ArticleJournal of virology2000
Cellular receptor traffic is essential for productive duck hepatitis B virus infection.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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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.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Characterization of Host Cell Potential Proteins Interacting with OsHV-1 Membrane Proteins.Viruses · 2021Article
- Natural resistance-associated macrophage protein is a cellular receptor for sindbis virus in both insect and mammalian hosts.Cell host & microbe · 2011Article
- Initiation of duck hepatitis B virus infection requires cleavage by a furin-like protease.Journal of virology · 2010Article
- Entry of duck hepatitis B virus into primary duck liver and kidney cells after discovery of a fusogenic region within the large surface protein.Journal of virology · 2007Article
- Viral and cellular determinants involved in hepadnaviral entry.World journal of gastroenterology · 2007Review
- Identification of a structural motif crucial for infectivity of hepatitis B viruses.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- A hydrophobic domain in the large envelope protein is essential for fusion of duck hepatitis B virus at the late endosome.Journal of virology · 2005Article
- Glycoprotein D receptor-dependent, low-pH-independent endocytic entry of herpes simplex virus type 1.Journal of virology · 2005Article
- NACA as a potential cellular target of hepatitis B virus preS1 protein.Digestive diseases and sciences · 2005Article
- Interactions between virus proteins and host cell membranes during the viral life cycle.International review of cytology · 2005Review
- Superinfection exclusion in duck hepatitis B virus infection is mediated by the large surface antigen.Journal of virology · 2004Article
- Study of the early steps of the Hepatitis B Virus life cycle.International journal of medical sciences · 2004Article
- Hepatitis B virus large envelope protein interacts with gamma2-adaptin, a clathrin adaptor-related protein.Journal of virology · 2001Article
- Envelope protein-mediated down-regulation of hepatitis B virus receptor in infected hepatocytes.Journal of virology · 2001Article
- A metastable form of the large envelope protein of duck hepatitis B virus: low-pH release results in a transition to a hydrophobic, potentially fusogenic conformation.Journal of virology · 2000Article
- Receptor recognition by a hepatitis B virus reveals a novel mode of high affinity virus-receptor interaction.The EMBO journal · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the mechanism of duck hepatitis B virus (DHBV) entry into susceptible primary duck hepatocytes (PDHs), using mutants of carboxypeptidase D (gp180), a transmembrane protein shown to act as the primary cellular receptor for avian hepatitis B virus uptake. The variant proteins were abundantly produced from recombinant adenoviruses and tested for the potential to functionally outcompete the endogenous wild-type receptor. Overexpression of wild-type gp180 significantly enhanced the efficiency of DHBV infection in PDHs but did not affect ongoing DHBV replication, an observation further supporting gp180 receptor function. A gp180 mutant deficient for endocytosis abolished DHBV infection, indicating endocytosis to be the route of hepadnaviral entry. With further gp180 variants, carrying mutations in the cytoplasmic domain and characterized by an accelerated turnover, the ability of gp180 to function as a DHBV receptor was found to depend on a wild-type-like sorting phenotype which largely avoids transport toward the endolysosomal compartment. Based on these data, we propose a model in which a distinct intracellular DHBV traffic to the endosome, but not beyond, is a prerequisite for completion of viral entry, i.e., for fusion and capsid release. Furthermore, the deletion of the two enzymatically active carboxypeptidase domains of gp180 did not lead to a loss of receptor function.
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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 OpenQuestion graph.