The role of the tvb locus in genetic resistance to RSV(RAV-0)

Crittenden, L. B.; Motta, J.

doi:10.1016/0042-6822(75)90434-1

Cited by 40 publications

(23 citation statements)

References 10 publications

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“…The second allele, tv-b s3 , can serve as a receptor for subgroups B and D only. Quail, turkey, and some related birds have an allele for a third type of receptor, tv-b q or tv-b t , conferring susceptibility to infection by subgroup E but not subgroup B and D viruses (2,13,14,26,35,48). Cells used for these studies are designated by the first letter of the species from which they are derived and the classical alpharetrovirus subgroups (A to E) to which the cells are resistant.…”

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confidence: 99%

Mechanisms of Avian Retroviral Host Range Extension

Rainey

Natonson

Maxfield

et al. 2003

J Virol

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Alpharetroviruses provide a useful system for the study of the molecular mechanisms of host range and receptor interaction. These viruses can be divided into subgroups based on diverse receptor usage due to variability within the two host range determining regions, hr1 and hr2, in their envelope glycoprotein SU (gp85). In previous work, our laboratory described selection from a subgroup B avian sarcoma-leukosis virus of an extended-host-range variant (LT/SI) with two adjacent amino acid substitutions in hr1. This virus retains its ability to use the subgroup BD receptor but can also infect QT6/BD cells, which bear a related subgroup E receptor (R. A. Taplitz and J. M. Coffin, J. Virol 71:7814-7819, 1997). Here, we report further analysis of this unusual variant. First, one (L154S) of the two substitutions is sufficient for host range extension, while the other (T155I) does not alter host range. Second, these mutations extend host range to non-avian cell types, including human, dog, cat, mouse, rat, and hamster. Third, interference experiments imply that the mutants interact efficiently with the subgroup BD receptor and possibly the related subgroup E receptor, but they have another means of entry that is not dependent on these interactions. Fourth, binding studies indicate that the mutant SU proteins retain the ability to interact as monomers with subgroup BD and BDE receptors but only bind the subgroup E receptor in the context of an Env trimer. Further, the mutant SU proteins bind well to chicken cells but do not bind any better than wild-type subgroup B to QT6 or human cells, even though the corresponding viruses are capable of infecting these cells.Alpharetroviruses, or avian sarcoma-leukosis viruses (ASLVs), display a great deal of diversity in their envelope glycoprotein (Env) sequences leading to diverse host range but, with the exception of the long terminal repeat (LTR), are nearly identical throughout the remainder of their genomes (11, 15, 16, 25-27, 29, 42). This pattern suggests a response to selective pressures to replicate in a variety of hosts. Alpharetroviruses are divided into subgroups (A to J) depending on host range, superinfection resistance patterns, and neutralizing antibody cross-reactivity. The surface (SU) subunit of the envelope glycoprotein is responsible for receptor recognition. Through a poorly characterized process, probably requiring a low-pH step (34), the SU-receptor interaction triggers the transmembrane (TM) subunit to mediate fusion between the viral envelope and the target cell membrane (10,26,48).Receptors for ASLV of subgroups A, B, D, and E have been cloned. The receptor for subgroup A viruses is a low-density lipoprotein receptor-like protein and is unrelated to any other known retroviral receptor (5, 51). The receptors for B, D, and E are encoded by orthologous genes in the tumor necrosis factor receptor family (2,3,8,40). Chickens have two alleles capable of acting as the receptor for these viruses. , conferring susceptibility to infection by subgroup E but not subgr...

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confidence: 99%

Mechanisms of Avian Retroviral Host Range Extension

Rainey

Natonson

Maxfield

et al. 2003

J Virol

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“…The R2 antiserum described here is similar to the Rl antiserum defined earlier (Crittenden et al, 1970(Crittenden et al, , 1973Crittenden & Motta, 1975) in that both agglutinated line 100B RBCs, but not une 7 2 RBCs (Table 1). The results from Tables 2 and 3 lead us to conclude that R2 agglutination occurs provided that the chicken expresses an ALV-E envelope and is also susceptible to subgroup E virus infection.…”

Section: Discussionmentioning

confidence: 78%

“…The tvb' strains with the positive agglutination phenotype were termed tvb' 1 , whereas non-agglutinating strains were termed tvb' 2 . The antigen identified by this antiserum was termed Rl (Crittenden et al, 1970;Crittenden & Motta, 1975). This Rl antiserum was, however, difficult to produce and did not identify all tvb' individuals and was subsequently not further investigated.…”

Section: Introductionmentioning

confidence: 99%

“…The tvb/e genes are classified into four alíeles: susceptibility to subgroups ALV-B and ALV-E (si or s2 alíeles as described below); susceptibility to ALV-B alone (s3), or resistant to both ALV-B and ALV-E (r). Chickens resistant to subgroup B but susceptible to ALV-E have not been identified (Crittenden & Motta, 1975;Crittenden, 1991). The absence of genes for subgroup E receptors, i.e.…”

Section: Introductionmentioning

confidence: 99%

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Development of an alloantiserum (R2) that detects susceptibility of chickens to subgroup E endogenous avian leukosis virus

et al. 1996

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SUMMARYAn alloantiserum, termed R2, specifically agglutinates red blood cells (RBC) from line 100B chickens that are susceptible to avian leukosis viruses (ALV) belonging to subgroups B and E, but does not agglutinate RBC from congenic inbred line 7 2 chickens that are resistant to ALV B and E. The R2 antigen was also detected on lymphocytes and thrombocytes. Using chickens from a special cross, it was found that R2 reactivity requires that the chickens must: (1) be susceptible to infection by ALV-E; and (2) express a viral envelope gene with subgroup E specificity. With R2 antiserum, a nearly perfect association was observed between agglutination and susceptibility to ALV-B in F 2 chickens containing endogenous viral genes ev2 and/or ev3. These results support earlier evidence that ALV-B and ALV-E share receptors. Moreover, the R2 antiserum was shown to neutralize ALV-E. The R2 antigen showed Mendelian segregation in chickens of a commercial White Leghorn straincross containing ev3, ev6 and ev9. However, commercial chickens with or without the R2 antigen did not differ in susceptibility to lymphoid leukosis induction or immune response on infection with ALV of subgroup A for complex reasons we discuss.

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“…The resistance to infection with subgroup E virus in line S and particularly in the I13 line (which completely lacked expression of chf), can therefore be assigned to an independent locus or loci. Two such loci have been postulated, TV-b and TV-e (Payne et al, 1971 ;Crittenden & Motta, 1975;Pani, 1976;Robinson et al, 1981), but whether these genes are identical or distinct (or act by complementary action) is not clear.…”

Section: Discussionmentioning

confidence: 99%

Variation in Susceptibility to Avian Sarcoma Viruses and Expression of Endogenous Avian Leukosis Virus Antigens in Specific Pathogen-free Chicken Lines

Ignjatovic

Bagust

1985

Journal of General Virology

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SUMMARYFive lines of chickens maintained as specific pathogen-free flocks in Australia were characterized in relation to endogenous antigens and endogenous avian leukosis virus expression. Embryos of line N were predominantly of C/E phenotype, uniformly positive for group-specific antigen and chick helper factor (gs+chf +) and 38~ expressed endogenous virus at a very low titre. Embryos of line M4 were uniformly of C/ABE phenotype and were either gs+chf + or gs-chf +. Line W19 embryos segregated for susceptibility to viruses of subgroup A, B and D and were either of C/E or C/ABE phenotype. The majority of W 19 embryos were gs+chf + with a small proportion being gs+chf -. Line I 13 embryos were either of C/0 or C/ABE phenotype, uniformly gs-chfand 44~ of embryos expressed endogenous virus at a low titre. Line S segregated for susceptibility to subgroup E virus and embryos were either of C/E or C/0 phenotype, while the majority of embryos from line S were gs-chf-with some embryos being gs+chf + or gs-chf +. The degree of interference of gs+chf + and gs-chf ÷ phenotypes with subgroup E virus infection was identical with the interference patterns of classical gs+chf + and gs-chf + phenotypes. The resistance to infection with avian sarcoma viruses of subgroups E in lines N and M4, and to a degree in line W19, was highly associated with the presence of chf. Resistance to subgroup E virus was independent of chf in lines S and I13, probably being under the control of an independent locus. Cellular restriction of endogenous virus replication existed in all subgroup E virussusceptible cells of line I 13 in contrast to cells of line S which supported replication of endogenous virus. The phenotype of chicken cells for the expression of endogenous gs antigen and chf could accurately be predicted from the test performed on whole blood cells.

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The role of the tvb locus in genetic resistance to RSV(RAV-0)

Cited by 40 publications

References 10 publications

Mechanisms of Avian Retroviral Host Range Extension

Mechanisms of Avian Retroviral Host Range Extension

Development of an alloantiserum (R2) that detects susceptibility of chickens to subgroup E endogenous avian leukosis virus

Variation in Susceptibility to Avian Sarcoma Viruses and Expression of Endogenous Avian Leukosis Virus Antigens in Specific Pathogen-free Chicken Lines

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