ArticleJournal of virology2001
A unique heparin-binding domain in the envelope protein of the neuropathogenic PVC-211 murine leukemia virus may contribute to its brain capillary endothelial cell tropism.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Heparan sulfate proteoglycan-mediated dynamin-dependent transport of neural stem cell exosomes in an in vitro blood-brain barrier model.The European journal of neuroscience · 2021Article
- Symmetry-related clustering of positive charges is a common mechanism for heparan sulfate binding in enteroviruses.Journal of virology · 2012Article
- Adeno-associated viral vectors based on serotype 3b use components of the fibroblast growth factor receptor signaling complex for efficient transduction.Human gene therapy · 2012Article
- Primate gammaretroviruses require an ancillary factor not required for murine gammaretroviruses to infect BHK cells.Journal of virology · 2011Article
- Importance of macrophage inflammatory protein-1α and splenic macrophages in neurodegeneration induced by PVC-211 murine leukemia virus.Virology · 2011Article
- Naturally Occurring Polymorphisms of the Mouse Gammaretrovirus Receptors CAT-1 and XPR1 Alter Virus Tropism and Pathogenicity.Advances in virology · 2011Article
- Cell entry of enveloped viruses.Advances in genetics · 2011Review
- Neurodegeneration induced by PVC-211 murine leukemia virus is associated with increased levels of vascular endothelial growth factor and macrophage inflammatory protein 1 alpha and is inhibited by blocking activation of microglia.Journal of virology · 2009Article
- A mouse-passaged dengue virus strain with reduced affinity for heparan sulfate causes severe disease in mice by establishing increased systemic viral loads.Journal of virology · 2008Article
- Changes in viral protein function that accompany retroviral endogenization.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Heparan sulfate proteoglycans mediate attachment and entry of human T-cell leukemia virus type 1 virions into CD4+ T cells.Journal of virology · 2005Article
- Human rhinovirus type 89 variants use heparan sulfate proteoglycan for cell attachment.Journal of virology · 2005Article
- Heparan sulfate-independent infection attenuates high-neurovirulence GDVII virus-induced encephalitis.Journal of virology · 2004Article
- Disparate regions of envelope protein regulate syncytium formation versus spongiform encephalopathy in neurological disease induced by murine leukemia virus TR.Journal of virology · 2004Article
- Identification of the receptor binding domain of the mouse mammary tumor virus envelope protein.Journal of virology · 2003Article
- G100R mutation within 4070A murine leukemia virus Env increases virus receptor binding, kinetics of entry, and viral transduction efficiency.Journal of virology · 2003Article
- Host range and receptor binding properties of vectors bearing feline leukemia virus subgroup B envelopes can be modulated by envelope sequences outside of the receptor binding domain.Journal of virology · 2002Article
- Heparin binds to murine leukemia virus and inhibits Env-independent attachment and infection.Journal of virology · 2002Article
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3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Previous studies from our laboratory demonstrated that PVC-211 murine leukemia virus (MuLV), a neuropathogenic variant of Friend MuLV (F-MuLV), had undergone genetic changes which allowed it to efficiently infect rat brain capillary endothelial cells (BCEC) in vivo and in vitro. Two amino acid changes from F-MuLV in the putative receptor binding domain (RBD) of the envelope surface protein of PVC-211 MuLV (Glu-116 to Gly and Glu-129 to Lys) were shown to be sufficient for conferring BCEC tropism on PVC-211 MuLV. Recent examination of the unique RBD of PVC-211 MuLV revealed that the substitution of Lys for Glu at position 129 created a new heparin-binding domain that overlapped a heparin-binding domain common to ecotropic MuLVs. In this study we used heparin-Sepharose columns to demonstrate that PVC-211 MuLV, but not F-MuLV, can bind efficiently to heparin and that one or both of the amino acids in the RBD of PVC-211 MuLV that are associated with BCEC tropism are responsible. We further showed that heparin can enhance or inhibit MuLV infection and that the mode of action is dependent on heparin concentration, sulfation of heparin, and the affinity of the virus for heparin. Our results suggest that the amino acid changes that occurred in the envelope surface protein of PVC-211 MuLV may allow the virus to bind strongly to the surface of BCEC via heparin-like molecules, increasing the probability that the virus will bind to its cell surface receptor and efficiently infect these cells.
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