Abstract

BackgroundBovine leukemia virus (BLV) is a member of retroviridae family, together with human T cell leukemia virus types 1 and 2 (HTLV-1 and -2) belonging to the genes deltaretrovirus, and infects cattle worldwide. Previous studies have classified the env sequences of BLV provirus from different geographic locations into eight genetic groups. To investigate the genetic variability of BLV in South America, we performed phylogenetic analyses of whole genome and partial env gp51 sequences of BLV strains isolated from Peru, Paraguay and Bolivia, for which no the molecular characteristics of BLV have previously been published, and discovered a novel BLV genotype, genotype-9, in Bolivia.ResultsIn Peru and Paraguay, 42.3 % (139/328) and over 50 % (76/139) of samples, respectively, were BLV positive. In Bolivia, the BLV infection rate was up to 30 % (156/507) at the individual level. In Argentina, 325/420 samples were BLV positive, with a BLV prevalence of 77.4 % at the individual level and up to 90.9 % at herd level. By contrast, relatively few BLV positive samples were detected in Chile, with a maximum of 29.1 % BLV infection at the individual level. We performed phylogenetic analyses using two different approaches, maximum likelihood (ML) tree and Bayesian inference, using 35 distinct partial env gp51 sequences from BLV strains isolated from Peru, Paraguay, and Bolivia, and 74 known BLV strains, representing eight different BLV genotypes from various geographical locations worldwide. The results indicated that Peruvian and Paraguayan BLV strains were grouped into genotypes-1, -2, and -6, while those from Bolivia were clustered into genotypes-1, -2, and -6, and a new genotype, genotype-9. Interestingly, these results were confirmed using ML phylogenetic analysis of whole genome sequences obtained by next generation sequencing of 25 BLV strains, assigned to four different genotypes (genotypes-1, -2, -6, and -9) from Peru, Paraguay, and Bolivia. Comparative analyses of complete genome sequences clearly showed some specific substitutions, in both structural and non-structural BLV genes, distinguishing the novel genotype-9 from known genotypes.ConclusionsOur results demonstrate widespread BLV infection in South American cattle and the existence of a new BLV genotype-9 in Bolivia. We conclude that at least seven BLV genotypes (genotypes-1, -2, -4, -5, -6, -7, and -9) are circulating in South America.Electronic supplementary materialThe online version of this article (doi:10.1186/s12977-016-0239-z) contains supplementary material, which is available to authorized users.

Highlights

  • Bovine leukemia virus (BLV) is a member of retroviridae family, together with human T cell leukemia virus types 1 and 2 (HTLV-1 and -2) belonging to the genes deltaretrovirus, and infects cattle worldwide

  • Bovine leukemia virus (BLV) is a member of retroviridae family belonging to the genes deltaretrovirus, being considered a model of pathogens for human T-cell leukemia virus types 1 (HTLV-1) [1], and is the etiological agent of enzootic bovine leukosis (EBL), the most common neoplastic disease of cattle [2, 3]

  • The samples were screened for BLV infection by nested polymerase chain reaction (PCR) to amplify BLV long terminal repeats (LTRs) (Table 1; Fig. 1)

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Summary

Introduction

Bovine leukemia virus (BLV) is a member of retroviridae family, together with human T cell leukemia virus types 1 and 2 (HTLV-1 and -2) belonging to the genes deltaretrovirus, and infects cattle worldwide. Bovine leukemia virus (BLV) is a member of retroviridae family belonging to the genes deltaretrovirus, being considered a model of pathogens for human T-cell leukemia virus types 1 (HTLV-1) [1], and is the etiological agent of enzootic bovine leukosis (EBL), the most common neoplastic disease of cattle [2, 3]. In addition to the above, BLV RNA polymerase III (pol III)-encoded viral microRNAs are strongly expressed in preleukemic and malignant cells, in which structural and regulatory gene expression is repressed, suggesting a possible key role in tumor onset and progression [14, 15]

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