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: 3.28). 02/2006; 344(1):25-9. DOI: 10.1016/j.virol.2005.09.021
Source: PubMed

ABSTRACT 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.

Download full-text


Available from: Daniel Elleder, Dec 25, 2013
  • Source
    • "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). "
    [Show abstract] [Hide abstract]
    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 · 3.28 Impact Factor
  • Source
    • "). 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.
  • Source
    • "To perform monosynaptic circuit tracing and target FP-expressing RV to desired neuronal subsets, the particles can first be pseudotyped with the foreign coat protein EnvA from avian sarcoma leukosis virus, which specifically binds to a class of avian membrane proteins called TVA receptors (Barnard et al., 2006). Genetic targeting of neuronal subsets for TVA expression directs RV infection to only those neurons. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Much has been learned about the environmental and molecular factors that influence the division, migration, and programmed cell death of adult-born neurons in the mammalian brain. However, detailed knowledge of the mechanisms that govern the formation and maintenance of functional circuit connectivity via adult neurogenesis remains elusive. Recent advances in genetic technologies now afford the ability to precisely target discrete brain tissues, neuronal subtypes, and even single neurons for vital reporter expression and controlled activity manipulations. Here, I review current viral tracing methods, heterologous receptor expression systems, and optogenetic technologies that hold promise toward elucidating the wiring diagrams and circuit properties of adult-born neurons.
    Frontiers in Neuroscience 04/2011; 5:48. DOI:10.3389/fnins.2011.00048 · 3.70 Impact Factor
Show more