ArticlePLoS pathogens2015
The Dual Role of an ESCRT-0 Component HGS in HBV Transcription and Naked Capsid Secretion.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 87 citations in OpenAlex.
- ESCRT Machinery in HBV Life Cycle: Dual Roles in Autophagy and Membrane Dynamics for Viral Pathogenesis.Cells · 2025Review
- Exosomes at the crossroads of HIV-1 pathogenesis and therapeutics.Frontiers in immunology · 2025Review
- Unveiling the Molecular Architecture of HBV Spherical Subviral Particles: Structure, Symmetry, and Lipid Dynamics.Viruses · 2024Review
- HRS Facilitates Newcastle Disease Virus Replication in Tumor Cells by Promoting Viral Budding.International journal of molecular sciences · 2024Article
- Identification of Host Proteins Involved in Hepatitis B Virus Genome Packaging.Journal of proteome research · 2024Article
- NEDD4 family ubiquitin ligase AIP4 interacts with Alix to enable HBV naked capsid egress in an Alix ubiquitination-independent manner.PLoS pathogens · 2024Article
- Significance of hepatitis B virus capsid dephosphorylation via polymerase.Journal of biomedical science · 2024Article
- Interconnection of cellular autophagy and endosomal vesicle trafficking and its role in hepatitis B virus replication and release.Virologica Sinica · 2024Review
- Review
- Excess filaggrin in keratinocytes is removed by extracellular vesicles to prevent premature death and this mechanism can be hijacked by Staphylococcus aureus in a TLR2-dependent fashion.Journal of extracellular vesicles · 2023Article
- The multifaceted interactions between pathogens and host ESCRT machinery.PLoS pathogens · 2023Review
- Release of hepatitis B virions is positively regulated by glucose-regulated protein 78 through direct interaction with preS1.Journal of medical virology · 2023Article
- Insights into the function of ESCRT and its role in enveloped virus infection.Frontiers in microbiology · 2023Review
- Small extracellular vesicles as key players in cancer development caused by human oncogenic viruses.Infectious agents and cancer · 2022Review
- Autophagic membranes participate in hepatitis B virus nucleocapsid assembly, precore and core protein trafficking, and viral release.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Hepatitis B virus virion secretion is a CRM1-spike-mediated late event.Journal of biomedical science · 2022Article
- Multiomics Analysis of Endocytosis upon HBV Infection and Identification of SCAMP1 as a Novel Host Restriction Factor against HBV Replication.International journal of molecular sciences · 2022Article
- A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion.Journal of biomedical science · 2021Article
- The Hepatitis B Virus Nucleocapsid-Dynamic Compartment for Infectious Virus Production and New Antiviral Target.Biomedicines · 2021Review
- The Role of Exosome and the ESCRT Pathway on Enveloped Virus Infection.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Endosomal Sorting Complex Required for Transport (ESCRT) is an important cellular machinery for the sorting and trafficking of ubiquitinated cargos. It is also known that ESCRT is required for the egress of a number of viruses. To investigate the relationship between ESCRT and hepatitis B virus (HBV), we conducted an siRNA screening of ESCRT components for their potential effect on HBV replication and virion release. We identified a number of ESCRT factors required for HBV replication, and focused our study here on HGS (HRS, hepatocyte growth factor-regulated tyrosine kinase substrate) in the ESCRT-0 complex. Aberrant levels of HGS suppressed HBV transcription, replication and virion secretion. Hydrodynamic delivery of HGS in a mouse model significantly suppressed viral replication in the liver and virion secretion in the serum. Surprisingly, overexpression of HGS stimulated the release of HBV naked capsids, irrespective of their viral RNA, DNA, or empty contents. Mutant core protein (HBc 1-147) containing no arginine-rich domain (ARD) failed to secrete empty virions with or without HGS. In contrast, empty naked capsids of HBc 1-147 could still be promoted for secretion by HGS. HGS exerted a strong positive effect on the secretion of naked capsids, at the expense of a reduced level of virions. The association between HGS and HBc appears to be ubiquitin-independent. Furthermore, HBc is preferentially co-localized with HGS near the cell periphery, instead of near the punctate endosomes in the cytoplasm. In summary, our work demonstrated the importance of an optimum level of HGS in HBV propagation. In addition to an effect on HBV transcription, HGS can diminish the pool size of intracellular nucleocapsids with ongoing genome maturation, probably in part by promoting the secretion of naked capsids. The secretion routes of HBV virions and naked capsids can be clearly distinguished based on the pleiotropic effect of HGS involved in the ESCRT-0 complex.
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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.