ArticleScientific reports2017
Heparin at physiological concentration can enhance PEG-free in vitro infection with human hepatitis B virus.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
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- Antibodies blocking PlGF or VEGF interactions with the NRP1 receptor mediate anti-proliferative effects.bioRxiv : the preprint server for biology · 2025Article
- Syndecan 2 proteoglycan serves as a hepatitis B virus cell attachment receptor.Journal of virology · 2025Article
- Epitranscriptomic cytidine methylation of the hepatitis B viral RNA is essential for viral reverse transcription and particle production.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Cell Culture Models for Hepatitis B and D Viruses Infection: Old Challenges, New Developments and Future Strategies.Viruses · 2024Review
- Significance of hepatitis B virus capsid dephosphorylation via polymerase.Journal of biomedical science · 2024Article
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- Cell-Responsive Shape Memory Polymers.ACS biomaterials science & engineering · 2022Article
- Antiviral strategies should focus on stimulating the biosynthesis of heparan sulfates, not their inhibition.Life sciences · 2021Review
- Advances in HBV infection and replication systems in vitro.Virology journal · 2021Review
- Novel Naturally Occurring Mutations of Enterovirus 71 Associated With Disease Severity.Frontiers in microbiology · 2020Article
- Molecular mechanisms of heparin-induced modulation of human interleukin 12 bioactivity.The Journal of biological chemistry · 2019Article
- N-Linked Glycosylation Is Not Essential for Sodium Taurocholate Cotransporting Polypeptide To Mediate Hepatitis B Virus InfectionJournal of virology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) is a blood-borne pathogen responsible for chronic hepatitis, cirrhosis, and liver cancer. The mechanism of HBV entry into hepatocytes remains to be investigated. Recently, sodium taurocholate cotransporting polypeptide (NTCP) was discovered as a major HBV receptor based on an in vitro infection system using NTCP-reconstituted HepG2 cells. However, this infection system relies on the compound polyethylene glycol (4% PEG), which is not physiologically relevant to human infection. High concentration of heparin has been commonly used as an inhibitor control for in vitro infection in the field. Surprisingly, we found that heparin at physiological concentration can enhance HBV infection in a PreS1-peptide sensitive, NTCP-dependent manner in both HepaRG and HepG2-NTCP-AS cells. O-sulfation of heparin is more important for the infection enhancement than N-sulfation. This system based on the HepG2-NTCP-AS cells can support in vitro infection with HBV genotypes B and C, as well as using serum samples from HBeAg positive and negative chronic carriers. In summary, our study provides a PEG-free infection system closely resembling human natural infection. In addition, it points to a future research direction for heparin and heparin-binding host factor(s) in the blood, which are potentially involved in viral entry. To our knowledge, this is the first soluble and circulatory host factor which can enhance HBV in vitro infection.
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