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Mapping of susceptibility to Marek's disease within the major histocompatibility ( B ) complex by refined typing of White Leghorn chickens
Author(s) -
Hepkema B. G.,
Hensen E. J.,
Blankert J. J.,
Zijpp A. J.,
Albers G. A. A.,
Tilanus M. G. J.,
Egberts E.
Publication year - 1993
Publication title -
animal genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.756
H-Index - 81
eISSN - 1365-2052
pISSN - 0268-9146
DOI - 10.1111/j.1365-2052.1993.tb00312.x
Subject(s) - biology , marek's disease , typing , white (mutation) , major histocompatibility complex , genetics , histocompatibility , virology , virus , antigen , gene , human leukocyte antigen
Summary The major histocompatibility ( B ) complex of a distinct commercial pure White Leghorn chicken line was characterized using serological, biochemical and restriction fragment length polymorphism (RFLP) typing. Line B chickens displayed a high recombination frequency within the B complex. Three recombinant haplo‐types were identified. The influence of these haplotypes was determined in relation to the haplotypes B l9 and B 21 on their resistance to Marek's disease (MD) in an experimental infection with the virus. Offspring of sires with a recombinant haplotype in combination with B 19 or B 21 , and dams, which were homozygous B 19 / B 19 or B 21 / B 21 were infected. The B type of the offspring had a significant effect upon survival. Animals with B complex types B 21 / B 21 , B 134 / B 21 and B 234 / B 21 were relatively resistant to MD (24–32% mortality), whereas B 19 / B 19 birds were highly susceptible (68% mortality). Animals with a recombinant halpotype B 19r21 ( B‐G 21 , B‐F 19 ) were equally susceptible to MD as birds with the complete B 19 haplotype. In contrast to earlier publications, resistance was not inherited as a dominant trait. Apparently, B 19 was associated with a dominant susceptibility. The gene(s) associated with the B complex and involved in resistance to MD were localized within the B‐F / B‐L region. However, the association with a presumably non‐coding subregion of B‐G could not be excluded.