ArticleJournal of virology2002
Heparin binds to murine leukemia virus and inhibits Env-independent attachment and infection.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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
19 citing papers in PubMed, 44 citations in OpenAlex.
- Pteropine orthoreoviruses use cell surface heparan sulphate as an attachment receptor.Emerging microbes & infections · 2023Article
- Heparanase is the possible link between monkeypox and Covid-19: robust candidature in the mystic and present perspective.AMB Express · 2023Review
- Heparin Protects Human Neural Progenitor Cells from Zika Virus-Induced Cell Death While Preserving Their Differentiation into Mature Neuroglial Cells.Journal of virology · 2022Article
- Lentiviral Vector Bioprocessing.Viruses · 2021Review
- Hypertension, Thrombosis, Kidney Failure, and Diabetes: Is COVID-19 an Endothelial Disease? A Comprehensive Evaluation of Clinical and Basic Evidence.Journal of clinical medicine · 2020Review
- Notable Aspects of Glycan-Protein Interactions.Biomolecules · 2015Review
- Shedding of clinical-grade lentiviral vectors is not detected in a gene therapy setting.Gene therapy · 2015Article
- Macropinocytosis is the entry mechanism of amphotropic murine leukemia virus.Journal of virology · 2015Article
- Human immunodeficiency virus and heparan sulfate: from attachment to entry inhibition.Frontiers in immunology · 2013Review
- Entry kinetics and cell-cell transmission of surface-bound retroviral vector particles.The journal of gene medicine · 2010Article
- Directional spread of surface-associated retroviruses regulated by differential virus-cell interactions.Journal of virology · 2010Article
- Identification of host proteins associated with retroviral vector particles by proteomic analysis of highly purified vector preparations.Journal of virology · 2008Article
- Matrix fibronectin binds gammaretrovirus and assists in entry: new light on viral infections.Journal of virology · 2007Article
- Primary attachment of murine leukaemia virus vector mediated by particle-associated heparan sulfate proteoglycan.The Biochemical journal · 2006Article
- Expression of HIV receptors, alternate receptors and co-receptors on tonsillar epithelium: implications for HIV binding and primary oral infection.Virology journal · 2006Article
- Early steps of retrovirus replicative cycle.Retrovirology · 2004Review
- The Trojan exosome hypothesis.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Determination of infectious retrovirus concentration from colony-forming assay with quantitative analysis.Journal of virology · 2003Article
- Evidence for nonspecific adsorption of targeted retrovirus vector particles to cells.Gene therapy · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Certain glycosaminoglycans (GAGs), including heparin, inhibit infection by murine leukemia virus (MLV). We now show that this is due to inhibition of virus attachment independent of the interaction between viral envelope proteins (Env) and their cellular receptors. Heparin blocked the binding of both Env-deficient and amphotropic MLV (MLV-A) particles to NIH 3T3 fibroblasts, CHO cells which lack the amphotropic retroviral receptor Pit-2, and CHO cells transfected with Pit-2 (CHO-Pit-2). Heparin also inhibited the transduction of NIH 3T3 cells by MLV-A over a similar concentration range. This effect was observed within 15 min of exposure to retrovirus. Preloading target cells with heparin had no effect on transduction and both MLV-A and Env-deficient retrovirus bound efficiently to heparin-coated agarose beads, suggesting that heparin interacts with the virus rather than the target cell. This requires both a strong negative charge and a specific structure since GAGs with different charge and carbohydrate composition inhibited virus infection variably. The specificity of GAG-virus interaction also depends on the producer cells, since virus packaged by murine GP+EnvAM12 cells was 1,000-fold more sensitive to inhibition by chondroitin sulfate A than was virus packaged by human FLYA13 packaging cells. No evidence for an interaction between MLV and cell surface proteoglycans was found, however, since the attachment of MLV-A and envelope-defective virus to proteoglycan-deficient CHOpgsA-745 cells was similar to that seen with both wild-type and CHO-Pit-2 cells. Although the molecular mechanism is unclear, this study presents evidence that Env receptor-independent attachment is an important step in MLV infection.
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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.