5- versus CXCR4-tropic HIV-1.Nature microbiology · 2024Article
- Hsp90 β is critical for the infection of severe fever with thrombocytopenia syndrome virus.Virologica Sinica · 2024Article
- Cellugyrin (synaptogyrin-2) dependent pathways are used by bacterial cytolethal distending toxin and SARS-CoV-2 virus to gain cell entry.Frontiers in cellular and infection microbiology · 2024Article
- Functional and evolutionary analysis of host Synaptogyrin-2 in porcine circovirus type 2 susceptibility.PLoS genetics · 2023Article
- Activation of the NLRP3 inflammasome and elevation of interleukin-1β secretion in infection by sever fever with thrombocytopenia syndrome virus.Scientific reports · 2022Article
- Host genetic factors associated with the range limit of a European hantavirus.Molecular ecology · 2022Article
- The Endless Wars: Severe Fever With Thrombocytopenia Syndrome Virus, Host Immune and Genetic Factors.Frontiers in cellular and infection microbiology · 2022Review
- Evidence for and localization of proposed causative variants in cattle and pig genomes.Genetics, selection, evolution : GSE · 2021Review
- The Role of Non-Structural Protein NSs in the Pathogenesis of Severe Fever with Thrombocytopenia Syndrome.Viruses · 2021Review
- A Look intoViruses · 2021Review
- Baseline mapping of severe fever with thrombocytopenia syndrome virology, epidemiology and vaccine research and development.NPJ vaccines · 2020Review
- Motor neuron translatome reveals deregulation of SYNGR4 and PLEKHB1 in mutant TDP-43 amyotrophic lateral sclerosis models.Human molecular genetics · 2020Article
- Severe Fever with Thrombocytopenia Syndrome Virus NSs Interacts with TRIM21 To Activate the p62-Keap1-Nrf2 Pathway.Journal of virology · 2020Article
- The Severe Fever with Thrombocytopenia Syndrome Virus NSs Protein Interacts with CDK1 To Induce GJournal of virology · 2020Article
- Internalization and Intoxication of Human Macrophages by the Active Subunit of theFrontiers in immunology · 2020Article
- Interferon-γ-Directed Inhibition of a Novel High-Pathogenic Phlebovirus and Viral Antagonism of the Antiviral Signaling by Targeting STAT1.Frontiers in immunology · 2019Article
- Synaptogyrin-2 influences replication of Porcine circovirus 2.PLoS genetics · 2018Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptogyrin-2 is a non-neuronal member of the synaptogyrin family involved in synaptic vesicle biogenesis and trafficking. Little is known about the function of synaptogyrin-2. Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease characterized by high fever, thrombocytopenia, and leukocytopenia with high mortality, caused by a novel tick-borne phlebovirus in the family Bunyaviridae. Our previous studies have shown that the viral nonstructural protein NSs forms inclusion bodies (IBs) that are involved in viral immune evasion, as well as viral RNA replication. In this study, we sought to elucidate the mechanism by which NSs formed the IBs, a lipid droplet-based structure confirmed by NSs co-localization with perilipin A and adipose differentiation-related protein (ADRP). Through a high throughput screening, we identified synaptogyrin-2 to be highly up-regulated in response to SFTS bunyavirus (SFTSV) infection and to be a promoter of viral replication. We demonstrated that synaptogyrin-2 interacted with NSs and was translocated into the IBs, which were reconstructed from lipid droplets into large structures in infection. Viral RNA replication decreased, and infectious virus titers were lowered significantly when synaptogyrin-2 was silenced in specific shRNA-expressing cells, which correlated with the reduced number of the large IBs restructured from regular lipid droplets. We hypothesize that synaptogyrin-2 is essential to promoting the formation of the IBs to become virus factories for viral RNA replication through its interaction with NSs. These findings unveil the function of synaptogyrin-2 as an enhancer in viral infection.
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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.