COMPLEMENTING MHC‐ AND NON‐MHC‐LINKED GENES AND RESISTANCE TO AVIAN SARCOMA VIRUS‐INDUCED TUMOURS IN INBRED LINES OF CHICKENS

Abstract

Schmidt-Ruppin Rous sarcoma virus, subgroup B (SR-RSV-B), was inoculated into the wingwebs of chickens from three partially congenic inbred lines, G-B1, G-B2 and G-B3, homozygous for different MHC (B region) haplotypes (genotypes =B¹/B¹, B²/B² and B³/B³ respectively). All birds developed tumours but only the G-B2 line resisted progressive tumour growth. Birds from lines G-B1 and G-B3 approached 100% susceptibility to progressive tumour growth, whereas most (G-B1 x G-B3) F₁ hybrids were resistant to tumours induced by SR-RSV-B. The association of the resistance trait in F₁ hybrids with genes of the B region was investigated by testing progeny of (G-B1 x G-B3) x G-B1 F₁ and (G-B1 x G-B2) x G-B3 F₁ backcross matings. Approximately 27% of the backcross population was resistant to SR-RSV-B-induced tumours and these resistant offspring were predominantly of the B₁/B₃ phenotype. We interpret these results to mean that resistance to progressive tumour growth involves complementation between genes (allelic or at separate loci) linked to or within the B region and that resistance is effective only when the complementing B region genes act in concert with complementing genes which assort independently of the MHC. We suggest that complementing B region-linked genes are homologues of complementing murine H-2-linked Ir genes. The function of the B region in determining growth of sarcomas may therefore be analogous to that of Ir genes.