ArticlePLoS pathogens2023
Hepatitis B virus hijacks TSG101 to facilitate egress via multiple vesicle bodies.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
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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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Pooled it
- A tale of dual role: HECT‑type E3 ubiquitin ligase mechanisms in liver diseases (Review).International journal of molecular medicine · 2026Review
- RANBP3 and RAN orchestrate CRM1-mediated nuclear export of hepatitis B virus RNAs.Journal of virology · 2026Article
- Ubiquitination dynamics in human tumour viruses: Viral infection, oncogenesis and antiviral therapy.The FEBS journal · 2026Review
- Innate immune recognition in hepatitis B virus infection.Virulence · 2025Review
- MCM7 promotes liver fibrosis by transcriptionally regulating IL11 via the SHCBP1-RACGAP1-STAT3 axis.Cell death & disease · 2025Article
- Screening of different species reveals cat hepatocytes support HBV infection.PLoS pathogens · 2025Article
- Targeting HBV cccDNA through chromatin destabilization: A new frontier in antiviral therapy.Infectious diseases & immunity · 2025Article
- Nonlytic Egress and Transmission in the Virus World.Annual review of biochemistry · 2025Review
- ESCRT Machinery in HBV Life Cycle: Dual Roles in Autophagy and Membrane Dynamics for Viral Pathogenesis.Cells · 2025Review
- The HBV large envelope protein initiates virion assembly by recruiting capsids at membrane rich domains related to late endosome.Cellular and molecular life sciences : CMLS · 2025Article
- Exosome in HBV infection: current concepts and future perspectives.Frontiers in cellular and infection microbiology · 2025Review
- Manganese is a potent inducer of lysosomal activity that inhibits de novo HBV infection.PLoS pathogens · 2025Article
- Hepatitis B virus entry, assembly, and egress.Microbiology and molecular biology reviews : MMBR · 2024Review
- SARS-CoV-2 nsp13 suppresses hepatitis B virus replication by targeting cccDNA transcription.Journal of virology · 2024Article
- Extracellular Vesicles in Viral Liver Diseases.Viruses · 2024Review
- NEDD4 family ubiquitin ligase AIP4 interacts with Alix to enable HBV naked capsid egress in an Alix ubiquitination-independent manner.PLoS pathogens · 2024Article
- Oncoviral Infections and Small Extracellular Vesicles.Viruses · 2024Review
- Hepatitis B virus RNAs co-opt ELAVL1 for stabilization and CRM1-dependent nuclear export.PLoS pathogens · 2024Article
- Interconnection of cellular autophagy and endosomal vesicle trafficking and its role in hepatitis B virus replication and release.Virologica Sinica · 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
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) chronically infects 296 million individuals and there is no cure. As an important step of viral life cycle, the mechanisms of HBV egress remain poorly elucidated. With proteomic approach to identify capsid protein (HBc) associated host factors and siRNA screen, we uncovered tumor susceptibility gene 101 (TSG101). Knockdown of TSG101 in HBV-producing cells, HBV-infected cells and HBV transgenic mice suppressed HBV release. Co-immunoprecipitation and site mutagenesis revealed that VFND motif in TSG101 and Lys-96 ubiquitination in HBc were essential for TSG101-HBc interaction. In vitro ubiquitination experiment demonstrated that UbcH6 and NEDD4 were potential E2 ubiquitin-conjugating enzyme and E3 ligase that catalyzed HBc ubiquitination, respectively. PPAY motif in HBc and Cys-867 in NEDD4 were required for HBc ubiquitination, TSG101-HBc interaction and HBV egress. Transmission electron microscopy confirmed that TSG101 or NEDD4 knockdown reduces HBV particles count in multivesicular bodies (MVBs). Our work indicates that TSG101 recognition for NEDD4 ubiquitylated HBc is critical for MVBs mediated HBV egress.
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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.