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Mechanisms of pathogenesis induced by bovine leukemia virus as a model for human T-cell leukemia virus

Yoko Aida, Hironobu Murakami, Masahiko Takahashi and 1 more

Frontiers in Microbiology · 2013 · Review

doi:10.3389/fmicb.2013.00328

Abstract

Bovine leukemia virus (BLV) and human T-cell leukemia virus type 1 (HTLV-1) make up a unique retrovirus family. Both viruses induce chronic lymphoproliferative diseases with BLV affecting the B-cell lineage and HTLV-1 affecting the T-cell lineage. The pathologies of BLV- and HTLV-induced infections are notably similar, with an absence of chronic viraemia and a long latency period. These viruses encode at least two regulatory proteins, namely, Tax and Rex, in the pX region located between the env gene and the 3' long terminal repeat. The Tax protein is a key contributor to the oncogenic potential of the virus, and is also the key protein involved in viral replication. However, BLV infection is not sufficient for leukemogenesis, and additional events such as gene mutations must take place. In this review, we first summarize the similarities between the two viruses in terms of genomic organization, virology, and pathology. We then describe the current knowledge of the BLV model, which may also be relevant for the understanding of leukemogenesis caused by HTLV-1. In addition, we address our improved understanding of Tax functions through the newly identified BLV Tax mutants, which have a substitution between amino acids 240 and 265.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 21, 2026. Paragraph numbers are ours, so an answer can point at one.

INTRODUCTION

Bovine leukosis was first reported in 1871 as the presence of slightly yellow nodules in the enlarged spleen of cattle. Spleen disruption consecutive to tumor formation is one of the most important clinical manifestations of bovine leukemia. Bovine leukosis is classified into two types, sporadic bovine leukosis (SBL) and enzootic bovine leukosis (EBL), which are characterized by T- and B-cell leukosis, respectively. The occurrence of EBL in cattle is much higher than that of SBL. Bovine leukemia virus (BLV), which belongs to the Retroviridae family and Deltaretrovirus genus, is the etiologic agent of EBL, although it remains unknown what causes SBL. The natural hosts of BLV are domestic cattle and water buffaloes; however, experimental infection with BLV in sheep can lead to the development of lymphoma. Interestingly, BLV is consistently associated with leukemia only in cattle and sheep, even though it can infect many cell lines and can be experimentally transmitted to rabbits, rats, chickens, pigs, goats, and sheep. Most BLV-infected cattle are asymptomatic, but approximately one-third of them suffer from persistent lymphocytosis (PL) characterized by non-malignant polyclonal B-cell expansion and 1–5% of them develop B-cell leukemia/lymphoma after a long latency period. On the other hand, sheep that are experimentally inoculated with BLV develop B-cell tumors at a higher frequency and with a shorter latency period than those observed in naturally infected cattle. Interestingly, the transformed B-lymphocytes in cattle are CD5+ IgM+ B-cells, whereas in sheep they are CD5- IgM+ B-cells, suggesting that the mechanisms of leukemogenesis induced by BLV may differ.

BLV is closely related to human T-cell leukemia virus type 1 (HTLV-1), which is the causative agent of adult T-cell leukemia (ATL) and a chronic neurological disorder known as tropical spastic paraparesis or HTLV-1-associated myelopathy HAM/TSP. Therefore, studies on BLV may facilitate our understanding of the mechanism of leukemogenesis induced by HTLV-1.

BLV AND HTLV-1

All retroviruses are encoded by gag, pro, pol, and env essential genes, which are necessary for the production of infectious virions, and are flanked by two identical long terminal repeats (LTRs; Figure 1). The gag, pro, pol, and env genes encode the internal structural proteins of the virion, the viral protease, the reverse transcriptase, and the envelope glycoproteins of the virion, respectively. The genome sequences of BLV and HTLV-1 are different, but have a unique sequence called the pX situated between the env gene and the 3′LTR and encoded by the regulatory gene (Figure 1). The pX sequence is not of host cell origin; that is, it is not an oncogene. It has been reported that both viruses have an ability to immortalize primary cells in vitro. Because their structure and properties differ from any other class of retroviruses, BLV and HTLV-1 viruses were classified into a new group of retroviruses. In both viruses the regulatory proteins Tax and Rex are encoded in the pX region. The R3 and G4 proteins are encoded in the BLV pX region, while p12I, p13II, and p30II are encoded in the HTLV-1 pX region (;; Figure 1). Interestingly, the HTLV-1 genome codes for HBZ, a unique gene encoded by the minus strand chain (; Figure 1). The major functions of the viral proteins encoded in the BLV and HTLV-1 pX regions are summarized in Table 1. The Tax protein has been extensively studied, and it is believed to play a critical role in leukemogenesis induced by BLV and HTLV-1. The Rex protein is responsible for nuclear export of viral RNA and promotes cytoplasmic accumulation and translation of viral messenger mRNA in BLV- and HTLV-1-infected cells. BLV R3 and G4 proteins contribute to the maintenance of high viral load. The G4 protein is particularly relevant to leukemogenesis, since it can immortalize primary rat embryo fibroblasts (REFs; ). HTLV-1 p12I is similar to the R3 protein, in that it contributes to the maintenance of infectivity, and both proteins are located in the nucleus and cellular membranes. On the other hand, HTLV-1 p13II protein resembles the G4 protein, since both proteins bind to farnesyl pyrophosphate synthetase, which farnesylates Ras, and the p13II protein promotes Ras-dependent apoptosis. HTLV-1 p30II protein regulates gene transcription through its interaction with the cAMP responsive element (CRE) binding protein (CREB)/p300. The HBZ protein plays a critical role in the leukemogenesis of HTLV-1, and HBZ knockdown inhibits the proliferation of ATL cells. However, since the BLV genome does not code for HBZ, it is assumed that the Tax protein plays a central role in the leukemogenesis of BLV.

The infection route of BLV and HTLV is by horizontal and vertical transmission. BLV is transmitted via direct contact, milk, and insect bites, while HTLV-1 is transmitted via milk and sexual intercourse. Moreover, the artificial transmission of BLV is caused by iatrogenic procedures such as dehorning, ear tattooing, and reuse of needles, whereas the artificial transmission of HTLV-1 is caused by blood transfusion and needle sharing among drug abusers. Since cell contact is required for the efficient transmission of both BLV and HTLV-1, cell-free infection by these viruses is believed to be very inefficient, most probably due to virion instability.

As shown in Figure 2, an infection with BLV is characterized by three progressive stages of disease, including an asymptomatic stage, PL, and lymphoma. Most BLV-infected cattle are asymptomatic, but approximately one-third of them suffer from PL characterized by a permanent and relatively stable increase in the number of B-lymphocytes in the peripheral blood. PL is considered to be a benign form of the disease resulting from the accumulation of untransformed B-lymphocytes. Finally, 1–5% of BLV-infected cattle develop B-lymphoma in various lymph nodes after a long latency period. Although BLV can also infect CD4+ T-cells, CD8+ T-cells, γ/δ T-cells, monocytes, and granulocytes in cattle, a large number of the tumor cells are derived from CD5+ IgM+ B-cell subpopulations. Interestingly, the full-length BLV proviral genome is maintained in each animal throughout the course of the disease. In addition, previous studies have shown that both large and small deletions of proviral genomes may be very rare events in BLV-infected cattle. Thus, the proviral loads were significantly increased at the PL stage compared with the aleukemic stage and were further increased at the lymphoma stage (,; Figure 2B). These findings clearly demonstrated that the BLV proviral copy number increases with increasing severity of the disease. On the other hand, unlike BLV, HTLV-1 is associated with ATL and with the chronic neurological disorder, HAM/TSP, and induces not only a malignant tumor but also an inflammatory disease. Although the pathogenesis of HTLV-1 is slightly different from BLV, HTLV-1, like BLV, can infect many cells in addition to T-cells, including B-cells and monocytes. In contrast to BLV, defective HTLV-1 proviral genomes have been found in more than half of all examined patients with ATL.

MECHANISM OF LEUKEMOGENESIS BY BLV

Animal retroviruses, which belong to the Alpharetrovirus and Gammaretrovirus genera, induce tumors by one of two mechanisms: either by activation of the “viral oncogene” or by “insertional activation” of a cellular gene such as a proto-oncogene (; Figure 1). By contrast, BLV lacks a known oncogene and does not integrate into preferred sites in their host cell genomes, which related to the disruption of the host gene but not to the suppression of viral gene expression.

Most studies of BLV-induced leukemogenesis have focused on the Tax protein because it is believed to be a potent transcriptional activator of viral gene expression. In addition to its function as a transcriptional activator, Tax induces immortalization of primary REFs. Furthermore, Tax cooperates with the Harvey rat sarcoma viral oncoprotein (Ha-ras) for the induction of full transformation of primary REF. Importantly, the Tax transformed cells induce tumors in nude mice. The ability of the Tax protein to induce immortalization may be the first step in the BLV-mediated transformation process. Moreover, after the infection of cattle and during the latency period, the expression of BLV becomes blocked at the transcriptional level. Such repression appears to be very important for the escape of BLV from the host’s immunosurveillance system, and later only a certain small proportion of infected animals rapidly develop a terminal disease. Indeed, transcription of the BLV genome in fresh tumor cells or in fresh peripheral blood mononuclear cells (PBMCs) from infected individuals is almost undetectable by conventional techniques. In situ hybridization has revealed the expression of viral RNA at low levels in many cells, and at a high level in only a few cells within PBMCs freshly isolated from BLV-infected asymptomatic animals. Thus, BLV infection is probably not sufficient for leukemogenesis and some additional events such as gene mutations might be involved in the leukemogenic process (Figure 2A). Taken together, Tax may induce immortalization of only CD5+ IgM+ B-cells among BLV-infected B-cells, CD4+ T-cells, CD8+ T-cells, γ/δ T-cells, monocytes, and granulocytes in cattle, thereby conferring a selective transformation advantage to the infected CD5+ IgM+ B-cells by a second event.

A mutation in the p53 tumor suppressor gene is one of several genetic changes known to be involved in the development of lymphoma (Figure 2A). The protein encoded by the p53 tumor suppressor gene plays a critical role in transducing a signal from the damaged DNA to genes that control cell cycle and apoptosis. Approximately half of the solid tumors induced by BLV in cattle and three of four bovine B-cell lymphoma lines were shown to harbor missense mutations in p53. By contrast, very few mutations were found in B-cells from cows with PL and none of the uninfected cattle harbored a mutated p53 gene. These observations indicate that p53 mutations frequently occur at the final stage of lymphoma in cattle. A previous study of the molecular mechanism of mutations at codons 206, 207, 241, and 242, which were identified in lymphoma, showed that these mutations may potentially alter the wild-type function of the bovine p53 protein, including the conformation and transactivator and growth suppressor activities, and then cause lymphoma. These four mutations were clearly divided into two functionally distinct groups: (i) the mutant forms with substitutions at codons 241 and 242, which were mapped within an evolutionarily conserved region and corresponded to the human “hot-spot” mutations, and had completely lost the capacity for transactivation and growth suppression while gaining transdominant repression activity in p53-null SAOS-2 cells; and (ii) the mutations at codons 206 and 207, which were located outside the evolutionarily conserved regions and partially retained the capacity for transactivation and growth suppression. Collectively, these naturally occurring mutations may potentially alter the wild-type function, and in addition, out of the four missense mutations, at least two mutations may be sufficient to cause lymphoma. However, since the other two mutations may be insufficient to induce lymphoma, it is possible that other cancer-related genes may contribute to lymphoma in concert with the p53 mutations.

A major factor involved in the clinical progression of BLV-infected animals is the bovine leukocyte antigen (BoLA; Figure 2A), which plays a crucial role in determining immune responsiveness. Several studies have shown that genetic variations in BoLA-DRB3, which is a functionally important and the most polymorphic BoLA class II locus in cattle, influence resistance and susceptibility to a wide variety of infectious diseases, including lymphoma and PL, and affect BLV proviral load. For example, the presence of the amino acids Glu–Arg (ER) at positions 70–71 of the BoLA-DRβ chain was associated with resistance to PL in BLV-infected cattle. Furthermore, the BoLA-DRB3 alleles encoding Glu, Arg, and Val at positions 74, 77, and 78, respectively, of the BoLA-DRβ chain might be associated with resistance to tumor development. In a related study, and found that the ovine leukocyte antigen (OLA)-DRB1 alleles encoding the Arg–Lys (RK) and the Ser–Arg (SR) motifs at positions 70–71 of the OLA-DRβ chain are associated with resistance (RK motif) and susceptibility (SR motif) to the development of lymphoma after experimental infection of sheep with BLV. The sheep with alleles encoding the RK motif produced neutralizing antibodies against BLV and interferon-γ, eliminated BLV completely, and did not develop lymphoma. The susceptibility to the monoclonal expansion of BLV-infected B-lymphocytes is thus associated with specific alleles of BoLA system.

A polymorphism in the promoter region of the tumor necrosis factor (TNF)-α gene is one of several genetic changes involved in the development of lymphoma (Figure 2A). A previous study found that, in sheep experimentally infected with BLV, the frequency of the TNF-α-824G allele, which has been associated with low transcription activity of the promoter/predicted enhancer region of the bovine TNF-α gene, was higher in animals with lymphoma than in asymptomatic carrier animals. In addition, a tendency was observed for increased BLV-provirus load in cattle homozygous for the TNF-α-824G/G allele compared to cattle homozygous for the TNF-α-824A/A or TNF-α-824A/G alleles. These data suggest that the observed polymorphism in the promoter region of the TNF-α gene could at least in part contribute to the progression of lymphoma in BLV infection.

The BLV studies have also focused on understanding the process of signal transduction such as B-cell receptor (BCR) signaling, since many signal transduction factors have been implicated in leukemogenesis of B-cells in humans. For example, the immunoreceptor tyrosine-based activation (ITAM) motifs present in the transmembrane gp30 proteins of the BLV envelope are important for the incorporation of envelope proteins into the virion and are required for infectivity in vivo. In addition to the viral signaling motif, the spleen tyrosine kinase (Syk) mRNA expression was significantly increased in PL samples, whereas it was decreased in tumor samples, suggesting that Syk mRNA expression dynamics is closely related to the progression of BLV-induced disease.

BLV Tax FUNCTION

As mentioned above, the Tax gene is a key contributor to the oncogenic potential, as well as a key protein involved in the replication of the virus. Table 1 summarizes the functions of the Tax protein. The Tax open reading frame is mainly encoded in the pX region, and its translation occurs upstream of the pol stop codon. The Tax protein is modified by phosphorylation of two serine residues and is detected as a 34–38 kDa product. In addition, the Tax protein has T- and B-cell epitopes corresponding to regions 110–130/131–150 and 261–280, respectively. One of the best characterized functions of Tax is the activation of viral transcription. The Tax protein acts on a triplicate 21 bp enhancer motif known as the Tax-responsive element (TxRE) in the U3 region of the 5′LTR, and it stimulates transactivation of the viral genome. The TxRE consists of a cyclic AMP-response element (CRE)-like sequence, and it has been suggested that Tax binds to this element indirectly through cellular factors, such as the members of the CREB/activating transcription factor (ATF) family of basic leucine zipper proteins that have been shown to bind to the CRE-like sequence. Furthermore, the Tax protein modulates the expression of cellular genes that are involved in the regulation of cell growth. In addition to its function in the regulation of cellular and viral transcription, the Tax protein can induce immortalization of primary REF and cooperates with Ha-Ras oncogene to fully transform the primary cells. On the other hand, the transactivation and transformation of Tax may be independently induced by each mechanism, since phosphorylation of Tax is required for its transformation but not for its activation. Moreover, the expression of Tax in primary ovine B-cells, which depends on CD154 and interleukin-4, affects B-cell proliferation, cell cycle phase distribution, and survival, leading to cytokine-independent growth. This immortalization process is also associated with increased B cell leukemia/lymphoma 2 (Bcl-2) protein levels, nuclear factor kappa B (NF-κB) accumulation, and a series of intracellular pathways that remain to be characterized. In addition, Tax inhibits base-excision DNA repair of oxidative damage, thereby potentially increasing the accumulation of ambient mutations in cellular DNA.

NEGATIVE REGULATION OF BLV Tax BY THE REGION BETWEEN RESIDUES 240–265

Our studies demonstrated new functions of the region between amino acids 240 and 265 of BLV Tax. As shown in Figure 3, a series of mutants with at least one amino acid substitution between amino acids 240 and 265 of BLV Tax were identified, including TaxD247G and TaxS240P, which exhibit an enhanced ability to stimulate and reduce viral LTR-directed transcription respectively, compared to the wild-type protein. Transient expression analysis revealed that the TaxD247G mutant increased the production of viral protein and particles from a defective recombinant proviral BLV clone to a greater extent than the wild-type Tax (TaxWT). Conversely, the TaxS240P mutant was unable to induce the release of viral particles. The microarray data in human HeLa cells and its validation of differentially expressed genes at the RNA and protein levels in bovine 23CLN cells revealed several alterations in genes involved in many cellular functions such as transcription, signal transduction, cell growth, apoptosis, and the immune response. In both of human HeLa cells and bovine 23CLN cells, the TaxD247G mutant induced higher gene expression compared with TaxWT and TaxS240P and many of these genes were expressed at the lowest level in the TaxS240P-transfected cells. In particular, our results showed that Tax activates the proteins which are involved in activator protein 1 (AP-1) signaling pathway [FBJ osteosarcoma oncogene (FOS), jun proto-oncogene (JUN), etc.] via interactions with other transcriptional pathways (G-protein, GTP-binding proteins, etc.). Likewise, the TaxD247G mutant induced apoptosis in transfected cells more effectively than the TaxWT. These results suggest that the region between amino acids 240 and 265 of the Tax protein might act as a negative regulatory domain, and missense mutations in this region might lead to enhanced transactivation activity of Tax, expression of many cellular genes and induction of apoptosis. Our results raise the possibility that the target sequence specificity of retroviral enhancers of Tax might be limited by this region because TaxD247G, but not TaxS240P, was found to activate other retroviral enhancers such as HTLV-1, HIV-1, and mouse mammary tumor virus (MMTV) and Moloney murine leukemia virus (M-MuLV), and c-fos, which are not activated by TaxWT (; Figure 3B). The microarray data also raised the possibility that BLV Tax regulates the innate immune response (Figure 3B): the largest group of downregulated genes was related to the immune response, and the majority of these genes belonged to the interferon family of antiviral factors, such as interferon-induced protein with tetratricopeptide repeats 1 (IFIT1; ). Interferons are major components of the innate immune system, and are recognized for their antiviral function in addition to their antiproliferative and immunomodulatory effects on cells. It is likely that BLV Tax downregulates the innate immune response, thereby increasing the production of viral protein.

An infectious molecular clone of BLV encoding the TaxD247G was examined for the viral expression and propagation, as well as for the induction of apoptosis in a sheep model. Interestingly, the infectious molecular clone of BLV encoding the TaxD247G produced more viral particles and was transmitted at an elevated rate in vitro, but with no significant differences in the proviral load and the expression of viral RNA between sheep experimentally injected with BLVs encoding the TaxWT or the mutant TaxD247G proteins. These findings suggest the presence of a dominant host defense mechanism regulating BLV–LTR-directed transcription by Tax that may play an important role in viral silencing in vivo (Figure 4). Likewise, although the transient expression of TaxD247G induced apoptosis in transfected cells in vitro more effectively than TaxWT, higher level of protection against apoptosis was observed in PBMCs isolated from sheep infected with TaxD247G-encoded BLV compared to TaxWT-encoded BLV (; Figure 4). These findings demonstrate that TaxD247G has an increased potential to induce apoptosis, which could be beneficial for BLV propagation like other viruses. One possible explanation for our results might be that TaxD247G-induced apoptosis is modulated by a dominant mechanism ex vivo, so the function might be suppressed.

CONCLUSION

BLV is the etiologic agent of EBL, which is the most common neoplastic disease in cattle. It infects cattle worldwide, thereby imposing a severe economic burden on the dairy cattle industry. In this review, we evaluated existing information on the mechanism of BLV-induced leukemogenesis. We propose that, since BLV Tax induces immortalization of only CD5+ IgM+ B-cells within BLV-infected B-cells, CD4+ T-cells, CD8+ T-cells, γ/δ T-cells, monocytes, and granulocytes in cattle, it may confer a selective transformation advantage to the infected CD5+ IgM+ B-cells by a second event, such as p53 mutation, polymorphisms of BoLA, or the promoter region of the TNF-α gene. We also propose new functions of the region between amino acids 240 and 265 of BLV Tax (Figure 3). Namely, the transactivation activity and target sequence specificity of BLV Tax might be limited or negatively regulated by this region. The most interesting point regarding the ability of TaxD247G to enhance BLV expression and apoptotic induction in vitro is that it might be suppressed in vivo or ex vivo. Thus, we hypothesize that there could be dominant mechanisms controlling the functions of TaxD247G ex vivo and in vivo, as shown in Figure 4. For HTLV-1, it has been reported that CD8+ cell-mediated cytotoxic T-lymphocytes (CTLs) target Tax-expressing cells, thereby reducing the number of infected cells. Likewise, BLV-infected cells expressing Tax may be exposed to the host defense system, and BLV may evolve in a manner that promotes the shielding of their potential abilities. Therefore, a strong transactivation activity of BLV Tax might not be advantageous for the propagation of BLV in vivo. Taken together, the findings discussed in this review suggest that there might be a dominant mechanism involved in the induction of apoptosis and expression of HTLV-1 in vivo. To address our hypothesis, it seems necessary to evaluate whether possible host responses against BLV infection, such as the induction of CTLs, genetic, and epigenetic alterations in apoptosis-regulatory genes, and DNA and chromatin modifications of BLV promoter for the suppression of viral expression, could be enhanced in animals infected with TaxD247G-encoded BLV. Thus, future investigations of the relationship between apoptosis and viral expression using BLV containing the mutant D247G Tax as a model will broaden our understanding of the replication and propagation of HTLV-1, and leukemia progression.

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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    Hanon E. Hall S. Taylor G. P. Saito M. Davis R. Tanaka Y. (2000 ). Abundant tax protein expression in CD4+ T cells infected with human T-cell lymphotropic virus type I (HTLV-I) is prevented by cytotoxic T lymphocytes. Blood 95 1386–1392

    Not in our library

  34. 34.

    Hiraragi H. Michael B. Nair A. Silic-Benussi M. Ciminale V. Lairmore M. (2005 ). Human T-lymphotropic virus type 1 mitochondrion-localizing protein p13II sensitizes Jurkat T cells to Ras-mediated apoptosis. J. Virol. 79 9449–9457

    Not in our library10.1128/jvi.79.15.9449-9457.2005

  35. 35.

    Hopkins S. G. DiGiacomo R. F. (1997 ). Natural transmission of bovine leukemia virus in dairy and beef cattle. Vet. Clin. North Am. Food Anim. Pract. 13 107–128

    Not in our library10.1016/s0749-0720(15)30367-4

  36. 36.

    Hu R. Gan Y. Liu J. Miller D. Zoon K. C. (1993 ). Evidence for multiple binding sites for several components of human lymphoblastoid interferon-alpha. J. Biol. Chem. 268 12591–12595

    Not in our library

  37. 37.

    Igakura T. Stinchcombe J. C. Goon P. K. Taylor G. P. Weber J. N. Griffiths G. M. (2003 ). Spread of HTLV-I between lymphocytes by virus-induced polarization of the cytoskeleton. Science 299 1713–1716

    Not in our library10.1126/science.1080115

  38. 38.

    Inabe K. Nishizawa M. Tajima S. Ikuta K. Aida Y. (1999 ). The YXXL sequences of a transmembrane protein of bovine leukemia virus are required for viral entry and incorporation of viral envelope protein into virions. J. Virol. 73 1293–1301

    Not in our library10.1128/jvi.73.2.1293-1301.1999

  39. 39.

    Ishiguro N. Furuoka H. Matsui T. Horiuchi M. Shinagawa M. Asahina M. (1997 ). p53 mutation as a potential cellular factor for tumor development in enzootic bovine leukosis. Vet. Immunol. Immunopathol. 55 351–358

    Not in our library10.1016/s0165-2427(96)05721-2

  40. 40.

    Jimba M. Takeshima S. N. Matoba K. Endoh D. Aida Y. (2010 ). BLV-CoCoMo-qPCR: quantitation of bovine leukemia virus proviral load using the CoCoMo algorithm. Retrovirology 7 91

    Not in our library10.1186/1742-4690-7-91

  41. 41.

    Jimba M. Takeshima S. N. Murakami H. Kohara J. Kobayashi N. Matsuhashi T. (2012 ). BLV-CoCoMo-qPCR: a useful tool for evaluating bovine leukemia virus infection status. BMC Vet. Res. 8:167

    Not in our library10.1186/1746-6148-8-167

  42. 42.

    Johnston E. R. Powers M. A. Kidd L. C. Radke K. (1996 ). Peripheral blood mononuclear cells from sheep infected with a variant of bovine leukemia virus synthesize envelope glycoproteins but fail to induce syncytia in culture. J. Virol. 70 6296–6303

    Not in our library10.1128/jvi.70.9.6296-6303.1996

  43. 43.

    Juliarena M. A. Poli M. Sala L. Ceriani C. Gutierrez S. Dolcini G. (2008 ). Association of BLV infection profiles with alleles of the BoLA-DRB3.2 gene. Anim. Genet. 39 432–438

    Not in our library10.1111/j.1365-2052.2008.01750.x

  44. 44.

    Kashanchi F. Brady J. N. (2005 ). Transcriptional and post-transcriptional gene regulation of HTLV-1. Oncogene 24 5938–5951

    Not in our library10.1038/sj.onc.1208973

  45. 45.

    Katoh I. Yoshinaka Y. Ikawa Y. (1989 ). Bovine leukemia virus trans-activator p38tax activates heterologous promoters with a common sequence known as a cAMP-responsive element or the binding site of a cellular transcription factor ATF. EMBO J. 8 497–503

    Not in our library10.1002/j.1460-2075.1989.tb03403.x

  46. 46.

    Kenyon S. J. Ferrer J. F. Mcfeely R. A. Graves D. C. (1981 ). Induction of lymphosarcoma in sheep by bovine leukemia virus. J. Natl. Cancer Inst. 67 1157–1163

    Not in our library

  47. 47.

    Kerkhofs P. Heremans H. Burny A. Kettmann R. Willems L. (1998 ). In vitro and in vivo oncogenic potential of bovine leukemia virus G4 protein. J. Virol. 72 2554–2559

    Not in our library10.1128/jvi.72.3.2554-2559.1998

  48. 48.

    Kettmann R. Deschamps J. Cleuter Y. Couez D. Burny A. Marbaix G. (1982 ). Leukemogenesis by bovine leukemia virus: proviral DNA integration and lack of RNA expression of viral long terminal repeat and 3′ proximate cellular sequences. Proc. Natl. Acad. Sci. U.S.A. 79 2465–2469

    Not in our library10.1073/pnas.79.8.2465

  49. 49.

    Klener P. Szynal M. Cleuter Y. Merimi M. Duvillier H. Lallemand F. (2006 ). Insights into gene expression changes impacting B-cell transformation: cross-species microarray analysis of bovine leukemia virus tax-responsive genes in ovine B cells. J. Virol. 80 1922–1938

    Not in our library10.1128/jvi.80.4.1922-1938.2006

  50. 50.

    Komori H. Ishiguro N. Horiuchi M. Shinagawa M. Aida Y. (1996 ). Predominant p53 mutations in enzootic bovine leukemic cell lines. Vet. Immunol. Immunopathol. 52 53–63

    Not in our library10.1016/0165-2427(95)05538-x

  51. 51.

    Konishi H. Kobayashi N. Hatanaka M. (1984 ). Defective human T-cell leukemia virus in adult T-cell leukemia patients. Mol. Biol. Med. 2 273–283

    Not in our library

  52. 52.

    Konnai S. Takeshima S. N. Tajima S. Yin S. A. Okada K. Onuma M. (2003 ). The influence of ovine MHC class II DRB1 alleles on immune response in bovine leukemia virus infection. Microbiol. Immunol. 47 223–232

    Not in our library10.1111/j.1348-0421.2003.tb03391.x

  53. 53.

    Konnai S. Usui T. Ikeda M. Kohara J. Hirata T. Okada K. (2006 ). Tumor necrosis factor-alpha genetic polymorphism may contribute to progression of bovine leukemia virus-infection. Microbes Infect. 8 2163–2171

    Not in our library10.1016/j.micinf.2006.04.017

  54. 54.

    Kono Y. Sentsui H. Arai K. Ishida H. Irishio W. (1983 ). Contact transmission of bovine leukemia virus under insect-free conditions. J. Vet. Med. Sci. 45 799–802

    Not in our library10.1292/jvms1939.45.799

  55. 55.

    Korber B. Okayama A. Donnelly R. Tachibana N. Essex M. (1991 ). Polymerase chain reaction analysis of defective human T-cell leukemia virus type I proviral genomes in leukemic cells of patients with adult T-cell leukemia. J. Virol. 65 5471–5476

    Not in our library10.1128/jvi.65.10.5471-5476.1991

  56. 56.

    Koyanagi Y. Itoyama Y. Nakamura N. Takamatsu K. Kira J. Iwamasa T. (1993 ). In vivo infection of human T-cell leukemia virus type I in non-T cells. Virology 196 25–33

    Not in our library10.1006/viro.1993.1451

  57. 57.

    Lagarias D. M. Radke K. (1989 ). Transcriptional activation of bovine leukemia virus in blood cells from experimentally infected, asymptomatic sheep with latent infections. J. Virol. 63 2099–2107

    Not in our library10.1128/jvi.63.5.2099-2107.1989

  58. 58.

    Lefebvre L. Vanderplasschen A. Ciminale V. Heremans H. Dangoisse O. Jauniaux J. C. (2002 ). Oncoviral bovine leukemia virus G4 and human T-cell leukemia virus type 1 p13(II) accessory proteins interact with farnesyl pyrophosphate synthetase. J. Virol. 76 1400–1414

    Not in our library10.1128/jvi.76.3.1400-1414.2002

  59. 59.

    Leisering A. (1871 ). Hypertrophy der Malpigischen Korperchen der Milz. Bericht uber das Veterinarwesen im Konigreich Sachsen 16 15–16

    Not in our library

  60. 60.

    Lemasson I. Lewis M. R. Polakowski N. Hivin P. Cavanagh M. H. Thebault S. (2007 ). Human T-cell leukemia virus type 1 (HTLV-1) bZIP protein interacts with the cellular transcription factor CREB to inhibit HTLV-1 transcription. J. Virol. 81 1543–1553

    Not in our library10.1128/jvi.00480-06

  61. 61.

    Lewin H. A. Bernoco D. (1986 ). Evidence for BoLA-linked resistance and susceptibility to subclinical progression of bovine leukaemia virus infection. Anim. Genet. 17 197–207

    Not in our library10.1111/j.1365-2052.1986.tb03191.x

  62. 62.

    Lewin H. A. Wu M. C. Stewart J. A. Nolan T. J. (1988 ). Association between BoLA and subclinical bovine leukemia virus infection in a herd of Holstein–Friesian cows. Immunogenetics 27 338–344

    Not in our library10.1007/bf00395129

  63. 63.

    Mammerickx M. Portetelle D. Burny A. (1981 ). Experimental cross-transmissions of bovine leukemia virus (BLV) between several animal species. Zbl. Vet. Med.B 28 69–81

    Not in our library10.1111/j.1439-0450.1981.tb01740.x

  64. 64.

    Matsuoka M. Jeang K. T. (2011 ). Human T-cell leukemia virus type 1 (HTLV-1) and leukemic transformation: viral infectivity, Tax, HBZ and therapy. Oncogene 30 1379–1389

    Not in our library10.1038/onc.2010.537

  65. 65.

    Mirsky M. L. Olmstead C. A. Da Y. Lewin H. A. (1996 ). The prevalence of proviral bovine leukemia virus in peripheral blood mononuclear cells at two subclinical stages of infection. J. Virol. 70 2178–2183

    Not in our library10.1128/jvi.70.4.2178-2183.1996

  66. 66.

    Miyasaka T. Takeshima S. N. Jimba M. Matsumoto Y. Kobayashi N. Matsuhashi T. (2013 ). Identification of bovine leukocyte antigen class II haplotypes associated with variations in bovine leukemia virus proviral load in Japanese Black cattle. Tissue Antigens 81 72–82

    Not in our library10.1111/tan.12041

  67. 67.

    Murakami H. Kuroiwa T. Suzuki K. Miura Y. Sentsui H. (2011a ). Analysis of Syk expression in bovine lymphoma and persistent lymphocytosis induced by bovine leukemia virus. J. Vet. Med. Sci. 73 41–45

    Not in our library10.1292/jvms.10-0225

  68. 68.

    Murakami H. Yamada T. Suzuki M. Nakahara Y. Suzuki K. Sentsui H. (2011b ). Bovine leukemia virus integration site selection in cattle that develop leukemia. Virus Res. 156 107–112

    Not in our library10.1016/j.virusres.2011.01.004

  69. 69.

    Murakami K. Aida Y. Kageyama R. Numakunai S. Ohshima K. Okada K. (1994a ). Immunopathologic study and characterization of the phenotype of transformed cells in sheep with bovine leukemia virus-induced lymphosarcoma. Am. J. Vet. Res. 55 72–80

    Not in our library

  70. 70.

    Murakami K. Okada K. Ikawa Y. Aida Y. (1994b ). Bovine leukemia virus induces CD5- B cell lymphoma in sheep despite temporarily increasing CD5+ B cells in asymptomatic stage. Virology 202 458–465

    Not in our library10.1006/viro.1994.1362

  71. 71.

    Nagaoka Y. Kabeya H. Onuma M. Kasai N. Okada K. Aida Y. (1999 ). Ovine MHC class II DRB1 alleles associated with resistance or susceptibility to development of bovine leukemia virus-induced ovine lymphoma. Cancer Res. 59 975–981

    Not in our library

  72. 72.

    Nicot C. Dundr M. Johnson J. M. Fullen J. R. Alonzo N. Fukumoto R. (2004 ). HTLV-1-encoded p30II is a post-transcriptional negative regulator of viral replication. Nat. Med. 10 197–201

    Not in our library10.1038/nm984

  73. 73.

    Ohshima K. Kikuchi M. Masuda Y. Kobari S. Sumiyoshi Y. Eguchi F. (1991 ). Defective provirus form of human T-cell leukemia virus type I in adult T-cell leukemia/lymphoma: clinicopathological features. Cancer Res. 51 4639–4642

    Not in our library

  74. 74.

    Onuma M. Honma T. Mikami T. Ichijo S. Konishi T. (1979 ). Studies on the sporadic and enzootic forms of bovine leukosis. J. Comp. Pathol. 89 159–167

    Not in our library10.1016/0021-9975(79)90055-0

  75. 75.

    Onuma M. Wada M. Yasutomi Y. Yamamoto M. Okada H. M. Kawakami Y. (1990 ). Suppression of immunological responses in rabbits experimentally infected with bovine leukemia virus. Vet. Microbiol. 25 131–141

    Not in our library10.1016/0378-1135(90)90072-4

  76. 76.

    Osame M. Usuku K. Izumo S. Ijichi N. Amitani H. Igata A. (1986 ). HTLV-I associated myelopathy, a new clinical entity. Lancet 1 1031–1032

    Not in our library10.1016/s0140-6736(86)91298-5

  77. 77.

    Panei C. J. Takeshima S. N. Omori T. Nunoya T. Davis W. C. Ishizaki H. (2013 ). Estimation of bovine leukemia virus (BLV) proviral load harbored by lymphocyte subpopulations in BLV-infected cattle at the subclinical stage of enzootic bovine leucosis using BLV-CoCoMo-qPCR. BMC Vet. Res. 9:95

    Not in our library10.1186/1746-6148-9-95

  78. 78.

    Philpott S. M. Buehring G. C. (1999 ). Defective DNA repair in cells with human T-cell leukemia/bovine leukemia viruses: role of tax gene. J. Natl. Cancer Inst. 91 933–942

    Not in our library10.1093/jnci/91.11.933

  79. 79.

    Richard A. Tulasne D. (2012 ). Caspase cleavage of viral proteins, another way for viruses to make the best of apoptosis. Cell Death Dis. 3 e277

    Not in our library10.1038/cddis.2012.18

  80. 80.

    Robert-Guroff M. Weiss S. H. Giron J. A. Jennings A. M. Ginzburg H. M. Margolis I. B. (1986 ). Prevalence of antibodies to HTLV-I, -II, and -III in intravenous drug abusers from an AIDS endemic region. JAMA 255 3133–3137

    Not in our library10.1001/jama.1986.03370220095034

  81. 81.

    Sagata N. Yasunaga T. Ogawa Y. Tsuzuku-Kawamura J. Ikawa Y. (1984a ). Bovine leukemia virus: unique structural features of its long terminal repeats and its evolutionary relationship to human T-cell leukemia virus. Proc. Natl. Acad. Sci. U.S.A. 81 4741–4745

    Not in our library10.1073/pnas.81.15.4741

  82. 82.

    Sagata N. Yasunaga T. Ohishi K. Tsuzuku-Kawamura J. Onuma M. Ikawa Y. (1984b ). Comparison of the entire genomes of bovine leukemia virus and human T-cell leukemia virus and characterization of their unidentified open reading frames. EMBO J. 3 3231–3237

    Not in our library10.1002/j.1460-2075.1984.tb02283.x

  83. 83.

    Sakakibara N. Kabeya H. Ohashi K. Sugimoto C. Onuma M. (1998 ). Epitope mapping of bovine leukemia virus transactivator protein tax. J. Vet. Med. Sci. 60 599–605

    Not in our library10.1292/jvms.60.599

  84. 84.

    Satou Y. Yasunaga J. Yoshida M. Matsuoka M. (2006 ). HTLV-I basic leucine zipper factor gene mRNA supports proliferation of adult T cell leukemia cells. Proc. Natl. Acad. Sci. U.S.A. 103 720–725

    Not in our library10.1073/pnas.0507631103

  85. 85.
    HTLV-1 bZIP Factor Induces T-Cell Lymphoma and Systemic Inflammation In Vivo · 2011
    No notice
  86. 86.

    Schwartz I. Bensaid A. Polack B. Perrin B. Berthelemy M. Levy D. (1994 ). In vivo leukocyte tropism of bovine leukemia virus in sheep and cattle. J. Virol. 68 4589–4596

    Not in our library10.1128/jvi.68.7.4589-4596.1994

  87. 87.

    Schwartz I. Levy D. (1994 ). Pathobiology of bovine leukemia virus. Vet. Res. 25 521–536

    Not in our library

  88. 88.

    Starkenburg R. J. Hansen L. B. Kehrli M. E. Jr. Chester-Jones H. (1997 ). Frequencies and effects of alternative DRB3.2 alleles of bovine lymphocyte antigen for Holsteins in milk selection and control lines. J. Dairy Sci. 80 3411–3419

    Not in our library10.3168/jds.s0022-0302(97)76316-1

  89. 89.

    Stott M. L. Thurmond M. C. Dunn S. J. Osburn B. I. Stott J. L. (1991 ). Integrated bovine leukosis proviral DNA in T helper and T cytotoxic/suppressor lymphocytes. J. Gen. Virol. 72(Pt 2) 307–315

    Not in our library10.1099/0022-1317-72-2-307

  90. 90.

    Sulimova G. E. Udina I. G. Shaikhaev G. O. Zakharov I. A. (1995 ). DNA polymorphism of the BoLA-DRB3 gene in cattle in connection with resistance and susceptibility to leukemia. Genetika 31 1294–1299

    Not in our library

  91. 91.

    Szynal M. Cleuter Y. Beskorwayne T. Bagnis C. Van Lint C. Kerkhofs P. (2003 ). Disruption of B-cell homeostatic control mediated by the BLV-Tax oncoprotein: association with the upregulation of Bcl-2 and signaling through NF-kappaB. Oncogene 22 4531–4542

    Not in our library10.1038/sj.onc.1206546

  92. 92.

    Tajima S. Aida Y. (2000 ). The region between amino acids 245 and 265 of the bovine leukemia virus (BLV) tax protein restricts transactivation not only via the BLV enhancer but also via other retrovirus enhancers. J. Virol. 74 10939–10949

    Not in our library10.1128/jvi.74.23.10939-10949.2000

  93. 93.

    Tajima S. Aida Y. (2002 ). Mutant tax protein from bovine leukemia virus with enhanced ability to activate the expression of c-fos. J. Virol. 76 2557–2562

    Not in our library10.1128/jvi.76.5.2557-2562.2002

  94. 94.

    Tajima S. Aida Y. (2005 ). Induction of expression of bovine leukemia virus (BLV) in blood taken from BLV-infected cows without removal of plasma. Microbes Infect. 7 1211–1216

    Not in our library10.1016/j.micinf.2005.04.010

  95. 95.

    Tajima S. Ikawa Y. Aida Y. (1998a ). Complete bovine leukemia virus (BLV) provirus is conserved in BLV-infected cattle throughout the course of B-cell lymphosarcoma development. J. Virol. 72 7569–7576

    Not in our library10.1128/jvi.72.9.7569-7576.1998

  96. 96.

    Tajima S. Zhuang W. Z. Kato M. V. Okada K. Ikawa Y. Aida Y. (1998b ). Function and conformation of wild-type p53 protein are influenced by mutations in bovine leukemia virus-induced B-cell lymphosarcoma. Virology 243 735–746

    Not in our library10.1006/viro.1998.9051

  97. 97.

    Tajima S. Takahashi M. Takeshima S. N. Konnai S. Yin S. A. Watarai S. (2003a ). A mutant form of the tax protein of bovine leukemia virus (BLV), with enhanced transactivation activity, increases expression and propagation of BLV in vitro but not in vivo. J. Virol. 77 1894–1903

    Not in our library10.1128/jvi.77.3.1894-1903.2003

  98. 98.

    Tajima S. Tsukamoto M. Aida Y. (2003b ). Latency of viral expression in vivo is not related to CpG methylation in the U3 region and part of the R region of the long terminal repeat of bovine leukemia virus. J. Virol. 77 4423–4430

    Not in our library10.1128/jvi.77.7.4423-4430.2003

  99. 99.

    Takahashi M. Tajima S. Okada K. Davis W. C. Aida Y. (2005 ). Involvement of bovine leukemia virus in induction and inhibition of apoptosis. Microbes Infect. 7 19–28

    Not in our library10.1016/j.micinf.2004.09.014

  100. 100.

    Takahashi M. Tajima S. Takeshima S. N. Konnai S. Yin S. A. Okada K. (2004 ). Ex vivo survival of peripheral blood mononuclear cells in sheep induced by bovine leukemia virus (BLV) mainly occurs in CD5- B cells that express BLV. Microbes Infect. 6 584–595

    Not in our library10.1016/j.micinf.2004.02.014

  101. 101.

    Takeshima S-N. Aida Y. (2006 ). Structure, function and disease susceptibility of the bovine major histocompatibility complex. Anim. Sci. J. 77 138–150

    Not in our library10.1111/j.1740-0929.2006.00332.x

  102. 102.

    Tanaka A. Takahashi C. Yamaoka S. Nosaka T. Maki M. Hatanaka M. (1990 ). Oncogenic transformation by the tax gene of human T-cell leukemia virus type I in vitro. Proc. Natl. Acad. Sci. U.S.A. 87 1071–1075

    Not in our library10.1073/pnas.87.3.1071

  103. 103.

    Theilen G. H. Dungworth D. L. (1965 ). Bovine lymphosarcoma in California. 3. The calf form. Am. J. Vet. Res. 26 696–709

    Not in our library

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    Tsukasaki K. Tsushima H. Yamamura M. Hata T. Murata K. Maeda T. (1997 ). Integration patterns of HTLV-I provirus in relation to the clinical course of ATL: frequent clonal change at crisis from indolent disease. Blood 89 948–956

    Not in our library

  105. 105.

    Voneche V. Portetelle D. Kettmann R. Willems L. Limbach K. Paoletti E. (1992 ). Fusogenic segments of bovine leukemia virus and simian immunodeficiency virus are interchangeable and mediate fusion by means of oblique insertion in the lipid bilayer of their target cells. Proc. Natl. Acad. Sci. U.S.A. 89 3810–3814

    Not in our library10.1073/pnas.89.9.3810

  106. 106.

    Weiss R. Teich N. Varmus H. Coffin J. (1985 ). RNA Tumor Viruses. New York: Cold Spring Harbor Laboratory

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  107. 107.

    Willems L. Gatot J. S. Mammerickx M. Portetelle D. Burny A. Kerkhofs P. (1995 ). The YXXL signalling motifs of the bovine leukemia virus transmembrane protein are required for in vivo infection and maintenance of high viral loads. J. Virol. 69 4137–4141

    Not in our library10.1128/jvi.69.7.4137-4141.1995

  108. 108.

    Willems L. Gegonne A. Chen G. Burny A. Kettmann R. Ghysdael J. (1987 ). The bovine leukemia virus p34 is a transactivator protein. EMBO J. 6 3385–3389

    Not in our library10.1002/j.1460-2075.1987.tb02661.x

  109. 109.

    Willems L. Grimonpont C. Kerkhofs P. Capiau C. Gheysen D. Conrath K. (1998 ). Phosphorylation of bovine leukemia virus Tax protein is required for in vitro transformation but not for transactivation. Oncogene 16 2165–2176

    Not in our library10.1038/sj.onc.1201765

  110. 110.

    Willems L. Heremans H. Chen G. Portetelle D. Billiau A. Burny A. (1990 ). Cooperation between bovine leukaemia virus transactivator protein and Ha-ras oncogene product in cellular transformation. EMBO J. 9 1577–1581

    Not in our library10.1002/j.1460-2075.1990.tb08277.x

  111. 111.

    Willems L. Kerkhofs P. Dequiedt F. Portetelle D. Mammerickx M. Burny A. (1994 ). Attenuation of bovine leukemia virus by deletion of R3 and G4 open reading frames. Proc. Natl. Acad. Sci. U.S.A. 91 11532–11536

    Not in our library10.1073/pnas.91.24.11532

  112. 112.

    Williams D. L. Barta O. Amborski G. F. (1988 ). Molecular studies of T-lymphocytes from cattle infected with bovine leukemia virus. Vet. Immunol. Immunopathol. 19 307–323

    Not in our library10.1016/0165-2427(88)90117-1

  113. 113.

    Wu D. Takahashi K. Murakami K. Tani K. Koguchi A. Asahina M. (1996 ). B-1a, B-1b and conventional B cell lymphoma from enzootic bovine leukosis. Vet. Immunol. Immunopathol. 55 63–72

    Not in our library10.1016/s0165-2427(96)05631-0

  114. 114.

    Wurzer W. J. Planz O. Ehrhardt C. Giner M. Silberzahn T. Pleschka S. (2003 ). Caspase 3 activation is essential for efficient influenza virus propagation. EMBO J. 22 2717–2728

    Not in our library10.1093/emboj/cdg279

  115. 115.

    Wyatt C. R. Wingett D. White J. S. Buck C. D. Knowles D. Reeves R. (1989 ). Persistent infection of rabbits with bovine leukemia virus associated with development of immune dysfunction. J. Virol. 63 4498–4506

    Not in our library10.1128/jvi.63.11.4498-4506.1989

  116. 116.

    Xu A. Van Eijk M. J. Park C. Lewin H. A. (1993 ). Polymorphism in BoLA-DRB3 exon 2 correlates with resistance to persistent lymphocytosis caused by bovine leukemia virus. J. Immunol. 151 6977–6985

    Not in our library

  117. 117.

    Zanotti M. Poli G. Ponti W. Polli M. Rocchi M. Bolzani E. (1996 ). Association of BoLA class II haplotypes with subclinical progression of bovine leukaemia virus infection in Holstein–Friesian cattle. Anim. Genet. 27 337–341

    Not in our library

  118. 118.

    Zhang W. Nisbet J. W. Albrecht B. Ding W. Kashanchi F. Bartoe J. T. (2001 ). Human T-lymphotropic virus type 1 p30(II) regulates gene transcription by binding CREB binding protein/p300. J. Virol. 75 9885–9895

    Not in our library10.1128/jvi.75.20.9885-9895.2001

  119. 119.

    Zhao T. Satou Y. Sugata K. Miyazato P. Green P. L. Imamura T. (2011 ). HTLV-1 bZIP factor enhances TGF-beta signaling through p300 coactivator. Blood 118 1865–1876

    Not in our library10.1182/blood-2010-12-326199

  120. 120.

    Zhao T. Yasunaga J. Satou Y. Nakao M. Takahashi M. Fujii M. (2009 ). Human T-cell leukemia virus type 1 bZIP factor selectively suppresses the classical pathway of NF-kappaB. Blood 113 2755–2764

    Not in our library10.1182/blood-2008-06-161729

  121. 121.

    Zhuang W. Tajima S. Okada K. Ikawa Y. Aida Y. (1997 ). Point mutation of p53 tumor suppressor gene in bovine leukemia virus-induced lymphosarcoma. Leukemia 11(Suppl 3) 344–346

    Not in our library

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