Alpharetrovirus Envelope-Receptor Interactions

Barnard, Richard; Young, John A. T.

doi:10.1007/978-3-642-19012-4_3

Cited by 36 publications

(37 citation statements)

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“…Other enveloped viruses that employ class I fusion proteins use the viral glycoprotein receptor interaction to traffic the viral particle to an endocytic compartment, where low pH is required to trigger conformational changes in the viral glycoproteins initiating the fusion process. The avian sarcoma and leukosis virus (ASLV) family of retroviruses uses a third mechanism of entry: the initial interaction of the ASLV glycoproteins with their receptor triggers an initial conformational change at the cell surface but then requires exposure to a low-pH environment to complete the conformational changes that can enable the completion of the fusion process (5,6).…”

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confidence: 99%

“…Five highly related ASLV envelope subgroups that infect chickens, ASLV subgroup A [ASLV(A)] through ALSV(E), likely evolved from a common ancestor: their envelope glycoproteins are highly conserved, except for five variable domains in SU glycoproteins (vr1, vr2, hr1, hr2, and vr3) (5)(6)(7)(8)(9)(10)(11)(12)(13). A variety of studies have identified hr1 and hr2 to be the principal binding domains between the viral glycoprotein and receptor, with vr3 contributing to the specificity of the receptor interaction for initiating a productive infection.…”

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confidence: 99%

“…TVC proteins, which are proteins related to mammalian butyrophilins, members of the immunoglobulin protein family, are receptors for ASLV(C) (20). These five ASLV subgroups are examples of the ability of retroviruses to evolve their highly conserved envelope glycoproteins to efficiently use different cell surface proteins as functional receptors for infection (5,6,9).…”

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Model of the TVA Receptor Determinants Required for Efficient Infection by Subgroup A Avian Sarcoma and Leukosis Viruses

Melder

Pike

VanBrocklin

et al. 2015

J Virol

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The study of the interactions of subgroup A avian sarcoma and leucosis viruses [ASLV(A)] with the TVA receptor required to infect cells offers a powerful experimental model of retroviral entry. Several regions and specific residues in the TVA receptor have previously been identified to be critical determinants of the binding affinity with ASLV(A) envelope glycoproteins and to mediate efficient infection. Two homologs of the TVA receptor have been cloned: the original quail TVA receptor, which has been the basis for most of the initial characterization of the ASLV(A) TVA, and the chicken TVA receptor, which is 65% identical to the quail receptor overall but identical in the region thought to be critical for infection. Our previous work characterized three mutant ASLV(A) isolates that could efficiently bind and infect cells using the chicken TVA receptor homolog but not using the quail TVA receptor homolog, with the infectivity of one mutant virus being >500-fold less with the quail TVA receptor. The mutant viruses contained mutations in the hr1 region of the surface glycoprotein. Using chimeras of the quail and chicken TVA receptors, we have identified new residues of TVA critical for the binding affinity and entry of ASLV(A) using the mutant glycoproteins and viruses to probe the function of those residues. The quail TVA receptor required changes at residues 10, 14, and 31 of the corresponding chicken TVA residues to bind wild-type and mutant ASLV(A) glycoproteins with a high affinity and recover the ability to mediate efficient infection of cells. A model of the TVA determinants critical for interacting with ASLV(A) glycoproteins is proposed. IMPORTANCE A detailed understanding of how retroviruses enter cells, evolve to use new receptors, and maintain efficient entry is crucial for identifying new targets for combating retrovirus infection and pathogenesis, as well as for developing new approaches for targeted gene delivery.Since all retroviruses share an envelope glycoprotein organization, they likely share a mechanism of receptor triggering to begin the entry process. Multiple, noncontiguous interaction determinants located in the receptor and the surface (SU) glycoprotein hypervariable domains are required for binding affinity and to restrict or broaden receptor usage. In this study, further mechanistic details of the entry process were elucidated by characterizing the ASLV(A) glycoprotein interactions with the TVA receptor required for entry. The ASLV(A) envelope glycoproteins are organized into functional domains that allow changes in receptor choice to occur by mutation and/or recombination while maintaining a critical level of receptor binding affinity and an ability to trigger glycoprotein conformational changes. For enveloped viruses to infect cells, they must fuse their viral membrane with a cellular membrane. For retroviruses, the interaction of the viral envelope glycoproteins with a cellular surface protein receptor initiates the entry and fusion process (1, 2). Retroviral envelope glycopro...

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Model of the TVA Receptor Determinants Required for Efficient Infection by Subgroup A Avian Sarcoma and Leukosis Viruses

Melder

Pike

VanBrocklin

et al. 2015

J Virol

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“…Genetic alteration(s) can account for resistance, resulting in the complete lack of receptor protein expression or the expression of an aberrant protein not suitable as a viral receptor. In addition, receptors can be saturated with viral glycoproteins expressed by the cell, physically blocking receptor accessibility, a phenomenon known as receptor interference (14, 24).The avian sarcoma and leukosis virus (ASLV) family of retroviruses contains five highly related envelope subgroups (A to E) thought to have evolved in the chicken population from a common viral ancestor (4,5,24). Three genetic loci in chickens determine the susceptibility or resistance of cells to infection by the subgroup A to E ASLVs.…”

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“…The avian sarcoma and leukosis virus (ASLV) family of retroviruses contains five highly related envelope subgroups (A to E) thought to have evolved in the chicken population from a common viral ancestor (4,5,24). Three genetic loci in chickens determine the susceptibility or resistance of cells to infection by the subgroup A to E ASLVs.…”

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A Single-Amino-Acid Substitution in the Tvb ^S1 Receptor Results in Decreased Susceptibility to Infection by Avian Sarcoma and Leukosis Virus Subgroups B and D and Resistance to Infection by Subgroup E In Vitro and In Vivo

Reinišová

Šenigl

Yin

et al. 2008

J Virol

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The avian sarcoma and leukosis virus (ASLV) family of retroviruses contains five highly related envelope subgroups (A to E) thought to have evolved from a common viral ancestor in the chicken population. Three genetic loci in chickens determine the susceptibility or resistance of cells to infection by the subgroup A to E ASLVs. Some inbred lines of chickens display phenotypes that are somewhere in between either efficiently susceptible or resistant to infection by specific subgroups of ASLV. The tvb gene encodes the receptor for subgroups B, D, and E ASLVs. The wild-type Tvb S1 receptor confers susceptibility to subgroups B, D, and E ASLVs. In this study, the genetic defect that accounts for the altered susceptibility of an inbred chicken Retroviruses cause serious diseases in animals and humans. The disease process begins with the virus infecting a cell(s), a process mediated by the interaction of the retroviral envelope glycoproteins with specific cell surface proteins that act as receptors (14,24). A proper viral-glycoprotein-receptor interaction initiates conformational changes in the viral glycoproteins that ultimately result in the fusion of the viral and cellular membranes and entry of viral components (9). Despite the complexity and specificity of the viral-glycoprotein-receptor interaction required for virus entry, families of closely related retroviruses have evolved their glycoproteins to use different cellular proteins as receptors. Presumably, the presence of multiple viral subgroups that utilize different receptors is an advantage for viruses in overcoming host resistance. Resistance to retroviral infection occurs when the specific receptor protein is not available. Genetic alteration(s) can account for resistance, resulting in the complete lack of receptor protein expression or the expression of an aberrant protein not suitable as a viral receptor. In addition, receptors can be saturated with viral glycoproteins expressed by the cell, physically blocking receptor accessibility, a phenomenon known as receptor interference (14, 24).The avian sarcoma and leukosis virus (ASLV) family of retroviruses contains five highly related envelope subgroups (A to E) thought to have evolved in the chicken population from a common viral ancestor (4,5,24). Three genetic loci in chickens determine the susceptibility or resistance of cells to infection by the subgroup A to E ASLVs. Susceptibility to subgroup A ASLVs is determined by the tva locus; susceptibility to subgroup C ASLVs by the tvc locus; and susceptibility to the subgroup B, D, and E ASLVs by the tvb locus. The Tva proteins are related to the low-density lipoprotein receptor family (6, 25). The Tvb proteins are related to the tumor necrosis factor receptor (TNFR) family (2, 3, 7). The Tvc proteins are most closely related to mammalian butyrophilins of the immunoglobulin superfamily (11). The normal functions and ligands of the Tva, Tvb, and Tvc proteins in birds are unknown.The genetic defects that account for resistance to infection by specific ASLVs, tv...

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Cellular Entry of Retroviruses

Lindemann

Steffen

Pöhlmann

2013

Viral Entry Into Host Cells

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The retrovirus family contains several important human and animal pathogens, including the human immunodeficiency virus (HIV), the causative agent of acquired immunodeficiency syndrome (AIDS). Studies with retroviruses were instrumental to our present understanding of the cellular entry of enveloped viruses in general. For instance, studies with alpharetroviruses defined receptor engagement, as opposed to low pH, as a trigger for the envelope protein-driven membrane fusion. The insights into the retroviral entry process allowed the generation of a new class of antivirals, entry inhibitors, and these therapeutics are at present used for treatment of HIV/AIDS. In this chapter, we will summarize key concepts established for entry of avian sarcoma and leukosis virus (ASLV), a widely used model system for retroviral entry. We will then review how foamy virus and HIV, primate- and human retroviruses, enter target cells, and how the interaction of the viral and cellular factors involved in the cellular entry of these viruses impacts viral tropism, pathogenesis and approaches to therapy and vaccine development.

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Alpharetrovirus Envelope-Receptor Interactions

Cited by 36 publications

References 118 publications

Model of the TVA Receptor Determinants Required for Efficient Infection by Subgroup A Avian Sarcoma and Leukosis Viruses

Model of the TVA Receptor Determinants Required for Efficient Infection by Subgroup A Avian Sarcoma and Leukosis Viruses

A Single-Amino-Acid Substitution in the Tvb ^S1 Receptor Results in Decreased Susceptibility to Infection by Avian Sarcoma and Leukosis Virus Subgroups B and D and Resistance to Infection by Subgroup E In Vitro and In Vivo

Cellular Entry of Retroviruses

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Alpharetrovirus Envelope-Receptor Interactions

Cited by 36 publications

References 118 publications

Model of the TVA Receptor Determinants Required for Efficient Infection by Subgroup A Avian Sarcoma and Leukosis Viruses

Model of the TVA Receptor Determinants Required for Efficient Infection by Subgroup A Avian Sarcoma and Leukosis Viruses

A Single-Amino-Acid Substitution in the Tvb S1 Receptor Results in Decreased Susceptibility to Infection by Avian Sarcoma and Leukosis Virus Subgroups B and D and Resistance to Infection by Subgroup E In Vitro and In Vivo

Cellular Entry of Retroviruses

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A Single-Amino-Acid Substitution in the Tvb ^S1 Receptor Results in Decreased Susceptibility to Infection by Avian Sarcoma and Leukosis Virus Subgroups B and D and Resistance to Infection by Subgroup E In Vitro and In Vivo