Identification of a cellular receptor for subgroup E avian leukosis virus

Adkins, Heather B.; Brojatsch, Jürgen; Naughton, John; Rolls, Melissa M.; Pesola, Jean M.; Young, John A. T.

doi:10.1073/pnas.94.21.11617

Cited by 89 publications

(88 citation statements)

References 23 publications

(22 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ALV uses certain membrane proteins as receptor sites to attach and get access into the cell. The main receptor proteins are those designated as Tva receptors for ALV subtype A (ALV-A), CAR1 for subtypes B & D, and SEAR for subtype E [2,15,55]. These proteins are encoded by autosomal genes called tumour virus (Tv) genes [7].…”

Section: Leukosis Virus Receptor Proteinsmentioning

confidence: 99%

Immunological basis of differences in disease resistance in the chicken

Zekarias

Huurne²,

Landman

et al. 2002

Vet. Res.

View full text Add to dashboard Cite

-Genetic resistance to diseases is a multigenic trait governed mainly by the immune system and its interactions with many physiologic and environmental factors. In the adaptive immunity, T cell and B cell responses, the specific recognition of antigens and interactions between antigen presenting cells, T cells and B cells are crucial. It occurs through a network of mediator proteins such as the molecules of the major histocompatibility complex (MHC), T cell receptors, immunoglobulins and secreted proteins such as the cytokines and antibodies. The diversity of these proteins that mainly is due to an intrinsic polymorphism of the genes causes phenotypic variation in disease resistance. The well-known linkage of MHC polymorphism and Marek's disease resistance difference represents a classic model revealing immunological factors in resistance differences and diversity of mediator molecules. The molecular bases in any resistance variation to infectious pathogens are vaguely understood. This paper presents a review of the major immune mediators involved in resistance and susceptibility to infectious diseases and their functional mechanisms in the chicken. The genetic interaction of disease resistance with production traits and the environment is mentioned. et les interactions entre les cellules présentant des antigènes, les cellules T et B, sont cruciales. Cela se produit à travers un réseau de protéines médiatrices telles que les molécules du complexe majeur d'histocompatibilité (CMH), les récepteurs des cellules T, les immunoglobulines et les protéines sé-crétées telles que les cytokines et les anticorps. La diversité de ces protéines, qui est surtout due au polymorphisme intrinsèque des gènes, entraîne une variation phénotypique dans la résistance aux maladies. Le lien bien connu entre le polymorphisme du CMH et les différences dans la résistance à la maladie de Marek représente un modèle classique révélant les facteurs immunologiques dans les différences de résistance et la diversité dans les molécules médiatrices. Les bases moléculaires impliquées dans toute variation de résistance aux pathogènes infectieux sont à peu près comprises. Cet article présente une synthèse sur les principaux médiateurs de l'immunité impliqués dans la résis-tance et la sensibilité aux maladies infectieuses chez le poulet et leurs mécanismes fonctionnels. L'interaction génétique entre la résistance aux maladies et les traits de production et l'environnement est mentionnée.

show abstract

Section: Leukosis Virus Receptor Proteinsmentioning

confidence: 99%

Immunological basis of differences in disease resistance in the chicken

Zekarias

Huurne²,

Landman

et al. 2002

Vet. Res.

View full text Add to dashboard Cite

show abstract

“…Although viruses in the ASLV-B, ASLV-D, and ASLV-E groups were initially thought to use different receptors based on their interference and host range properties, it is now clear that they all use closely related orthologs of a member of the tumor necrosis factor (TNF) receptor family denoted Tvb (also called CAR1 [for "cytopathic ASLV receptor"] for ASLV-B and ASLV-D and SEAR [for "subgroup E ASLV receptor"] for ASLV-E) (2,27). Tvb is most closely related to the human TNF receptor family members TRAIL-R1 and TRAIL-R2 and is likely to mediate the cell killing induced by ASLV-B and ASLV-D. As with ASLV-A and LDL proteins, it is interesting to hypothesize that the ASLV-B, ASLV-D, and ASLV-E Env proteins might show some amino acid similarity to TNF family proteins, the natural ligands for TNF receptor family proteins, and this might explain the Env specificity for Tvb; however, no such similarity is apparent.…”

Section: Receptors With a Single Membrane-spanning Region Single Tranmentioning

confidence: 99%

Receptors and Entry Cofactors for Retroviruses Include Single and Multiple Transmembrane-Spanning Proteins as well as Newly Described Glycophosphatidylinositol-Anchored and Secreted Proteins

Overbaugh

Miller

Eiden³

2001

Microbiol Mol Biol Rev

172

165

View full text Add to dashboard Cite

SUMMARY In the past few years, many retrovirus receptors, coreceptors, and cofactors have been identified. These molecules are important for some aspects of viral entry, although in some cases it remains to be determined whether they are required for binding or postbinding stages in entry, such as fusion. There are certain common features to the molecules that many retroviruses use to gain entry into the cell. For example, the receptors for most mammalian oncoretroviruses are multiple membrane-spanning transport proteins. However, avian retroviruses use single-pass membrane proteins, and a sheep retrovirus uses a glycosylphosphatidylinositol-anchored molecule as its receptor. For some retroviruses, particularly the lentiviruses, two cell surface molecules are required for efficient entry. More recently, a soluble protein that is required for viral entry has been identified for a feline oncoretrovirus. In this review, we will focus on the various strategies used by mammalian retroviruses to gain entry into the cell. The choice of receptors will also be discussed in light of pressures that drive viral evolution and persistence.

show abstract

“…The cellular receptor(s) for HTLV- 1 have not yet been identified. Based on results from receptor interference assays, HTLV-1 is believed to share a common receptor with HTLV-2 and other primate T-cell leukemia/lymphoma viruses (64,55).…”

mentioning

confidence: 99%

Similar Regulation of Cell Surface Human T-Cell Leukemia Virus Type 1 (HTLV-1) Surface Binding Proteins in Cells Highly and Poorly Transduced by HTLV-1-Pseudotyped Virions

Jones

Nath

Petrow‐Sadowski

et al. 2002

J Virol

View full text Add to dashboard Cite

Little is known about the requirements for human T-cell leukemia virus type 1 (HTLV-1) entry, including the identity of the cellular receptor(s).Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus which is the etiological agent of a severe lymphocyte neoplasia called adult T-cell leukemia/lymphoma (ATL) (53, 77) and a progressive neurological disease known as HTLV-1-associated myelopathy/tropical spastic paraparesis (19,48). The virus is endemic in southern Japan, the Caribbean basin, Central and South America, and portions of West Africa. HTLV-1 and the closely related human T-cell leukemia virus type 2 (HTLV-2) are uncommon in the general populations of the United States and Europe. However, one recent study revealed that HTLV is prevalent in the United States among paid blood donors, African-American health care clinic patients, Amerindians, intravenous drug users, and patients with other-than-low-grade non-Hodgkin's lymphoma (52).ATL is a malignancy of CD4 ϩ T cells. It has been generally believed that the majority of the cells infected by HTLV-1 in vivo are CD4 ϩ T cells (30, 54). However, HTLV-1 can infect all subsets of human lymphocytes in vitro, and recent studies indicate that both CD4 ϩ and CD8 ϩ T cells serve as viral reservoirs in HTLV-1-associated myelopathy/tropical spastic paraparesis patients (42). Although capable of infecting a number of different cell types, HTLV-1 is poorly infectious in both primary cells and established cell lines in vitro.As for all retroviruses, entry of HTLV-1 into target cells is mediated by the envelope glycoproteins (Env), a surface glycoprotein (SU), and a transmembrane glycoprotein (TM). The HTLV-1 Env proteins are initially synthesized as precursor proteins, which are subsequently glycosylated and cleaved in the Golgi apparatus by a furin-like cellular protease to yield the SU (gp46) and the TM (gp21) glycoproteins. Following cleavage, the SU and the TM remain associated with each other through noncovalent interactions (51). As for other retroviruses, it is believed that the HTLV-1 SU glycoprotein specifically binds to a cellular receptor, inducing a conformational change in the SU-TM complex. This change activates a fusion domain within TM, allowing fusion of the viral and cellular membranes (5,9,10,37,51,55,56). Recent work using HTLV/ murine leukemia virus (MLV) envelope chimeras strongly suggests that the region of SU that interacts with the receptor is located within the N-terminal two-thirds of the protein (29). For HTLV-1, both SU and TM appear to play an additional role in a postfusion event critical for infectivity (11,28).The cellular receptor(s) for HTLV-1 have not yet been identified. Based on results from receptor interference assays, HTLV-1 is believed to share a common receptor with HTLV-2 and other primate T-cell leukemia/lymphoma viruses (64, 55). The gene encoding the receptor was mapped to chromosome 17 and further localized to 17q23. 2-25.3 (18, 35, 55), although later studies have questioned this assignment (27,47,67).A number of diffe...

show abstract

Identification of a cellular receptor for subgroup E avian leukosis virus

Cited by 89 publications

References 23 publications

Immunological basis of differences in disease resistance in the chicken

Immunological basis of differences in disease resistance in the chicken

Receptors and Entry Cofactors for Retroviruses Include Single and Multiple Transmembrane-Spanning Proteins as well as Newly Described Glycophosphatidylinositol-Anchored and Secreted Proteins

Similar Regulation of Cell Surface Human T-Cell Leukemia Virus Type 1 (HTLV-1) Surface Binding Proteins in Cells Highly and Poorly Transduced by HTLV-1-Pseudotyped Virions

Contact Info

Product

Resources

About