Avian sarcoma and leukosis virus-receptor interactions: From classical genetics to novel insights into virus - Cell membrane fusion

The Infectious Disease Laboratory, The Salk Institute, La Jolla, San Diego, CA 92037-1099, USA.
Virology (Impact Factor: 3.32). 02/2006; 344(1):25-9. DOI: 10.1016/j.virol.2005.09.021
Source: PubMed


For over 40 years, avian sarcoma and leukosis virus (ASLV)-receptor interactions have been employed as a useful model system to study the mechanism of retroviral entry into cells. Pioneering studies on this system focused upon the genetic basis of the differential susceptibilities of different lines of chickens to infection by distinct subgroups of ASLV. These studies led to the definition of three distinct autosomal recessive genes that were predicted to encode cellular receptors for different viral subgroups. They also led to the concept of viral interference, i.e. the mechanism by which infection by one virus can render cells resistant to reinfection by other viruses that use the same cellular receptor. Here, we review the contributions that analyses of the ASLV-receptor system have made in unraveling the mechanisms of retroviral entry into cells and focus on key findings such as identification and characterization of the ASLV receptor genes and the subsequent elucidation of an unprecedented mechanism of virus-cell fusion. Since many of the initial findings on this system were published in the early volumes of Virology, this subject is especially well suited to this special anniversary issue of the journal.

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Available from: Daniel Elleder, Dec 25, 2013
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    • "However, because the cellular receptor for CrERV is not known, we cannot exclude that it is mutated in deer. Selection for such mutations in receptors for ERVs has been documented in endogenous avian leukosis viruses (ALV) and murine leukemia viruses (MLVs) (Barnard et al., 2006; Kozak, 2015). Treatment with tunicamycin, inhibitor of N-linked glycosylation, has been shown in some cases to abrogate resistance to retrovirus entry, by deglycosylation of the cellular receptors or the virus envelope proteins (Koo et al., 1994; Miller and Miller, 1992). "
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    ABSTRACT: Endogenous retroviruses (ERVs) were acquired during evolution of their host organisms after infection and mendelian inheritance in the germline by their exogenous counterparts. The ERVs can spread in the host genome and in some cases they affect the host phenotype. The cervid endogenous gammaretrovirus (CrERV) is one of only a few well-defined examples of evolutionarily recent invasion of mammalian genome by retroviruses. Thousands of insertionally polymorphic CrERV integration sites have been detected in wild ranging mule deer (Odocoileus hemionus) host populations. Here, we describe for the first time induction of replication competent CrERV by cocultivation of deer and human cells. We characterize the physical properties and tropism of the induced virus. The genomic sequence of the induced virus is phylogenetically related to the evolutionarily young endogenous CrERVs described so far. We also describe the level of replication block of CrERV on deer cells and its capacity to establish superinfection interference. Copyright © 2015 Elsevier Inc. All rights reserved.
    Virology 07/2015; 485. DOI:10.1016/j.virol.2015.07.003 · 3.32 Impact Factor
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    • "). EnvA limits infection to cells that express the TVA receptor, a protein found in birds but not mammals (Barnard et al., 2006). As developed by Wickersham et al. (2007b) for the resulting pseudotyped virus, EnvA-SAD∆G-GFP, to work as a 'singlecell tracer' three genes must be delivered to the target neuron prior to delivering the virus (Fig. 13 "

    Mononegaviruses of Veterinary Importance: Pathobiology and Molecular Diagnosis, Edited by Muhammad Munir, 09/2013: chapter 13: pages 209-229; CAB International.
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    • "Fusion mediated by ASLV Env and Tva800 or Tva950 requires a low pH step for entry via endosomes [13,14]. Virus binding triggers a conformational change in Env that exposes the fusion peptide, which is then inserted into the cellular membrane [13,15]. Exposure of the sensitised Env to low pH in the endosomes will lead to fusion of viral and cellular membranes [16]. "
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    ABSTRACT: Understanding the mechanism by which viruses enter their target cell is an essential part of understanding their infectious cycle. Previous studies have focussed on the multiplicity of viral envelope proteins that need to bind to their cognate receptor to initiate entry. Avian sarcoma and leukosis virus Envelope protein (ASLV Env) mediates entry via a receptor, Tva, which can be attached to the cell surface either by a phospholipid anchor (Tva800) or a transmembrane domain (Tva950). In these studies, we have now investigated the number of target receptors necessary for entry of ASLV Env-pseudotyped virions. Using titration and modelling experiments we provide evidence that binding of more than one receptor, probably two, is needed for entry of virions via Tva800. However, binding of just one Tva950 receptor is sufficient for successful entry. The different modes of attachment of Tva800 and Tva950 to the cell membrane have important implications for the utilisation of these proteins as receptors for viral binding and/or uptake.
    Retrovirology 11/2011; 8(1):96. DOI:10.1186/1742-4690-8-96 · 4.19 Impact Factor
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