Genetic control of Rous sarcoma regression in chickens: Linkage with the major histocompatibility complex

Schierman, Louis W.; Watanabe, Daniel H.; McBride, Raymond A.

doi:10.1007/bf01570489

Cited by 107 publications

(49 citation statements)

References 14 publications

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“…Senseney et al [37] in a cross segregating for two haplotypes (B Q and B 17 ) found no effect of MHC on the regression of tumors at a high dose of virus but an effect at a lower dose of the same virus and in the same genetic stock with an allelic complementation between the two alleles, the heterozygote state showing an advantage towards tumor regression. The superiority of other heterozygote combination were found elsewhere [6,27,39]. The effect of the resistance genes may clearly depend on the degree of pathogenicity of the virus.…”

Section: Discussionmentioning

confidence: 79%

“…Indeed, early studies on RSV stipulated that only a very restricted number of genes and even one single gene would be involved in the control of tumor regression or progression. This was in some cases because of the easiness to select for the trait or because of the observation of the segregation of different phenotypes [21] or because of the particular genetic background of some inbred lines used intensively for the study of the fate of RSV tumors [10,33,39]. Naturally, most of the studies on RSV tumor control consider MHC as the natural candidate of choice as far as disease resistance is concerned, and showed an effect of the avian B-complex on either the progression or regression, as reviewed by Schierman and Collins [38].…”

Section: Introductionmentioning

confidence: 99%

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Genetic analysis of a divergent selection for resistance to Rous sarcomas in chickens

et al. 2004

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-Selection for disease resistance related traits is a tool of choice for evidencing and exploring genetic variability and studying underlying resistance mechanisms. In this framework, chickens originating from a base population, homozygote for the B 19 major histocompatibility complex (MHC) were divergently selected for either progression or regression of tumors induced at 4 weeks of age by a SR-D strain of Rous sarcoma virus (RSV). The first generation of selection was based on a progeny test and subsequent selections were performed on full-sibs. Data of 18 generations including a total of 2010 birds measured were analyzed for the tumor profile index (TPI), a synthetic criterion of resistance derived from recording the volume of the tumors and mortality. Response to selection and heritability of TPI were estimated using a restricted maximum likelihood method with an animal model. Significant progress was shown in both directions: the lines differing significantly for TPI and mortality becoming null in the "regressor" line. Heritability of TPI was estimated as 0.49 ± 0.05 and 0.53 ± 0.06 within the progressor and regressor lines respectively, and 0.46 ± 0.03 when estimated over lines. Preliminary results showed within the progressor line a possible association between one Rfp-Y type and the growth of tumors.chicken / selection / resistance / Rous sarcoma / Rfp-Y † This article is dedicated to the memory of Pierrick Thoraval

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Section: Discussionmentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Genetic analysis of a divergent selection for resistance to Rous sarcomas in chickens

et al. 2004

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“…The B6 haplotype was associated with regression and the B13 haplotype with susceptibility in backcross segregants of the GB-2 line (B6, then called B2) and line GB-1 (B13, then called Bl) infected with Schmidt-Ruppin strain of RSV (Schierman et al, 1977). Similarly, the B2 haplotype was associated with regression and the B5 haplotype with susceptibility in F2 segregants of the 151 line (B5) and line 61 (B2) infected with Bryan high titre BH-RSV (RAV-1) (Collins et al, 1977).…”

Section: Rous Sarcoma Virus and The Mhcmentioning

confidence: 99%

The importance of MHC for Rous sarcoma virus and Marek's disease virus—Some Payne‐ful considerations

Kaufman

Venugopal

1998

Avian Pathology

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In contrast to mammals, there are several viral diseases for which resistance and susceptibility are determined by particular chicken MHC haplotypes. At least one reason for this is that mammals express a multigene family of class I molecules, while common chicken haplotypes express only one class I molecule at high levels. We have determined the peptide-binding motifs for the some dominantly-expressed chicken class I molecules and found that they can explain the outcome of infections with the classic transforming retrovirus, Rous sarcoma virus (RSV). We have also found that the level of cell-surface expression of chicken class I molecules varies between MHC haplotypes, and that this correlates inversely with the MHC-determined resistance reported for classical Marek's disease virus (MDV). In this paper we consider two difficulties with these explanations. First, we examine the question of why the response to RSV depends on the MHC haplotype while the response to avian leukosis viruses (ALVs) does not. It would appear that the v-src gene present in RSV but not ALVs is responsible, and we find that, of three peptides derived from the v-src protein that bind the class I molecule of the resistant line CB, two differ quite significantly in sequence from the normal c-src protein sequence. Second, we examine the issue of resistance and susceptibility to MDV due to genes outside of the MHC. It is possible that such genes interact with the class I genes in the MHC, which puts the recent observation that a gene on chicken chromosome I that determines resistance and susceptibility to MDV may be the natural killer (NK) locus in an attractive perspective.

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“…For example, a specific haplotype, say B 13 , is assumed to carry the allele R-Rs-13 or r-Rs-13. This designation is somewhat at variance with that originally proposed by Schierman et al 1977). For simplicity we use "tv" and "rs" to represent, in general, any cellular res/susc locus and any tumour regr/progr gene, respectively.…”

Section: Chorioallantoic Membrane Inoculation and Observationmentioning

confidence: 99%

Influence of B complex versus non B genetic background on cellular resistance and on Rous Sarcoma virus‐induced tumour regression in chickens¹

Gebriel

Nordskog

1983

Avian Pathology

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SUMMARYSix of eight inbred lines, segregating for the same B complex alleles, permitted a comparison of genetic backgrounds on resistance to Bryan high titre Rous sarcoma virus (RSV) of subgroups A, B and C. Tests were based both on wing web challenge (WWC), using 682 five-week-old chicks, and on the chorioallantoic membranes (CAMs) of 606 twelve-day-old embryos (CAM test). Absence of tumour development on WWC and of pock formation on CAMs indicated cellular resistance to RSV (primary mechanism of genetic resistance). The differential response of tumours (regressive or progressive tumour growth in WWC) measured the secondary mechanism of genetic resistance.The results verified previously reported studies that the tv loci for cellular resistance map outside the B histocompatibility complex, and that variation in RSV-induced tumour regression was mostly but not entirely linked to the B complex. Although cellular resistance and tumour regression are not wholly independent events, the data generally support the dual mechanism hypothesis of resistance.The ratios of variance between lines with the same B serotype, σ2L, to that between serotypes with common inbred line background, σ2B, demonstrated that σ5L were 3.2 and 17.3-fold larger than σ2B, respectively, to the CAM and WWC tests of cellular resistance (tv genes). In contrast, σ2B was 5-fold larger than σ2L for tumour regression (rs genes).The results further indicate that segregation at both the tv and rs loci is greater than expected within these inbred lines in view of their high coefficients of inbreeding. Theoretical expectations show that for eight inbred lines, each with an inbreeding coefficient of 80% assuming initial gene frequencies of .5, the probability of complete gene fixation at the same tv locus is .43 and the probability that only one line is segregating is .38.

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Genetic control of Rous sarcoma regression in chickens: Linkage with the major histocompatibility complex

Cited by 107 publications

References 14 publications

Genetic analysis of a divergent selection for resistance to Rous sarcomas in chickens

Genetic analysis of a divergent selection for resistance to Rous sarcomas in chickens

The importance of MHC for Rous sarcoma virus and Marek's disease virus—Some Payne‐ful considerations

Influence of B complex versus non B genetic background on cellular resistance and on Rous Sarcoma virus‐induced tumour regression in chickens¹

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Genetic control of Rous sarcoma regression in chickens: Linkage with the major histocompatibility complex

Cited by 107 publications

References 14 publications

Genetic analysis of a divergent selection for resistance to Rous sarcomas in chickens

Genetic analysis of a divergent selection for resistance to Rous sarcomas in chickens

The importance of MHC for Rous sarcoma virus and Marek's disease virus—Some Payne‐ful considerations

Influence of B complex versus non B genetic background on cellular resistance and on Rous Sarcoma virus‐induced tumour regression in chickens1

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Influence of B complex versus non B genetic background on cellular resistance and on Rous Sarcoma virus‐induced tumour regression in chickens¹