ENZOOTIC BOVINE LEUCOSIS IN SOUTH EAST QUEENSLAND

The reverse strategy of the genome of the enzootic bovine leucosis (EBL) virus and all retroviruses as pathogens represents the peak of the evolutionary perdection of parasitism with the preservation of their biological species at the level of only the genotype and the complete loss of trivial phenotypic characters (structure, morphology, reproduction). This explains many features of pathobiosis in leucosis, especially the malignant transformation of the host cell and the reproduction of the viral genome in the context of unlimited proliferation of lymphocytes, absolute immune evasion in relation to the antiviral protective effectors of both innate and acquired immunity, and intracellular transmission of the infection by the epizootic chain. The principal feature of EBL is clinical dimorphism, i.e. the status of latent infection an absolute quantitative and chronological predominance of the incubation period of the course, essentially a cryptic form of infection throughout a productive life of the animal, and the illness per se in a pathological sense, extremely rare sporadic cases of a manifest form of lymphosarcomatosis that arise and really recorded only in old animals, outside of productive age. In this article the transmission of infection and the pathogenesis of EBL are interpreted from modern parasitic systemic positions as aspects of this problem that are little being considered in the home publications.

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Enzootic bovine leucosis

Veterinary Record ◽

10.1136/vr.103.10.194 ◽

1978 ◽

Vol 103 (10) ◽

pp. 194-198 ◽

Cited By ~ 5

Author(s):

L. Tyler

Keyword(s):

Enzootic Bovine Leucosis

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BoLA-DRB3 Polymorphism is Associated with Differential Susceptibility to Bovine Leukemia Virus-Induced Lymphoma and Proviral Load

Viruses ◽

10.3390/v12030352 ◽

2020 ◽

Vol 12 (3) ◽

pp. 352 ◽

Cited By ~ 5

Author(s):

Chieh-Wen Lo ◽

Liushiqi Borjigin ◽

Susumu Saito ◽

Koya Fukunaga ◽

Etsuko Saitou ◽

...

Keyword(s):

Bovine Leukemia Virus ◽

Proviral Load ◽

Disease Susceptibility ◽

Leukemia Virus ◽

Differential Susceptibility ◽

Leukocyte Antigen ◽

Polymorphic Gene ◽

Host Genetic ◽

The Relationship ◽

Enzootic Bovine Leucosis

Bovine leukemia virus (BLV) is the causative agent of enzootic bovine leucosis. However, less than 5% of BLV-infected cattle will develop lymphoma, suggesting that, in addition to viral infection, host genetic polymorphisms might play a role in disease susceptibility. Bovine leukocyte antigen (BoLA)-DRB3 is a highly polymorphic gene associated with BLV proviral load (PVL) susceptibility. Due to the fact that PVL is positively associated with disease progression, it is believed that controlling PVL can prevent lymphoma development. Thus, many studies have focused on the relationship between PVL and BoLA-DRB3. Despite this, there is little information regarding the relationship between lymphoma and BoLA-DRB3. Furthermore, whether or not PVL-associated BoLA-DRB3 is linked to lymphoma-associated BoLA-DRB3 has not been clarified. Here, we investigated whether or not lymphoma-associated BoLA-DRB3 is correlated with PVL-associated BoLA-DRB3. We demonstrate that two BoLA-DRB3 alleles were specifically associated with lymphoma resistance (*010:01 and *011:01), but no lymphoma-specific susceptibility alleles were found; furthermore, two other alleles, *002:01 and *012:01, were associated with PVL resistance and susceptibility, respectively. In contrast, lymphoma and PVL shared two resistance-associated (DRB3*014:01:01 and *009:02) BoLA-DRB3 alleles. Interestingly, we found that PVL associated alleles, but not lymphoma associated alleles, are related with the anti-BLV gp51 antibody production level in cows. Overall, our study is the first to demonstrate that the BoLA-DRB3 polymorphism confers differential susceptibility to BLV-induced lymphoma and PVL.

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