Abstract
ABSTRACT Bovine leukemia virus (BLV) is an oncogenic retrovirus of the Deltaretrovirus genus, which causes persistent infection in its natural hosts – cattle, zebu, and water buffalo with diverse clinical manifestations through the defeat of B-cells. The BLV proviral genome, along with structural genes (gag, pro, pol, and env), includes nonstructural ones (R3, G4, tax, rex, AS, pre-miRs (for miRNAs). We have shown in our previous data the association of some pre-miRs-B’ (for BLV miRNA) alleles with leukocyte (WBC – white blood cell) number in BLV-infected cows. Multifunctional properties of Tax protein have led us to an assumption that tax gene/Tax protein could have too population variations related to WBC counts. Here we report about several tax alleles/Tax protein variants, which have a highly significant association with an increase or a decrease of WBC number in BLV-infected cows. We have provided evidence that Tax A, H variants (tax b, c, d, f, e alleles) are correlated with reduced WBC counts at the level of BLV-negative groups of animals and thus could be the feature of the aleukemic (AL) form of BLV infection. We suggest this finding could be used in BLV testing for the presence of Tax A, H in the proviral DNA consider such strains of BLV as AL ones, and because of this, minimize the clinical losses due to BLV infection in cattle.
Highlights
Bovine leukemia virus (BLV) is an oncogenic retrovirus of the Deltaretrovirus genus, which causes persistent infection in its natural hosts – cattle, zebu, and water buffalo with diverse clinical manifestations through the defeat of B-cells
BLV causes a persistent infection of B-cells in natural hosts – cattle, yak, zebu, and water buffalo resulting in the disease called Enzootic Bovine Leukosis (EBL)
Persistent Lymphocytosis (PL) is a subclinical form of the BLV infection
Summary
Bovine leukemia virus (BLV) is an oncogenic retrovirus of the Deltaretrovirus genus, which causes persistent infection in its natural hosts – cattle, zebu, and water buffalo with diverse clinical manifestations through the defeat of B-cells. BLV Tax and host Drosha interaction has not been found, but it has been shown for miRs-B that their production increased so much, that BLV proviral DNA has been called “a prodigious producer of viral microRNAs” in host cells [7].
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