ArticleScientific reports2015
Identification of BST-2/tetherin-induced hepatitis B virus restriction and hepatocyte-specific BST-2 inactivation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 38 citations in OpenAlex.
- Real-Time Imaging of HIV-1 Protease Activation and Substrate Cleavage in Single Virions Assembling on the Plasma Membrane.Viruses · 2026Article
- BST-2 inhibits SARS-CoV-2 egress at intracellular membranes and is neutralized by ORF7a.Scientific reports · 2026Article
- Emerging Oncogenic and Immunoregulatory Roles of BST2 in Human Cancers.Biomedicines · 2026Review
- CD317 functions as a key antiviral factor in human herpesvirus 6 (HHV-6) infection.Journal of virology · 2025Article
- Review
- TLR-mediated aggresome-like induced structures comprise antimicrobial peptides and attenuate intracellular bacterial survival.Molecular biology of the cell · 2024Article
- Galectin-9 restricts hepatitis B virus replication via p62/SQSTM1-mediated selective autophagy of viral core proteins.Nature communications · 2022Article
- BST2 Suppresses LINE-1 Retrotransposition by Reducing the Promoter Activity of LINE-1 5' UTR.Journal of virology · 2022Article
- Deubiquitinating Enzyme USP21 Inhibits HIV-1 Replication by Downregulating Tat Expression.Journal of virology · 2021Article
- Increased BST-2 expression by HBV infection promotes HBV-associated HCC tumorigenesis.Journal of gastrointestinal oncology · 2021Article
- Specific Deubiquitinating Enzymes Promote Host Restriction Factors Against HIV/SIV Viruses.Frontiers in immunology · 2021Article
- The Hepatitis B Virus Interactome: A Comprehensive Overview.Frontiers in microbiology · 2021Review
- Review
- ATP1B3 cooperates with BST-2 to promote hepatitis B virus restriction.Journal of medical virology · 2020Article
- TRIM21-mediated proteasomal degradation of SAMHD1 regulates its antiviral activity.EMBO reports · 2020Article
- SERINC5 Inhibits the Secretion of Complete and Genome-Free Hepatitis B Virions Through Interfering With the Glycosylation of the HBV Envelope.Frontiers in microbiology · 2020Article
- Long Noncoding RNA ITPRIP-1 Positively Regulates the Innate Immune Response through Promotion of Oligomerization and Activation of MDA5.Journal of virology · 2018Article
- Development of a cell-based assay to identify hepatitis B virus entry inhibitors targeting the sodium taurocholate cotransporting polypeptide.Oncotarget · 2018Article
- Review
- A robust cell culture system supporting the complete life cycle of hepatitis B virus.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BST-2/tetherin is an interferon-inducible antiviral protein that blocks the release of various enveloped viruses, including HIV-1. Hepatitis B virus (HBV), a major cause of liver disease, belongs to the Hepadnaviridae family of enveloped DNA viruses. Whether BST-2 regulates HBV production is largely unknown. In this report, we have demonstrated that HBV particle release is modulated by BST-2 in a cell type-dependent fashion. In HEK293T cells, ectopically expressed or interferon-induced BST-2 strongly inhibited HBV release. BST-2 co-localized with HBV surface protein at multivesicular bodies (MVBs) and physically interacted with HBV particles. However, exogenous BST-2-induced HBV restriction was weak in Huh-7 hepatoma cells, and the interferon-induced anti-HBV effect was independent of BST-2 induction in hepatic L02 cells. Notably, HBV could promote HIV-1 ΔVpu virus release from BST-2-positive HepG2 hepatoma cells but not HeLa cells, whereas Vpu failed to efficiently inhibit BST-2-induced HBV restriction. HBx exhibited an enhanced interaction and co-localization with BST-2 in hepatocytes. These observations indicate that BST-2 restricts HBV production at intracellular MVBs but is inactivated by HBV through a novel mechanism requiring hepatocyte-specific cellular co-factors or a hepatocyte-specific environment. Further understanding of BST-2-induced HBV restriction may provide new therapeutic targets for future HBV treatments.
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