Bovine leukemia virus (BLV), proposed control and eradication programs by marker assisted breeding of genetically resistant cattle

ESTEBAN EDUARDO; POLI MARIO; POIESZ BERNARD; CERIANI MARIA CAROLINA; DUBE SYAMALIMA; GUTIERREZ SE; DOLCINI GUILLERMINA; GAGLIARDI ROBERTO; PEREZ SANDRA E; LUTZELSCHWAB CLAUDIA; FELDMAN LEONARDO; JULIARENA MARCELA

Animal Genetics

Nova Science Publishers Inc.

Lugar: Hauppauge, New York; Año: 2010; p. 1 - 26

Ninety three years after Siedamgrotzky first reported cases of bovine lymphocytic malignancies in Germany in 1876, bovine leukemia virus (BLV) was identified in cultured neoplastic cells from affected cattle. Epidemiological studies carried out in herds with a high frequency of mature B-cell lymphoma/leukemia proved that BLV was the causative agent of these diseases and also of persistent lymphocytosis (PL). This latter condition results in the benign expansion of BLV-infected peripheral blood B-cell lymphocytes.BLV is identified in almost every case of bovine B-cell lymphoma/leukemia; however, less than 10% of BLV-infected cattle develop these diseases, while about 30% of BLV-infected animals develop PL. Early observations of the increased incidence of B-cell lymphocytic neoplasias or PL in certain bovine pedigrees, but not in others, suggested that host-genetic factors were involved in the development of these conditions after BLV-infection. There were also indications that host-genetic factors influenced the susceptibility to one condition or the other independently. Epidemiological data also indicate that 2/3 of all cases of B-cell neoplasia occur in cattle with pre-existing PL, while 1/3 of cases come from animals with a normal blood profile. The major histocompatibility complex of cattle, termed Bovine Lymphocyte Antigens (BoLA) was discovered in 1978. The BoLA complex is a multiallelic or polymorphic genetic region located on chromosome 23 at band 22, and is organized into class I, II, and III genes, which encode proteins with different tissue distributions and functions. B-lymphocytic leukemia/lymphoma, PL and even the number of BLV-infected peripheral blood lymphocytes were subsequently found to be associated with certain BoLA-genotypes. Due to the wide dissemination of BLV among dairy cattle in Argentina and other countries, control and eradication programs based on the serological detection of BLV-infected cattle and the subsequent culling of infected animals has several drawbacks. A new approach to classify BLV-infected Holstein cattle belonging to high prevalence BLV-infected herds was recently reported. Two BLV-infection profiles: low and high proviral load (LPL and HPL, respectively) showed a strong association with certain BoLA-DRB3.2 polymorphisms. LPL was more frequently associated with BoLA-DRB3.2*0902, and HPL with BoLA-DRB3.2*1501 or 03. Further experimentation has indicated that these alleles are good candidates for genetic markers of resistance or susceptibility to BLV transmission, and would serve as powerful tools toward controlling BLV dissemination by marker assisted breeding of genetically-selected cattle. The dynamic between BLV and the BoLA complex should serve as a model for studying the interaction between host and virus. Such understanding should prove important to, not only veterinary medicine, but also to human oncology, wherein human T-cell lymphoma/leukemia virus, a member of the same genus of retroviruses as BLV, causes T-lymphocytic malignancies.