Expression of NK-lysin, blvr, ifn-a and blood cell populations in cows infected by bovine leukemia virus

At now, it is impossible to prevent or control the spread of retroviral infections, in particular, bovine leukemia virus (BLV). The existing methods of vaccination and detection of infected animals remain insufficient (G. Gutiérrez et al., 2014; M. Nishiike et al., 2016) which necessitates further investigations of the interactions between pathogen and host organism. Previously, we obtained evidence that a common characteristic for BLV infected animals with moderate and high leukocytosis was the increase in platelets, and in cows with a pronounced leukocytosis the decrease in the number of neutrophils (G.Yu. Kosovovskii et al. 2017). In order to assess the relationship between BLV infection in animals, the ratio of cell populations in the peripheral blood and the expression of the genes, encoding the BLV receptor ( blvr gene), a comparative analysis of antivirus protection protein, interferon alpha (INFΑ), and effector protein of innate immunity, NK-lysine, was carried out in two groups of cows that differed in origin and farm conditions. In result, the evidences were obtained that cows from two farms differed mainly in the amount of peripheral blood neutrophils and platelets. However, in both farms the BLV infected animals had the reduced gene expression of NK-lysin and an increased number of platelets compared to cows free from infection. Relatively increased expression of blvr was observed in BLV infected cows, reflecting, apparently, the increase in the proportion of the young forms of B-lymphocytes (M. Lavanya et al., 2008). On the basis of the own obtained findings and literature data the scheme is proposed of the influence of BLV on the expression of NK-lysin and the suppression of apoptosis. As per the scheme, viral protein TAX (a transcription activator) induces the expression of host tnf -a gene (M. Arainga et al., 2012) which, in turn, activates the Treg regulators of immune homeostasis (L.Y. Chang et al., 2015); Treg produces TGF-β (transforming growth factor beta), TGF-β inhibits the proliferation and activity of T-killers and NK-cells, the producers of NK-lysine, and increases the number and activity of platelets which inhibits the apoptosis (K. Ohira et al., 2016; S.C. Tao et al., 2016). The proposed scheme suggested that the key event in pathogenesis, induced by BLV, is the effect on the innate immune system