ArticleJournal of virology1999
Induction of syncytia by neuropathogenic murine leukemia viruses depends on receptor density, host cell determinants, and the intrinsic fusion potential of envelope protein.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- A Replication-Competent Retroviral Vector Expressing the HERV-W Envelope Glycoprotein is a Potential Tool for Cancer Gene Therapy.Journal of microbiology and biotechnology · 2024Article
- Review
- Mutation of the Putative Immunosuppressive Domain of the Retroviral Envelope Glycoprotein Compromises Infectivity.Journal of virology · 2017Article
- Targeted entry via somatostatin receptors using a novel modified retrovirus glycoprotein that delivers genes at levels comparable to those of wild-type viral glycoproteins.Journal of virology · 2012Article
- Ephrin-B2 expression critically influences Nipah virus infection independent of its cytoplasmic tail.Virology journal · 2008Article
- Mouse mammary tumor virus uses mouse but not human transferrin receptor 1 to reach a low pH compartment and infect cells.Virology · 2008Article
- The MuLV 4070A G541R Env mutation decreases the stability and alters the conformation of the TM ectodomain.Virology · 2008Article
- Differential resistance to cell entry by porcine endogenous retrovirus subgroup A in rodent species.Retrovirology · 2007Article
- Changes in viral protein function that accompany retroviral endogenization.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- TR1.3 viral pathogenesis and syncytium formation are linked to Env-Gag cooperation.Journal of virology · 2007Article
- Feline leukemia virus T entry is dependent on both expression levels and specific interactions between cofactor and receptor.Virology · 2007Article
- Linkage of reduced receptor affinity and superinfection to pathogenesis of TR1.3 murine leukemia virus.Journal of virology · 2006Article
- HTLV-1 and -2 envelope SU subdomains and critical determinants in receptor binding.Retrovirology · 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
- Complementation of a binding-defective retrovirus by a host cell receptor mutant.Journal of virology · 2004Article
- G541R within the 4070A TM protein regulates fusion in murine leukemia viruses.Journal of virology · 2003Article
- Membrane fusion tropism and heterotypic functional activities of the Nipah virus and Hendra virus envelope glycoproteins.Journal of virology · 2002Article
- Relationship between SU subdomains that regulate the receptor-mediated transition from the native (fusion-inhibited) to the fusion-active conformation of the murine leukemia virus glycoprotein.Journal of virology · 2002Article
- Activation of membrane fusion by murine leukemia viruses is controlled in cis or in trans by interactions between the receptor-binding domain and a conserved disulfide loop of the carboxy terminus of the surface glycoprotein.Journal of virology · 2001Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Infection by the neuropathogenic murine leukemia virus (MLV) TR1.3 results in hemorrhagic disease that correlates directly to in vivo syncytium formation of brain capillary endothelial cells (BCEC). This phenotype maps to amino acid 102 in the envelope (Env) protein of TR1.3. Substitution of glycine (G) for tryptophan (W) at this position (W102G Env) in the nonpathogenic MLV FB29 induces both syncytium formation and neurologic disease in vivo. Using an in vitro gene reporter cell fusion assay, we showed that fusion either with murine NIH 3T3 cells or with nonmurine target cells that expressed receptors at or below endogenous murine levels mirrored that seen in BCEC in vivo. In these instances only TR1.3 and W102G Env induced cell fusion. In contrast, when receptor levels on nonmurine cells were raised above endogenous murine levels, FB29 Env was as fusogenic as the neuropathogenic TR1.3 and W102G Env. These results indicate that TR1.3 Env and W102G Env are intrinsically more fusogenic than FB29 Env, that the induction of fusion requires a threshold number of receptors that is greater for FB29 Env than for TR1.3 or W102G Env, and that receptor density on murine NIH 3T3 cells and BCEC is below the threshold for FB29-dependent fusion. Surprisingly, receptor density on NIH 3T3 cells could not be increased by stable expression of exogenous receptors, and FB29-dependent fusion was not observed in NIH 3T3 cells that transiently expressed elevated receptor numbers. These results suggest that an additional undefined host cell factor(s) may limit both receptor expression and fusion potential in murine cells.
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