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.
Investigation of Enzootic Bovine Leucosis (EBL) infection by Clinical, Serological, Haematological and Pathological Examinations in the Three Dairy Cows
