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Evidence for BoLA‐linked resistance and susceptibility to subclinical progression of bovine leukaemia virus infection
Author(s) -
LEWIN H. A.,
BERNOCO D.
Publication year - 1986
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.1365-2052.1986.tb03191.x
Subject(s) - biology , lymphocytosis , bovine leukemia virus , subclinical infection , immunology , virology , haplotype , major histocompatibility complex , virus , antigen , allele , genetics , gene
Summary The role of the bovine major histocompatibility complex in bovine leukaemia virus (BLV) infection and disease progression was investigated in a herd of Shorthorn cattle ( n = 117). The frequency of cows that were seropositive to BLV‐glycoprotein antigen was 51%. Twenty‐three per cent of the seropositive cows were lymphocytotic. At the herd level, relative resistance to BLV‐dependent B‐cell proliferation and lymphocytosis among seropositive cows was associated with bovine lymphocyte antigen (BoLA)‐DA7, whereas susceptibility was associated with BoLA‐DA12·3. These associations were also confirmed at the family level, where BoLA phenotypes were used as haplotypic markers. Among the offspring of one BoLA‐heterozygous sire ( n = 33), resistance segregated with the DA7 haplotype and susceptibility with the DA12·3 haplotype. In this sire group, maternal transmission of the BoLA‐w8 allele was associated with increased susceptibility to B‐cell proliferation and lymphocytosis in w8/DA12·3 heterozygotes. These data provide the first evidence that subclinical progression of BLV infection is under the control of the BoLA complex, and suggest that the BoLA system can be used to select for resistance to B‐cell proliferation and the development of lymphocytosis in BLV‐infected herds.