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Preventive and Therapeutic Strategies for Bovine Leukemia Virus: Lessons for HTLV

Sabrina M. Rodríguez, Arnaud Florins, Nicolas Gillet and 9 more

Viruses · 2011 · Review · CC BY

Abstract

Bovine leukemia virus (BLV) is a retrovirus closely related to the human T-lymphotropic virus type 1 (HTLV-1). BLV is a major animal health problem worldwide causing important economic losses. A series of attempts were developed to reduce prevalence, chiefly by eradication of infected cattle, segregation of BLV-free animals and vaccination. Although having been instrumental in regions such as the EU, these strategies were unsuccessful elsewhere mainly due to economic costs, management restrictions and lack of an efficient vaccine. This review, which summarizes the different attempts previously developed to decrease seroprevalence of BLV, may be informative for management of HTLV-1 infection. We also propose a new approach based on competitive infection with virus deletants aiming at reducing proviral loads.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 25, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

1As early as in the 19th century, a series of reports already described the occurrence of clinical signs associated with enzootic bovine leukosis (EBL). Initial observations from Leisering of yellowish nodules in the enlarged spleen of a leukocytic cow were communicated in the German literature in 1871 (, cited by). Three years later, Bollinger described bovine leukemia as a well-defined clinical entity, and in 1876 Siedamgrotzky and Hofmeister recorded the first cases of bovine lymphocytic malignancies (; cited by). Thus, Europe, and more specifically the Memel area, then regarded as East Prussia and now located in the contemporary Lithuania, might be thought of as the cradle of enzootic bovine leukemia (; cited by). Diffusion and wide spread of the disease occurred by the introduction of European cattle breeds in countries free of the disease. Despite all these pieces of evidence, the infectious nature of EBL etiological agent was discovered many decades later based on epidemiological evidence. Finally, the causative agent of this malignant disease was isolated in culture in 1969 and designated bovine leukemia virus (BLV).

2BLV is an oncogenic B-lymphocytotropic retrovirus that infects cattle inducing a persistent infection with diverse outcomes. The great majority of BLV-infected animals (around 70%) are asymptomatic carriers of the virus. In these animals, neither clinical symptoms nor alteration of the total lymphocyte count are evidenced. Thus, they can only be identified by the presence of anti-BLV antibodies and/or of proviral DNA. Approximately, one-third of BLV-infected bovines develop a benign polyclonal proliferation of B cells called persistent lymphocytosis (PL). This clinical condition is characterized by an increase in the absolute number of peripheral blood circulating B lymphocytes associated with an inversion of the B/T lymphocyte ratio. Despite these hematologic alterations, PL animals do not develop any other apparent clinical signs. PL is usually stable for several years but can also progress to the tumor phase.

3The most conspicuous clinical manifestation of BLV infection is the development of lymphoid tumors. Fatal lymphoma or lymphosarcoma (LS) occurs in less than 5–10% of infected animals, predominantly adult cattle older than 4–5 years old. The development of tumors is not necessarily preceded by a phase of PL, but this is the case in two-thirds of the animals. Unlike persistent lymphocytosis, B-cell expansion is of mono- or oligo-clonal origin. Local proliferation of B cells, called lymphosarcoma, can occur within different organs and tissues leading to a series of defects that are finally incompatible with the survival of the animal. In addition, transformed B cells can also induce the enlargement of lymph nodes and cause lymphoma. Besides an impact on survival, BLV infection also impairs the immune system leading to opportunistic infections.

Transmission

4BLV is transmitted horizontally, essentially through the transfer of infected cells. Since free virus is very unstable, BLV-infected cells (B-lymphocytes, monocytes/macrophages, etc.) present in blood or milk appear to be the best vehicles of natural transmission. Due to the high number of infected cells they contain, animals with PL are particularly efficient in transmitting the virus. In herds, iatrogenic procedures largely account for the propagation of the infection. Cattle management procedures which involve transfer of infected blood (i.e., dehorning, ear tattooing, rectal palpation, and, essentially, the use of infected needles) were postulated as a common mode of transmission. In addition, prolonged direct contact between infected and healthy animals has also been considered as a risk factor for BLV transmission. Transfer of infected blood might also occur in regions with high density of hematophagous insects. Perinatal or postnatal transmission of BLV frequently happens in herd conditions. The rate of transmission in utero varies between 4 and 18%, with highest risk in calves born from cows with PL. Although BLV transmission has been postulated to occur from cow to calves via milk, this route of infection was only demonstrated experimentally. Despite the presence of BLV proviral DNA in colostrum and milk from infected cows, calves can remain uninfected over extended periods of time likely due to the protective role of maternal antibodies present in the colostrum.

Epidemiology

5Sero-epidemiological surveys have shown that BLV infection is widespread in all continents except in Europe. Efforts in the implementation of control measures and campaigns to eradicate BLV infection in Western Europe have been successful. Recently, the European Economic Community (EEC) declared most of its member states as officially free of EBL. In contrast, the situation is different in Eastern Europe where the disease is still present in several countries (Bulgaria, Croatia, Estonia, Latvia, Poland, Romania, Ukraine).

6Similar attempts to eradicate BLV infection in Australia and New Zealand dairy herds began in the mid-1990s. More than 98% of dairy herds were negative in 2005.

7Detailed information about the epidemiological situation in the United States of America was collected through the National Animal Health Monitoring (NAHMS). Survey studies in 2007 revealed that 83.9% of U.S. dairy herds were positive for BLV. Recent epidemiological data is available for several provinces in Canada. All agree in indicating high seroprevalence rates reaching up to 89% and 20.8%–37.4% at herd and individual levels, respectively.

8In South America, individual infection rates between 34 and 50% were reported in Colombia, Venezuela, Chile and Uruguay. In Argentina, individual and herd prevalence levels scale up to 32.8% and 84%, respectively. In Brazil, the individual prevalence of BLV infection varies considerably among states and reaches levels beyond 50%.

9The epidemiological situation in Asia is more uncertain. The International Organization of Epizootics (OIE) recognizes that BLV is present in Indonesia, Taipei (China) and Mongolia. Surprisingly, only about 5% of animals were positive for BLV in Cambodia and Taiwan. The seroprevalence rates in Japan were found to be 28.6% and 68.1% at the individual and herd levels, respectively. In Korea, individual seroprevalence rates exceeded 50% whilst 86.8% of dairy herds were infected.

10Regarding the Middle East countries, reports indicate that the prevalence of BLV infection is somewhat lower than in other regions of the world, i.e., about 20%. Exceptions in this region include Turkey and Iran where the herd seroprevalence levels climb to 48.3% and 64.7%, respectively, while the individual seroprevalence in Iran was estimated between 17 and 24.6%, although some argue that prevalence levels are lower.

Preventive and Therapeutic Strategies

11Understanding the mechanisms of pathogenesis has been instrumental for developing therapeutic and preventive strategies against BLV infection. The different approaches that were developed are reviewed in this section.

Test and Eliminate

12A first strategy is to identify and eliminate BLV-infected cattle. This approach requires identification of BLV-positive animals either by hematological, genomic or serological methods, immediate removal of positive cases from the herd and, finally, prompt slaughtering.

13This “test and elimination” methodology has been instrumental in accomplishing the BLV-free status at herd and regional scales within a relatively brief period of time when compared to other alternatives. Evidence of the efficiency of this strategy is illustrated by the successful eradication of the disease in several countries of Western Europe.

14Although this approach has been efficient, its feasibility faces some important restrictions. A key limitation is that the initial prevalence rate of infection should not be high due to its very high economic cost. Hence, this strategy can be particularly justified in pedigree breeds having high genetic potential as well as for export to BLV-free countries. Nevertheless, even when the rates of infection are low, the “test and eliminate” approach is a burdensome strategy due to diagnostics, premature culling and replacement of reactors. Loss of genetic and reproductive potential must also be considered.

15In fact, this strategy requires governmental economic compensation policies to be successful. If no official subsidizing action is adopted by the local authorities, the costs of implementation of such a strategy quickly exceeds the potential benefits. Countries such as USA, Canada, Argentina, and Japan lacking financial compensatory policies usually failed to obtain adherence to enroll in these programs.

16To summarize, the pros and cons of the “test and eliminate” strategy are outlined in Table 1.

Test and Segregate

17Another approach aims at reducing part of these costs by segregating instead of culling infected animals. Control programs based on segregation require detection of seropositive animals and confinement of BLV-infected and seronegative herds in strictly separated areas. It has been proposed that a minimum distance of 200 meters must separate the two herds to avoid transmission. An alternative option is to keep the animals in the same farm and to manage them separately. For optimal results with any of these options, separate equipment or at least careful disinfection and hygiene of non-disposable equipment should be implemented (Table 1). The main advantage of this approach is the reduction of costly losses due to compulsory premature culling and replacement of BLV-positive animals. Although quite demanding, this type of program has been useful to decrease prevalence or even achieve eradication of the disease. The disadvantage is that there is a permanent risk of reintroducing infected animals and, therefore, it may be slower than the ‘test and eliminate’ option.

18The removal/segregation approaches both require specific and regular identification of infected animals. Discrimination of BLV-infected animals from the herd was originally performed by hematologic screening based on leukocyte counts. Later on, more sensitive and specific techniques (i.e., AGID, agar gel-immunodiffusion test and ELISA, enzyme-linked immunosorbent assay) became routine diagnostic methods. These serologic assays performed on serum or milk were widely used and became the official tests recommended for international trade. However, these tests can be misleading since the presence of anti-BLV antibodies does not necessarily imply that the animals are infected and vice versa. Indeed, there is a “latency” period of several weeks between infection and seroconversion. Also, calves can have anti-BLV antibodies due to maternal antibodies from the colostrum or to parturition. A significant fraction of these calves will remain uninfected although they carry anti-BLV antibodies.

19Therefore, a more accurate way to monitor BLV infection is PCR. BLV-infected cattle can further be classified according to their proviral load (PVL). In fact, the proviral load in the peripheral blood is a predictive marker of transmission risk. Thus, PVL can be used as a criterion to discriminate and eliminate/segregate highly infected cows. Besides technical challenges (contaminations), the disadvantages of PCR-based diagnostics are higher costs and the need of more complex equipment.

Corrective Management and Veterinary Practices

20This type of approach aims at limiting transfer of BLV-infected cells present in blood, milk, secretions, excretions, syringes or surgical instruments.

21Among the diverse control measures that can be implemented in a preventive or corrective management control plan, the following constitute essential practices: - (i) use of individual, single-use needles and syringes during vaccination or therapeutic protocols;- (ii) use of individual, single-use obstetrical sleeves (or at least replacement between examination of BLV-reactors and non-infected animals);- (iii) use of disposable equipment (or at least cleaning, disinfection or sterilization of reusable materials and surgical instruments) in procedures such as dehorning, tattooing, implanting, cauterizing, castration or ear-tagging;- (iv) use of electrical or gas burning devices rather than gouging equipment during dehorning;- (v) feeding calves with colostrum or whole milk from non-infected dams, pasteurized colostrum from BLV-infected cows or milk replacer;- (vi) elimination of insects, particularly in densely populated farm areas (milking areas, free-stalls, barns) in order to minimize potential transmission between animals through arthropod vectors;- (vii) natural and/or artificial insemination and embryo transfer with BLV-free dams and bulls.

22- (i) use of individual, single-use needles and syringes during vaccination or therapeutic protocols;

23- (ii) use of individual, single-use obstetrical sleeves (or at least replacement between examination of BLV-reactors and non-infected animals);

24- (iii) use of disposable equipment (or at least cleaning, disinfection or sterilization of reusable materials and surgical instruments) in procedures such as dehorning, tattooing, implanting, cauterizing, castration or ear-tagging;

25- (iv) use of electrical or gas burning devices rather than gouging equipment during dehorning;

26- (v) feeding calves with colostrum or whole milk from non-infected dams, pasteurized colostrum from BLV-infected cows or milk replacer;

27- (vi) elimination of insects, particularly in densely populated farm areas (milking areas, free-stalls, barns) in order to minimize potential transmission between animals through arthropod vectors;

28- (vii) natural and/or artificial insemination and embryo transfer with BLV-free dams and bulls.

29Other potentially beneficial management control measures might include: (i) prevent introduction of infected animals into the herd by testing and quarantining/isolating newcomers; (ii) separate animals by age to decrease contacts (iii) minimize movement of animals between milking/feeding groups; (iv) use individual calf hutches for newborn calves; and (v) limit access to outside visitors.

30Compared to the test and eliminate/segregate strategies, the “corrective management and veterinary practices” approach is clearly more cost-effective. Neither investments on facilities nor removal of infected cattle nor constant surveillance of the herd serological status are required. The disadvantages of the corrective management approach are that practices are intensively laborious and vulnerable to environmental and human variables. In this regard, careful appraisal of the effort required before the enrolment into a corrective management control plan must be considered. Strict compliance to the rigorous measures should be enforced and a long-term engagement with the program is required until fruitful benefits of this strategy are observed (see Table 1). In addition, adequate training of personnel and farm employees on BLV prevention and biosecure practices might be considered. The efficacy of a “corrective management and veterinary practices” strategy based exclusively on strict sanitary measures is still controversial.

Selection of BLV-Resistant Cattle

31Livestock breeding programs exploit selection of genetic traits beneficial for production (e.g., milk yield, growth, reproduction). In principle, it would be possible to select breeds that are less susceptible or even resistant to BLV infection. Immune responsiveness and heritable resistance or susceptibility to infection are influenced by the host major histocompatibilty complex (MHC). The Bovine Lymphocyte Antigen (BoLA) refers to the major histocompatibilty complex in bovine species (Bos taurus and Bos indicus). Pioneering work suggested that host genetics factors determined cattle susceptibility to BLV infection. Early studies initially attributed a linkage between resistance or susceptibility of cattle to development of subclinical PL and serologically defined class I BoLA-A alleles. However, frequencies of BoLA-A alleles diverge considerably between breeds and the association was not confirmed at the population level. More sensitive analyses showed that the development of PL was apparently more closely related to class II DRB2 genes. Further characterization of genes within the class II BoLA locus evidenced that the strongest association with resistance or susceptibility to PL corresponded to polymorphisms of the class II DRB3 gene, the only one actively transcribed among the three DRB genes. Reduced proviral loads were observed in animals carrying the resistance-associated DRB3.2*11 allele, conferring biological significance to this association. These observations were later confirmed and extended to other breeds. More recently, a strong linkage between the allele DRB3.2*0902 and genetic resistance to PL was demonstrated in Holstein cows. The presence of DRB3.2*0902 allele correlates with a low proviral load profile (LPL). It was proposed that cattle harboring the *0902 allele and presenting this LPL profile might be unable to transmit BLV in herd conditions. Polymorphisms in the BoLA-DRB3 genes were also correlated with resistance and susceptibility to leukemia/lymphoma in cows. In the experimental sheep model, gene polymorphisms of ovine leukocyte antigen (OLA)-DRB1 can predict the frequency of tumor development.

32Besides the polymorphic BoLA-DRB3 gene, other non-MHC genes are also considered to be involved in the development or progression of BLV infection. An association between TNF-alpha and BLV pathogenesis has been established in ovine and bovine species. In the latter, a polymorphism in the promoter region of the TNF-α gene (allele -824G) might contribute to PL susceptibility. Furthermore, polymorphisms in alpha-albumin genes might also be associated with resistance to BLV infection.

33Selection of BLV resistant animals based on genetic traits faces a series of limitations. First, the relevance and statistical significance of the identified markers must be analyzed at the population level. Large-scale studies in different breeds are required to assess the efficiency and the consequences of selection based on these markers. It is likely that identification of other BoLA polymorphisms or resistance genes will be required to achieve robust and efficient selection. Genetic resistance to BLV infection appears to be a complex mechanism under the control of multiple genes, each contributing slightly to the phenotype. Poor correspondence between the specific alleles and development of PL or LS clearly indicates that other viral or host genetic, epigenetic and/or environmental factors contribute to the outcome of infection. In this scenario, it might become difficult to prioritize one allele over other/s as an absolute genetic selection marker for selecting BLV resistant cattle.

34A second limitation is that selection of BLV-resistant animals encounters a major risk due to the narrowing of the genetic pool of the cattle population. This loss of biodiversity is particularly important in resistance to other pathogens. On the other hand, selection for BLV resistance may also have adverse effects on beneficial productivity traits. In this sense, it should be mentioned that humoral immune response to other economically important viral diseases (i.e., foot and mouth disease, bovine herpesvirus type 1 and bovine viral diarrhea virus) was not adversely affected in bovines carrying the DRB3.2*0902 allele. Perhaps a more important problem is that selection based on disease resistance might also have adverse effects on productivity traits.

35Due to these limitations, the benefits of selection programs for BLV resistance might not reach a positive benefit:cost ratio.

Epigenetic Modulation of Viral Expression as Therapy

36This type of approach issued from fundamental research on viral dynamics in BLV-infected sheep. Conceptually, the host-pathogen interplay during infection is characterized by a very dynamic kinetics resulting in a subtle equilibrium between the virus, which attempts to replicate, and the immune response, which seeks to exert tight control of the pathogen. This equilibrium appeared to be tightly regulated by epigenetic mechanisms. In particular, the extent of chromatin condensation is an essential epigenetic control mechanism determining gene expression and is partly dependent on the level of histone acetylation. In a certainly oversimplified model, chromatin relaxation results from acetylation of the conserved N-terminal histone tails that reduces the interaction with the negatively charged phosphate backbone. This allows unwinding of DNA, leading to gene expression by favoring access of transcriptional activators to their target sites. Conversely, gene silencing or transcriptional repression is the consequence of preventing access of transcriptional activators due to DNA packaging into condensed chromatin. This is mediated by acetyl removal of lysine residues from histone N-terminal tails, restoring a positive charge and increasing the affinity of histones for DNA. The degree of acetylation of the core histones reflects an intrinsic balance between the activities of two families of functionally antagonistic enzymes: histone deacetylases (HDACs) and histone acetyltransferases (HATs), which withdraw or incorporate acetyl groups into core histones, respectively.

37In BLV infected cells, the virus is stably integrated apparently in a transcriptionally silent state. Two epigenetic mechanisms, histone acetylation and DNA hypermethylation, correlate with BLV transcriptional repression. The lack of viral expression in a large proportion of infected cells prevents efficient clearance of the virus by the immune system despite the presence of a vigorous immune response. The rationale of a potential therapy consists in inducing viral expression in provirus-carrying cells, thereby exposing infected cells to the host immune response. A key observation for this working model was that increasing the BLV promoter efficiency paradoxically decreases proviral loads. In this context, a therapeutic approach based on the modulation of host epigenetic mechanisms was proposed to treat BLV infection and disease. Different HDAC inhibitors (valproate VPA, trichostatin A TSA, trapoxin TPX) efficiently enhance viral transcription directed by the BLV promoter in vitro. HDAC inhibitors also increase viral expression during ex vivo short-term culture of peripheral blood mononuclear cells (PBMCs) from BLV-infected sheep and cattle. Consistent with its inhibitory activity, VPA induces hyperacetylation of histone H3. VPA treatment, in the absence of any other cytotoxic drug, induced tumor regression in BLV-infected sheep and was efficient for leukemia/lymphoma therapy in the sheep model. However, VPA treatment was inefficient in preventing primary infection and reducing PVL in asymptomatic sheep.

38The efficacy of VPA in BLV-infected cows is presently unknown. However, large scale treatment of BLV infected herds with HDAC inhibitors such as VPA is not justified mainly due to costs. Nevertheless, a treatment with VPA, alone or possibly in combination with antiretroviral drugs (AZT) may still be useful to treat animals with high genetic value.

39This strategy might also hold promise for treating adult T cell leukemia (ATL) or human T-lymphotropic virus-associated myelopathy/tropical spastic paraparesis (HAM/TSP), diseases for which no satisfactory treatment currently exists (see Section 5). It is noteworthy that VPA alone had no effect in simian T lymphotropic virus type 1 (STLV-1) infected monkeys but significantly reduced the PVL when combined with AZT.

Vaccination

40During the last few decades, a series of attempts were performed to develop a vaccine against BLV.

Inactivated Virus Vaccines

41Early studies evaluated preparations of inactivated BLV obtained from persistently infected cell lines (fetal lamb kidney or FLK, LK15, Bat2Cl1 cell lines). Inactivation was obtained by treatment of the virus with different chemical agents (N-acetylethylenimine, 0.1% Triton X-100, 0.1% formalin, formaldehyde, aminomethylated compounds). These inactivated virus vaccines induced a strong specific neutralizing humoral response and partially protected sheep and cattle from low dose viral challenge. Protection roughly correlated with the efficiency of the vaccine to induce a strong neutralizing humoral response. However, vaccinated animals became infected with high challenge doses.

Cell-Derived Vaccines

42Several tentative vaccines were based on cell lysates from: - plasma membranes or cell extracts from BLV tumors.- BLV-infected FLK or SF-28 cells fixed with 3% glutaraldehyde.- ovine virus non-producing NP2 cells synthesizing only the env gene products (gp51 and gp30) and the capsid protein (p24) of BLV.

43- plasma membranes or cell extracts from BLV tumors.

44- BLV-infected FLK or SF-28 cells fixed with 3% glutaraldehyde.

45- ovine virus non-producing NP2 cells synthesizing only the env gene products (gp51 and gp30) and the capsid protein (p24) of BLV.

46Although some of these trials led to partial protection, this strategy has the intrinsic risk of transmitting infection. Therefore, viral subunits were tested for prophylactic immunization.

Viral Subunit Vaccines

47First subunit vaccines were designed with the gp51 surface envelope glycoprotein. The gp51 sequence is indeed well conserved among BLV isolates and carries at least three neutralizing epitopes.

48A subunit vaccine including purified gp51 obtained from culture supernatant of FLK cells inactivated with 0.01% N-acetylethylenimine was immunogenic but did not consistently protect from BLV challenge. Native viral gp51 glycoprotein obtained from FLK cell culture supernatant absorbed in Al(OH)3 also failed to prevent BLV infection in calves. A similar unsuccessful attempt was undertaken with the p24 protein.

49Based on the ability of anti-BLV antibodies in the colostrum to prevent infection, the three aforementioned conventional approaches were focused on inducing an optimal humoral response. Further experimental evidence supporting the role of the humoral response was obtained by successful immunization of naïve sheep with immunoglobulin G from BLV-infected sheep. It should be emphasized that these early vaccination trials included only few animals and were performed over short periods of time. More importantly, the main concern of these experiments was to determine the correct challenge dose encountered under real herd conditions. On the other hand, a major problem of these vaccines was the fast decline of protective antibody titers. Therefore, the significance of these vaccination strategies in herd conditions remains questionable.

50Although important, the humoral response quickly appeared to be insufficient for achieving full protection against BLV infection. Additionally, antibody titers showed fast decline in vaccinated animals, an undesired feature in an effective vaccine. Due to these initial failures in vaccination against BLV, more emphasis was given on the cellular component of the immune response.

Recombinant Vaccinia Virus

51Recombinant vaccinia virus (RVV) was used as a vehicle for immunization against BLV antigens. RVV is a live recombinant vector having a broad host range specificity, the capacity to carry a large amount of genetic information and, most importantly, the ability to elicit both humoral and cell-mediated immunity.

52Preliminary studies with RVV coding for gp51 alone induced neither a humoral response nor protected against BLV in sheep or rabbits. In contrast, RVV harboring the complete env gene (RVV-env) which encodes both gp51 and gp30 glycoproteins produced a neutralizing humoral response in rabbits and sheep. In one study, RVV-env failed to induce detectable neutralizing specific antibodies and conferred only partial protection in naïve sheep after challenge with BLV. However, the BLV proviral loads were decreased in vaccinated sheep. An efficient immune response correlated with type 1 helper T cell proliferation and delayed hypersensitivity with predominant involvement of CD8 cytotoxic T lymphocytes. In two other studies, similar RVV-env vaccines induced a strong humoral and CD4+ T cell response and protected against BLV challenge. Unfortunately, the RVV-env vaccines were inefficient in cows. Remarkably, vaccination with RVV-env in cattle resulted in increasing titers of IgG1 antibodies which might indicate a type 2 response. A RVV vector expressing the gag, pol and env genes also failed to protect cattle after challenge.

Synthetic Peptides

53Short peptides mimicking gp51 B- and T-cell epitopes were tested as potential immunogens. Preliminary analyses with peptides encapsulated in mannan-coated liposomes as delivery system induced significant humoral response and specific Th1 type immunity in mice and sheep models. A different cocktail that included multiple synthetic peptides of Th, Tc and B epitopes failed to induce protection after challenge despite a cell mediated immune response. In the short term, the peptide vaccine partially reduced BLV replication. Finally, a peptide encompassing a minimal 9-mer CTL epitope of gp51 mixed with Freund’s adjuvant induced a cell-mediated response but did not protect most vaccinated sheep against infection.

54Synthetic peptide-based vaccines showed poor performance possibly due to inadequate stereochemical structure and partial epitope presentation.

DNA Vaccines

55DNA vaccines can induce a long-lasting immunity engaging both humoral and cellular components of the immune responses.

56A DNA vaccine containing the env gene under the control of the cytomegalovirus promoter did not induce a vigorous antibody response but stimulated cellular mediated immunity in vaccinated calves. Partial protection was achieved after BLV challenge.

57Another DNA vaccine was designed to express the Tax transactivator protein. The Tax vector suppressed BLV replication in immunized sheep likely through a Th1-cell response involving CTL activity. However, a more recent study showed that a Tax DNA vaccine elicited a cytotoxic response in the early phase of infection but did not prevent later infection. Neither Tax-specific cytotoxic responses nor the proviral loads were predictive of disease outcome.

58As other previously developed immunogens, DNA vaccines were thus disappointing.

Competitive Infection by Attenuated Proviruses

59Failure of “traditional vaccines” was likely due to inadequate or short-lived stimulation of all immunity components. Ideally, the optimal vaccine would therefore contain a large number of viral factors permanently stimulating the immune response. Attenuated derivatives of BLV proviruses meet these requirements.

60Replication-competent BLV proviruses lacking accessory genes and cis-acting LTR sequences were designed and evaluated in rats and rabbits. A first generation of these genetically simpler viruses was constructed by co-injection of independent vectors encoding gag-pol and env genes. These constructs were devoid of tax, rex, R3 and G4 and contained promoter cis-acting regulatory sequences of spleen necrosis virus (SNV). These BLV simpler hybrid derivatives were infectious and induced specific antibodies in a rat model. A second type of virus contained gag, pol and env genes in a single genome under the control of SNV regulatory sequences. This viral vector was competent for replication and induced antibody responses against gag and env structural proteins in rats and rabbits. While PVL were decreased, the viral vector induced protection against viral challenge in a rabbit model.

61Another approach to design attenuated BLV viruses was to delete genes dispensable for infectivity but required for efficient replication. Using an infectious molecular clone, a series of BLV mutant or deletant proviruses were engineered and evaluated for infectivity, replication and pathogenicity in sheep. As predicted, large deletions in the structural genes (gag, pol, and env) abrogated infectivity. Other specific mutations within the genome (the capsid major homology region, the catalytic sites of the integrase) were deleterious. A mutation (nucleotide coordinate 6073) of the immunoreceptor tyrosine-based activation (ITAM) motifs localized in the cytoplasmic tail of the transmembrane gp30 glycoprotein impaired replication but not infectivity. Importantly, the pathogenic potential of the 6073-mutated provirus was significantly reduced but the anti-viral humoral response was preserved.

62Other attenuated BLV proviruses were obtained by deletion of the region expanding from the end of the env gene to the splice acceptor site of the tax/rex mRNA. These mutants lacking R3 and G4 sequences were infectious but replicated at extremely low levels. Similar conclusions were drawn from HTLV mutant proviruses deleted in the ORFs encoding the p12I and p13II/p30II orthologs of R3 and G4. The BLV R3+G4 deletant (pBLVDX) elicited a wild type humoral response but was only very rarely pathogenic in sheep, with a single exception among 20 sheep observed after an unusually long period of latency (7 years).

63To summarize, two types of BLV mutants (pBLV6073 and pBLVDX) were infectious, replicated at low levels but elicited a wild-type like immune response. Importantly, these attenuated viruses conferred long-term protection after challenge with a wild-type strain in sheep and partly in cattle. Indeed, the idea is that these deleted viruses persistently infect cows and interfere with wild-type BLV propagation in herds. The number of BLV-positive cells is also expected to be reduced in the milk of vaccinated cows, impairing the efficiency of BLV transmission to calves. However, calves born from vaccinated cows with these attenuated mutants would be protected through passive immunization. Whether the attenuated strain is transmitted from cow to calf is presently unknown.

64Since attenuated viruses can sometimes be pathogenic, an important issue of these vaccines is biosafety. Pathogenicity can be reduced by combining multiple mutations and deletions that do not affect infectivity but reduce replication. Another risk is conversion of the attenuated vaccine to wild-type. Conceptually, this conversion would only be possible by recombination with another BLV strain. Since the very large majority of the cattle are infected in endemic areas (see Section 3. Epidemiology), the risk is that a fraction of vaccinated animals would become infected with a wild-type virus, a process that occurs anyway with high frequencies. It should also be emphasized that virus recombinations were not observed with attenuated strains even under enforced conditions.

65Trials are currently ongoing to evaluate efficacy and safety of this competitive infection strategy in real herd conditions.

BLV as a Model for HTLV Therapy and Prevention

66BLV and HTLV-1 are closely related deltaretroviruses sharing a similar genomic organization. Although HTLV and BLV infect different target cells (T and B lymphocytes, respectively) and induce distinct hematological disorders, the two viruses persist, spread and transform through similar mechanisms. A shared feature of their replication strategy is transcriptional silencing, a process that allows escape from the host immune response. Both viruses replicate by colonizing new lymphocytes (infectious cycle) as well as by mitosis of the host cell (clonal expansion). A major driving force of viral spread is delivered by the Tax oncoprotein that continuously stimulates proliferation of the infected cell.

67In a perspective of comparative virology, the BLV system is a model of pathogenesis for HTLV (see Table 2). Important outcomes are outlined in this section.

Prevention

68In the absence of an effective vaccine, control of HTLV-1 infection relies on prevention practices aiming to reduce viral transmission.

Interruption or Short-Term Breast-Feeding

69Vertical transmission via postnatal breast-feeding is considered as the most clinically relevant route for HTLV-1 transmission, particularly when practiced over long periods. Cell-associated but not free virus in breast milk appears to be the source of infection. Consistently, the main preventive measure to decrease the risk of mother to child transmission would be to avoid breast feeding. However, this measure is not always easy to adopt due to behavioral, social and societal reasons. For example, refraining from breast-feeding can lead to social stigma or discrimination and explain why women might have difficulties to follow this recommendation. Furthermore, when sanitary conditions are not met, it might be hazardous to use reconstituted milk with contaminated water. Malnutrition being a primary cause of infant death, poverty can also hamper the use of artificial milk. Finally, there is no optimal substitute for natural milk that provides passive immunity, as described earlier for BLV. Therefore, whilst avoiding or limiting breast-feeding is an effective preventive measure in developed countries where safer alternatives exist, it is frequently not adequate for other regions.

70Other strategies also used for BLV include: - limit the duration of breast feeding (to less than 6 months).- inactivate the virus by heating or freezing-thawing.

71- limit the duration of breast feeding (to less than 6 months).

72- inactivate the virus by heating or freezing-thawing.

73Besides milk, pre- and perinatal infection with HTLV-1 occurs less frequently through transfer of cord blood and placenta syncytiotrofoblastic cells. When the PVLs are high, HTLV-1 transmission could be impaired with anti-retroviral drugs such as AZT.

Prevention of Sexual Transmission

74Sexual intercourse is another route of HTLV-1 transmission that occurs more efficiently from men to women. As for HIV, the use of condoms is the optimal measure preventing HTLV-1 transmission.

Prevention of Iatrogenic Transmission

75Although less frequent, iatrogenic transmission of HTLV-1 occurs with low efficacy due to needle sharing by intravenous drug users. In fact, HTLV-2 appears to be more prevalent in this group. Therefore, individuals are strongly recommended to refrain from sharing needles or syringes. Iatrogenic transmission of HTLV-1 also occurs in organ transplanted recipients and long-term hemodialyzed patients.

76Parenteral infection by transfusion of contaminated blood is a potential threat for HTLV-1 transmission. Rates of 5–6% infection were found among blood donors of highly endemic areas, such as the Caribbean Islands and Japan. In medium prevalence areas of South America, these rates are close to 2%. Systematic screening for HTLV-1 in blood banks has become compulsory in many countries. Rapid implementation measures were adopted in highly endemic areas like Japan (1986), Brazil (1993), the Caribbean and the French Isles (1989), as well as in many other developed countries despite low seroprevalence rates (France, USA, Canada, Australia, Netherlands or Denmark). Later on, blood bank screening was applied in developing countries with medium to high seroprevalence among blood donors (Argentina: 2004, Peru: 1999). This policy proved to be successful to decrease HTLV-1 spread by blood transfusion. Unfortunately, official screening programs still lack in other regions with high prevalence (Middle East), further reflecting differences between industrialized and developing countries.

Vaccination Strategies

77Vaccination is probably the best strategy against HTLV-1 infection particularly in endemic areas with high prevalence and in developing economies where other control measures are not implemented. Unfortunately, an efficient, safe and cost-effective vaccine is not available.

78As for BLV, an efficient HTLV-1 vaccine should elicit both humoral response and cell-mediated immunity. Focus was also given to the envelope glycoproteins (gp46 and gp21) and the Tax transactivator. Attempts included: - heat-inactivated HTLV-1;- env glycoproteins produced in Escherichia coli;- DNA vaccines encoding tax or env genes (in combination with RVV-env or RVV-env+gag);- synthetic peptide derived from env gp46 and Tax;- complex chimeric synthetic multivalent peptide vaccines;- recombinant vaccinia viruses expressing gag and/or env proteins.

79- heat-inactivated HTLV-1;

80- env glycoproteins produced in Escherichia coli;

81- DNA vaccines encoding tax or env genes (in combination with RVV-env or RVV-env+gag);

82- synthetic peptide derived from env gp46 and Tax;

83- complex chimeric synthetic multivalent peptide vaccines;

84- recombinant vaccinia viruses expressing gag and/or env proteins.

85Despite interesting preliminary data, none of these vaccines achieved final development mainly due to partial or short-lived response, safety concerns and perhaps also a lack of interest from an industrial partner. No matter the reasons, a vaccine for HTLV or BLV is currently unavailable and will clearly require significant further development.

Epigenetic Modulation Strategy and Gene Activation Therapy

86In the absence of satisfactory therapy and based on preclinical trials performed in animal models, gene activation therapy is an option to improve treatment of HTLV-infected patients. As previously described for BLV (see Section 3.4), this approach is designed to activate viral gene expression with VPA in order to expose virus-positive cells to the host immune response.

87In primary cells freshly isolated from HAM/TSP patients, VPA induced hyperacetylation, triggered viral expression and was proapoptotic. Despite early fluctuations, the PVLs were however not significantly affected after two years of VPA treatment. Importantly, VPA did not alter the anti-viral CTL response and generated only minor side effects. Long term treatment with VPA is thus safe but does not alleviate the condition of HAM/TSP. Further attempts to improve treatment are ongoing. Among these, the combination of VPA and AZT can reduce PVL in STLV-1 infected P. papio. If applicable to humans, this treatment could be rapidly translated into clinical therapy and reduce the risk of developing HAM/TSP.

88For ATLL, the standard treatment is currently a combination of AZT and alpha-interferon. This regimen is partly efficient for the acute form but unfortunately inoperant for lymphoma ATLL. Very recently, an exciting perspective has been presented at the 15th International Conference on Human Retrovirology: VPA combined with AZT and PEG-alpha-interferon induced complete response in 33% of patients associated with molecular remissions (i.e., drop of PVL below threshold levels).

89The epigenetic therapy initially developed in the BLV model may thus provide novel opportunities for HTLV-induced diseases.

Conclusion

90In this review, we outlined the currently available approaches to decrease infection rates of BLV: test and eliminate, segregate or manage (see Table 1). Treatment of BLV leukemia with VPA is not economically sustainable except for animals with high genetic value. In the absence of an efficient vaccine, a new strategy based on competitive infection with deletant viruses is presently being evaluated.

91Although aims and ethical rules are different for HTLV and BLV, there is an interesting parallelism in prevention and therapeutic measures (see Table 2). An effective vaccine against these viruses is still desperately lacking. Both systems have benefited from each other leading to a better understanding of the mechanisms of viral persistence and pathogenesis.

References 331

1.
Leisering A. Hypertrophy der Malpighischen Körperoen der Milz. Berl Vet West Kgr Sachsen. 1871;16:15-16.
Not in our library
2.
Olson C, Miller J, Burny A, Mammerickx M. History and terminology of enzootic bovine leukosis. Enzootic Bovine Leukosis and Bovine Leukemia Virus. 1987;3-14.
Not in our library
3.
Bollinger O. Über Leukämie bei den Haustieren. Virchows Arch. 1874;59:341-349.
Not in our library
4.
Siedamgrotzky O, Hofmeister V. Anleitung zur mikroskopischen und chemischen Diagnostik der Krankheiten der Hausthiere: für Thierärzte und Landwirthe/bearb. 1876;192.
Not in our library
5.
Schöttler F, Schöttler H. Über Ätiologie und Therapie der Aleukämischen Lymphadenose des Rindes. Berl Muench Tierarztl Wochenschr. 1934;50:497-502.
Not in our library
6.
Johnson R, Kaneene JB. Bovine leukaemia virus and enzootic bovine leukosis. Vet Bull. 1992;62:287-312.
Not in our library
7.
Bendixen HJ. Bovine enzootic leukosis. Adv Vet Sci. 1965;10:129-204.
Not in our library
8.
Miller JM, Miller LD, Olson C, Gillette KG. Virus-like particles in phytohemagglutinin-stimulated lymphocyte cultures with reference to bovine lymphosarcoma. J Natl Cancer Inst. 1969;43:1297-1305.
Not in our library
9.
Ferrer JF, Marshak RR, Abt DA, Kenyon SJ. Persistent lymphocytosis in cattle: Its cause, nature and relation to lymphosarcoma. Ann Rech Vet. 1978;9:851-857.
Not in our library
10.
Ferrer JF. Bovine lymphosarcoma. Adv Vet Sci Comp Med. 1980;24:1-68.
Not in our library
11.
Burny A, Bex F, Chantrenne H, Cleuter Y, Dekegel D, Ghysdael J, Kettmann R, Leclercq M, Leunen J, Mammerickx M, et al. Bovine leukemia virus involvement in enzootic bovine leukosis. Adv Cancer Res. 1978;28:251-311.
Not in our library10.1016/s0065-230x(08)60649-1
12.
Burny A, Bruck C, Chantrenne H, Cleuter Y, Dekegel D, Ghysdael J, Kettmann R, Leclercq M, Leunen J, Mammerickx M, Klein G, et al. Bovine leukemia virus: Molecular biology and epidemiology. Viral Oncology. 1980.
Not in our library
13.
Burny A, Bruck C, Cleuter Y, Couez D, Deschamps J, Gregoire D, Ghysdael J, Kettmann R, Mammerickx M, Marbaix G, et al. Bovine leukaemia virus and enzootic bovine leukosis. Onderstepoort J Vet Res. 1985;52:133-144.
Not in our library
14.
Burny A, Cleuter Y, Kettmann R, Mammerickx M, Marbaix G, Portetelle D, van den Broeke A, Willems L, Thomas R. Bovine leukaemia: Facts and hypotheses derived from the study of an infectious cancer. Vet Microbiol. 1988;17:197-218.
Not in our library10.1016/0378-1135(88)90066-1
15.
Kettmann R, Portetelle D, Mammerickx M, Cleuter Y, Dekegel D, Galoux M, Ghysdael J, Burny A, Chantrenne H. Bovine leukemia virus: An exogenous RNA oncogenic virus. Proc Natl Acad Sci U S A. 1976;73:1014-1018.
Not in our library10.1073/pnas.73.4.1014
16.
Kettmann R, Burny A, Levy JA. Bovine Leukemia Virus. The Retroviridae. 1994;3:39-81.
Not in our library
17.
Kenyon SJ, Piper CE. Cellular basis of persistent lymphocytosis in cattle infected with bovine leukemia virus. Infect Immun. 1977;16:891-897.
Not in our library10.1128/iai.16.3.891-897.1977
18.
Ferrer JF, Marshak RR, Abt DA, Kenyon SJ. Relationship between lymphosarcoma and persistent lymphocytosis in cattle: A review. J Am Vet Med Assoc. 1979;175:705-708.
Not in our library
19.
Schwartz I, Levy D. Pathobiology of bovine leukemia virus. Vet Res. 1994;25:521-536.
Not in our library
20.
Kettmann R, Burny A, Cleuter Y, Ghysdael J, Mammerickx M. Distribution of bovine leukemia virus proviral sequences in tissues of bovine, ovine and human origin. Ann Rech Vet. 1978;9:837-844.
Not in our library
21.
Kettmann R, Meunier-Rotival M, Cortadas J, Cuny G, Ghysdael J, Mammerickx M, Burny A, Bernardi G. Integration of bovine leukemia virus DNA in the bovine genome. Proc Natl Acad Sci U S A. 1979;76:4822-4826.
Not in our library10.1073/pnas.76.10.4822
22.
Kettmann R, Meunier-Rotival M, Cortadas J, Cuny G, Ghysdael J, Mammerickx M, Burny A, Bernardi G. Integration site of bovine leukemia virus DNA in the bovine genome [proceedings]. Arch Int Physiol Biochim. 1979;87:818-819.
Not in our library
23.
Kettmann R, Cleuter Y, Mammerickx M, Meunier-Rotival M, Bernardi G, Burny A, Chantrenne H. Genomic integration of bovine leukemia provirus: Comparison of persistent lymphocytosis with lymph node tumor form of enzootic. Proc Natl Acad Sci U S A. 1980;77:2577-2581.
Not in our library10.1073/pnas.77.5.2577
24.
Jacobs RM, Song Z, Poon H, Heeney JL, Taylor JA, Jefferson B, Vernau W, Valli VE. Proviral detection and serology in bovine leukemia virus-exposed normal cattle and cattle with lymphoma. Can J Vet Res. 1992;56:339-348.
Not in our library
25.
Thurmond MC, Burny A, Mammerickx M. Economics of enzootic bovine leukosis. Enzootic bovine leukosis and bovine leukemia virus. 1987;71-86.
Not in our library
26.
Pelzer KD. Economics of bovine leukemia virus infection. Vet Clin North Am Food Anim Pract. 1997;13:129-141.
Not in our library10.1016/s0749-0720(15)30368-6
27.
Trainin Z, Brenner J. The direct and indirect economic impacts of bovine leukemia virus infection on dairy cattle. Isr J Vet Med. 2005;60:90-105.
Not in our library
28.
Johnson R, Gibson CD, Kaneene JB. Bovine leukemia virus: A herd-based control strategy. Prev Vet Med. 1985;3:339-349.
Not in our library
29.
Hopkins SG, DiGiacomo RF. Natural transmission of bovine leukemia virus in dairy and beef cattle. Vet Clin North Am Food Anim Pract. 1997;13:107-128.
Not in our library10.1016/s0749-0720(15)30367-4
30.
Ohshima K, Okada K, Numakunai S, Yoneyama Y, Sato S, Takahashi K. Evidence on horizontal transmission of bovine leukemia virus due to blood-sucking tabanid flies. Nippon Juigaku Zasshi. 1981;43:79-81.
Not in our library10.1292/jvms1939.43.79
31.
Perino LJ, Wright RE, Hoppe KL, Fulton RW. Bovine leukosis virus transmission with mouthparts from Tabanus abactor after interrupted feeding. Am J Vet Res. 1990;51:1167-1169.
Not in our library
32.
Ferrer JF, Piper CE, Abt DA, Marshak RR, Bhatt DM. Natural mode of transmission of the bovine C type leukemia virus (BLV). Bibl Haematol. 1975;43:235-237.
Not in our library10.1159/000399138
33.
Lassauzet ML, Thurmond MC, Johnson WO, Holmberg CA. Factors associated with in utero or periparturient transmission of bovine leukemia virus in calves on a California dairy. Can J Vet Res. 1991;55:264-268.
Not in our library
34.
Piper CE, Ferrer JF, Abt DA, Marshak RR. Postnatal and prenatal transmission of the bovine leukemia virus under natural conditions. J Natl Cancer Inst. 1979;62:165-168.
Not in our library
35.
Agresti A, Ponti W, Rocchi M, Meneveri R, Marozzi A, Cavalleri D, Peri E, Poli G, Ginelli E. Use of polymerase chain reaction to diagnose bovine leukemia virus infection in calves at birth. Am J Vet Res. 1993;54:373-378.
Not in our library
36.
Ferrer JF, Piper CE. Role of colostrum and milk in the natural transmission of the bovine leukemia virus. Cancer Res. 1981;41:4906-4909.
Not in our library
37.
Ferrer JF, Piper CE. An evaluation of the role of milk in the natural transmission of BLV. Ann Rech Vet. 1978;9:803-807.
Not in our library
38.
Ferrer JF, Kenyon SJ, Gupta P. Milk of dairy cows frequently contains a leukemogenic virus. Science. 1981;213:1014-1016.
Not in our library10.1126/science.6267692
39.
Van Der Maaten MJ, Miller JM, Schmerr MJ. Effect of colostral antibody on bovine leukemia virus infection of neonatal calves. Am J Vet Res. 1981;42:1498-1500.
Not in our library
40.
Van der Maaten MJ, Miller JM, Bentvelzen P, Hilgers J, Yohn DS. Susceptibility of cattle to bovine leukemia virus infection by various routes of exposure. Advances in Comparative Leukemia Research. 1978;29-32.
Not in our library
41.
Lassauzet ML, Johnson WO, Thurmond MC, Stevens F. Protection of colostral antibodies against bovine leukemia virus infection in calves on a California dairy. Can J Vet Res. 1989;53:424-430.
Not in our library
42.
Forschner E, Bunger I, Krause HP. Surveillance investigations of brucellosis-, leukosis- and BHV-free cattle herds. ELISA-based bulk milk studies compared to single animal sample studies with traditional test systems. Safety and cost. Dtsch Tierarztl Wochenschr. 1988;95:214-218.
Not in our library
43.
Knapen K, Kerkhofs P, Mammerickx M. Eradication of enzootic bovine leukosis in Belgium: Results of the mass detection on the national cattle population in 1989, 1990 and 1991. Ann Med Vet. 1993;137:197-201.
Not in our library
44.
Nuotio L, Rusanen H, Sihvonen L, Neuvonen E. Eradication of enzootic bovine leukosis from Finland. Prev Vet Med. 2003;59:43-49.
Not in our library10.1016/s0167-5877(03)00057-6
45.
Acaite J, Tamosiunas V, Lukauskas K, Milius J, Pieskus J. The eradication experience of enzootic bovine leukosis from Lithuania. Prev Vet Med. 2007;82:83-89.
Not in our library10.1016/j.prevetmed.2007.05.010
46.
OIE World Animal Health InformationDatabase (WAHID Interface).
Not in our library
47.
NAHIS-AHA Enzootic Bovine Leukosis.
Not in our library
48.
Hayes D, Burton L. Enzootic bovine leucosis eradication scheme. Surveillance. 1998;25:3-5.
Not in our library
49.
NAHMS-USDA Bovine Leukosis Virus on U.S. Dairy Operations. 2007.
Not in our library
50.
Jacobs RM, Pollari FL, McNab WB, Jefferson B. A serological survey of bovine syncytial virus in Ontario: associations with bovine leukemia and immunodeficiency-like viruses, production records, and management practices. Can J Vet Res. 1995;59:271-278.
Not in our library
51.
Van Leeuwen JA, Keefe GP, Tremblay R, Power C, Wichtel JJ. Seroprevalence of infection with Mycobacterium avium subspecies paratuberculosis, bovine leukemia virus, and bovine viral diarrhea virus in maritime Canada dairy cattle. Can Vet J. 2001;42:193-198.
Not in our library
52.
Van Leeuwen JA, Forsythe L, Tiwari A, Chartier R. Seroprevalence of antibodies against bovine leukemia virus, bovine viral diarrhea virus, Mycobacterium avium subspecies paratuberculosis, and Neospora caninum in dairy cattle in Saskatchewan. Can Vet J. 2005;46:56-58.
Not in our library
53.
Van Leeuwen JA, Tiwari A, Plaizier JC, Whiting TL. Seroprevalence of antibodies against bovine leukemia virus, bovine viral diarrhea virus, Mycobacterium avium subspecies partuberculosis, and Neospora caninum in beef and dairy cattle in Manitoba. Can Vet J. 2006;47:783-786.
Not in our library
54.
Scott HM, Sorensen O, Wu JT, Chow EY, Manninen K, Van Leeuwen JA. Seroprevalence of Mycobacterium avium subspecies paratuberculosis, Neospora caninum, Bovine leukemia virus, and Bovine viral diarrhea virus infection among dairy cattle and herds in Alberta and agroecological risk factors associated with seropositivity. Can Vet J. 2006;47:981-991.
Not in our library
55.
Marin C, de López NM, Álvarez L, Lozano O, España W, Castaños H, León A. Epidemiology of bovine leukemia in Venezuela. Ann Rech Vet. 1978;9:743-746.
Not in our library
56.
Islas LA, Inchaurtieta SC, Muñoz PG. Prevalencia de leucosis enzoótica bovina (LEB) en lecherías de las comunas de San Fernando, Chimbarongo y Placilla. Monograf Med Vet. 1990;12:64-70.
Not in our library
57.
Alfonso R, Almansa JE, Barrera JC. Serological prevalence and evaluation of the risk factors of bovine enzootic leukosis in the Bogota savannah and the Ubate and Chiquinquira Valleys, Colombia. Rev Sci Tech. 1998;17:723-732.
Not in our library
58.
Rama G, Moratorio G, Greif G, Obal G, Bianchi S, Tomé L, Carrion F, Meikle A, Pritsch O. Development of a real time PCR assay using SYBR Green chemistry for bovine leukemia virus detection. Retrovirology. 2011;8:A17.
Not in our library
59.
Trono KG, Perez-Filgueira DM, Duffy S, Borca MV, Carrillo C. Seroprevalence of bovine leukemia virus in dairy cattle in Argentina: Comparison of sensitivity and specificity of different detection methods. Vet Microbiol. 2001;83:235-248.
Not in our library10.1016/s0378-1135(01)00420-5
60.
D’Angelino JL, Garcia M, Birgel EH. Epidemiological study of enzootic bovine leukosis in Brazil. Trop Anim Health Prod. 1998;30:13-15.
Not in our library10.1023/a:1005053124518
61.
Abreu VLV, Silva JA, Modena CM, Moreira ÉC, Figueiredo MMN. Prevalência da leucose enzoótica bovina nos estados de Rondônia e Acre. Arq Bras Med Vet Zootec. 1990;42:203-210.
Not in our library
62.
Melo LEH. Leucose enzoótica dos bovinos. Prevalência da infecção em rebanhos leiteiros criados no agreste meridional do estado de Pernambuco. 102.
Not in our library
63.
Melo CB, Oliveira AM, Figueiredo HCP, Leite RC, Lobato ZIP. Prevalência de anticorpos contra Herpesvírus Bovino-1, vírus da Diarréia Bovina a Vírus e vírus da Leucose Enzoótica Bovina em bovinos do Estado de Sergipe, Brasil. Rev Bras Reprod Anim. 1997;21:160-161.
Not in our library
64.
Molnár E, Molnár L, Tavares Dias H, da Silva AOA, Gomes Vale W. Ocorrência da Leucose Enzoótica dos Bovinos no Estado do Pará, Brasil. Pesq Vet Bras. 1999;19:7-11.
Not in our library
65.
Leuzzi Junior LÁ, Fernandes Alfieri A, Alfieri AA. Leucose enzoótica bovina e vírus da leucemia bovina. Semina. 2001;22:211-221.
Not in our library
66.
Cerqueira-Leite R, Portela Lobato ZI, Fernandes Camargos M. Leucose Enzoótica Bovina. Revista CFMFVZ. 2001;24:20-28.
Not in our library
67.
Del Fava C, Pituco EM. Infecção pelo vírus da leucemia bovina (BLV) no Brasil. Biológico. 2004;66:1-8.
Not in our library
68.
Wang CT. Bovine leukemia virus infection in Taiwan: Epizdemiological study. J Vet Med Sci. 1991;53:395-398.
Not in our library10.1292/jvms.53.395
69.
Meas S, Ohashi K, Tum S, Chhin M, Te K, Miura K, Sugimoto C, Onuma M. Seroprevalence of bovine immunodeficiency virus and bovine leukemia virus in draught animals in Cambodia. J Vet Med Sci. 2000;62:779-781.
Not in our library10.1292/jvms.62.779
70.
Murakami K, Kobayashi S, Konishi M, Kameyama K, Yamamoto T, Tsutsui T. The recent prevalence of bovine leukemia virus (BLV) infection among Japanese cattle. Vet Microbiol. 2011;148:84-88.
Not in our library10.1016/j.vetmic.2010.08.001
71.
Suh GH, Lee JC, Lee CY, Hur TY, Son DS, Ahn BS, Kim NC, Lee CG. Establishment of a bovine leukemia virus-free dairy herd in Korea. J Vet Sci. 2005;6:227-230.
Not in our library
72.
Hafez SM, Sharif M, Al-Sukayran A, Dela-Cruz D. Preliminary studies on enzootic bovine leukosis in Saudi dairy farms. Dtsch Tierarztl Wochenschr. 1990;97:61-63.
Not in our library
73.
Meas S, Seto J, Sugimoto C, Bakhsh M, Riaz M, Sato T, Naeem K, Ohashi K, Onuma M. Infection of Bovine Immunodeficiency Virus and Bovine Leukemia Virus in Water Buffalo and Cattle Populations in Pakistan. J Vet Med Sci. 2000;62:329-331.
Not in our library10.1292/jvms.62.329
74.
Pourjafar M, Mahzonieh MR, Heidari Borujeni M. Serological study of bovine viral leukosis in Borujen, Lordegan and Farsan. 338.
Not in our library
75.
Burgu I, Alkan F, Karaoglu T, Bilge-Dagalp S, Can-Sahna K, Gungor B, Demir B. Control and eradication programme of enzootic bovine leucosis (EBL) from selected dairy herds in Turkey. Dtsch Tierarztl Wochenschr. 2005;112:271-274.
Not in our library
76.
Haghparast A, Mohammadi G, Mousavi S, Harapin I, Kos J. Seroepidemiology of bovine leukemia virus (BLV) infection in the north eastern provinces of Iran. 2008;504.
Not in our library
77.
Brujeni GN, Poorbazargani TT, Nadin-Davis S, Tolooie M, Barjesteh N. Bovine immunodeficiency virus and bovine leukemia virus and their mixed infection in Iranian Holstein cattle. J Infect Dev Ctries. 2010;4:576-579.
Not in our library10.3855/jidc.711
78.
Tan MT, Yildirim Y, Erol N, Gungor AB. The seroprevalence of bovine herpes virus type 1 (BHV-1) and bovine leukemia virus (BLV) in selected dairy cattle herds in Aydin province, Turkey. Turk J Vet Anim Sci. 2006;30:353-357.
Not in our library
79.
Ferrer JF. Bovine leukosis: Natural transmission and principles of control. J Am Vet Med Assoc. 1979;175:1281-1286.
Not in our library
80.
DiGiacomo RF. The epidemiology and control of bovine leukemia virus infection. Vet Med. 1992;87:248-257.
Not in our library
81.
Mammerickx M, Cormann A, Burny A, Dekegel D, Portetelle D. Eradication of enzootic bovine leukosis based on the detection of the disease by the GP immunodiffusion test. Ann Rech Vet. 1978;9:885-894.
Not in our library
82.
Straub OC. First results of a new sanitation program concerning the eradication of enzootic bovine leukosis. Ann Rech Vet. 1978;9:895-898.
Not in our library
83.
Maas-Inderwiesen F, Albrecht A, Bause I, Osmers M, Schmidt FW. Effect of leukosis control on the development of enzootic bovine leukosis in Lower Saxony. Dtsch Tierarztl Wochenschr. 1978;85:309-313.
Not in our library
84.
Van Der Maaten MJ, Miller JM. Appraisal of control measures for bovine leukosis. J Am Vet Med Assoc. 1979;175:1287-1290.
Not in our library
85.
Roberts DH, Bushnell S. Herd eradication of enzootic bovine leukosis. Vet Rec. 1982;111:487.
Not in our library10.1136/vr.111.21.487
86.
Schmidt FW, Straub OC. Results and observations of an EBL eradication programme based on AGIDT diagnosis and culling of reactors. 1982;491-497.
Not in our library
87.
Yoshikawa T, Yoshikawa H, Koyama H, Tsubaki S. Preliminary attempts to eradicate infection with bovine leukemia virus from a stock farm in Japan. Nippon Juigaku Zasshi. 1982;44:831-843.
Not in our library10.1292/jvms1939.44.831
88.
Ohshima K, Okada K, Numakunai S, Kayano H, Goto T. An eradication program without economic loss in a herd infected with bovine leukemia virus (BLV). Nippon Juigaku Zasshi. 1988;50:1074-1078.
Not in our library10.1292/jvms1939.50.1074
89.
Wang CT, Onuma M. Attempt to eradicate bovine leukemia virus-infected cattle from herds. Jpn J Vet Res. 1992;40:105-111.
Not in our library
90.
Asfaw Y, Tsuduku S, Konishi M, Murakami K, Tsuboi T, Wu D, Sentsui H. Distribution and superinfection of bovine leukemia virus genotypes in Japan. Arch Virol. 2005;150:493-505.
Not in our library10.1007/s00705-004-0433-5
91.
Monti G, Schrijver R, Beier D. Genetic diversity and spread of Bovine leukaemia virus isolates in Argentine dairy cattle. Arch Virol. 2005;150:443-458.
Not in our library10.1007/s00705-004-0437-1
92.
Shettigara PT, Samagh BS, Lobinowich EM. Control of bovine leukemia virus infection in dairy herds by agar gel immunodiffusion test and segregation of reactors. Can J Vet Res. 1989;53:108-110.
Not in our library
93.
Brenner J, Meiron R, Avraham R, Savir S, Trainin Z. Trial of two methods for the eradication of bovine leucosis virus infection from two large dairy herds in Israel. Isr J Vet Med. 1988;44:168-175.
Not in our library
94.
Kaja RW, Olson C, Rowe RF, Stauffacher RH, Strozinski LL, Hardie AR, Bause I. Establishment of a bovine leukosis virus-free dairy herd. J Am Vet Med Assoc. 1984;184:184-185.
Not in our library
95.
Otachel-Hawranek J. Eradication of enzootic bovine leukosis in dairy cattle from the lower Silesia region. Bull Vet Inst Pulawy. 2007;51:465-469.
Not in our library
96.
OIE. Enzootic bovine leukosis. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. 2008;2:729-738.
Not in our library
97.
Evermann JF, DiGiacomo RF, Ferrer JF, Parish SM. Transmission of bovine leukosis virus by blood inoculation. Am J Vet Res. 1986;47:1885-1887.
Not in our library
98.
Burridge MJ, Thurmond MC, Miller JM, Schmerr MJ, Van Der Maaten MJ. Duration of colostral antibodies to bovine leukemia virus by two serologic tests. Am J Vet Res. 1982;43:1866-1867.
Not in our library
99.
Burridge MJ, Thurmond MC, Miller JM, Schmerr MJ, Van Der Maaten MJ. Fall in antibody titer to bovine leukemia virus in the periparturient period. Can J Comp Med. 1982;46:270-271.
Not in our library
100.
Lew AE, Bock RE, Miles J, Cuttell LB, Steer P, Nadin-Davis SA. Sensitive and specific detection of bovine immunodeficiency virus and bovine syncytial virus by 5′ Taq nuclease assays with fluorescent 3′ minor groove binder-DNA probes. J Virol Methods. 2004;116:1-9.
Not in our library10.1016/j.jviromet.2003.10.006
101.
Jimba M, Takeshima SN, Matoba K, Endoh D, Aida Y. BLV-CoCoMo-qPCR: Quantitation of bovine leukemia virus proviral load using the CoCoMo algorithm. Retrovirology. 2010;7:91.
Not in our library10.1186/1742-4690-7-91
102.
Juliarena MA, Gutierrez SE, Ceriani C. Determination of proviral load in bovine leukemia virus-infected cattle with and without lymphocytosis. Am J Vet Res. 2007;68:1220-1225.
Not in our library10.2460/ajvr.68.11.1220
103.
Esteban EN, Poli M, Poiesz B, Ceriani C, Dube S, Gutierrez S, Dolcini G, Gagliardi R, Perez S, Lützelschwab C, Rechi LJ, et al. Bovine leukemia virus (BLV), proposed control and eradication programs by marker assisted breeding of genetically resistant cattle. Animal Genetics. 2009;107-130.
Not in our library
104.
Gutiérrez G, Alvarez I, Politzki R, Lomónaco M, Dus Santos MJ, Rondelli F, Fondevila N, Trono K. Natural progression of bovine leukemia virus infection in Argentinean dairy cattle. Vet Microbiol. 2011.
Not in our library10.1016/j.vetmic.2011.03.035
105.
Ruppanner R, Behymer DE, Paul S, Miller JM, Theilen GH. A strategy for control of bovine leukemia virus infection: test and corrective management. Can Vet J. 1983;24:192-195.
Not in our library
106.
Sprecher DJ, Pelzer KD, Lessard P. Possible effect of altered management practices on seroprevalence of bovine leukemia virus in heifers of a dairy herd with history of high prevalence of infection. J Am Vet Med Assoc. 1991;199:584-588.
Not in our library
107.
Bacon LD. Influence of the major histocompatibility complex on disease resistance and productivity. Poult Sci. 1987;66:802-11.
Not in our library10.3382/ps.0660802
108.
Gogolin-Ewens KJ, Meeusen EN, Scott PC, Adams TE, Brandon MR. Genetic selection for disease resistance and traits of economic importance in animal production. Rev Sci Tech. 1990;9:865-896.
Not in our library10.20506/rst.9.3.519
109.
Warner CM, Meeker DL, Rothschild MF. Genetic control of immune responsiveness: A review of its use as a tool for selection for disease resistance. J Anim Sci. 1987;64:394-406.
Not in our library10.2527/jas1987.642394x
110.
Lamont SJ. Impact of genetics on disease resistance. Poult Sci. 1998;77:1111-1118.
Not in our library10.1093/ps/77.8.1111
111.
Amorena B, Stone WH. Serologically defined (SD) locus in cattle. Science. 1978;201:159-160.
Not in our library10.1126/science.663645
112.
Spooner RL, Leveziel H, Grosclaude F, Oliver RA, Vaiman M. Evidence for a possible major histocompatibility complex (BLA) in cattle. J Immunogenet. 1978;5:325-346.
Not in our library
113.
Spooner RL, Oliver RA, Sales DI, McCoubrey CM, Millar P, Morgan AG, Amorena B, Bailey E, Bernoco D, Brandon M, et al. Analysis of alloantisera against bovine lymphocytes. Joint report of the 1st International Bovine Lymphocyte Antigen (BoLA) workshop. Anim Blood Groups Biochem Genet. 1979;10:63-86.
Not in our library10.1111/j.1365-2052.1979.tb01009.x
114.
Burridge MJ, Wilcox CJ, Hennemann JM. Influence of genetic factors on the susceptibility of cattle to bovine leukemia virus infection. Eur J Cancer. 1979;15:1395-1400.
Not in our library10.1016/0014-2964(79)90117-8
115.
Lewin HA, Bernoco D. Evidence for BoLA-linked resistance and susceptibility to subclinical progression of bovine leukaemia virus infection. Anim Genet. 1986;17:197-207.
Not in our library10.1111/j.1365-2052.1986.tb03191.x
116.
Stear MJ, Dimmock CK, Newman MJ, Nicholas FW. BoLA antigens are associated with increased frequency of persistent lymphocytosis in bovine leukaemia virus infected cattle and with increased incidence of antibodies to bovine leukaemia virus. Anim Genet. 1988;19:151-158.
Not in our library10.1111/j.1365-2052.1988.tb00800.x
117.
Lewin HA, Wu MC, Stewart JA, Nolan TJ. Association between BoLA and subclinical bovine leukemia virus infection in a herd of Holstein-Friesian cows. Immunogenetics. 1988;27:338-344.
Not in our library10.1007/bf00395129
118.
Bull RW, Lewin HA, Wu MC, Peterbaugh K, Antczak D, Bernoco D, Cwik S, Dam L, Davies C, Dawkins RL, et al. Joint report of the Third International Bovine Lymphocyte Antigen (BoLA) Workshop, Helsinki, Finland, 27 July 1986. Anim Genet. 1989;20:109-132.
Not in our library10.1111/j.1365-2052.1989.tb00849.x
119.
Palmer C, Thurmond M, Picanso J, Brewer AW, Bernoco D. Susceptibility of cattle bovine leukemia virus infection associated with BoLA type. 1987;218-228.
Not in our library
120.
van Eijk MJ, Stewart-Haynes JA, Beever JE, Fernando RL, Lewin HA. Development of persistent lymphocytosis in cattle is closely associated with DRB2. Immunogenetics. 1992;37:64-68.
Not in our library10.1007/bf00223546
121.
Xu A, van Eijk MJ, Park C, Lewin HA. Polymorphism in BoLA-DRB3 exon 2 correlates with resistance to persistent lymphocytosis caused by bovine leukemia virus. J Immunol. 1993;151:6977-6985.
Not in our library
122.
van Eijk MJ, Stewart-Haynes JA, Lewin HA. Extensive polymorphism of the BoLA-DRB3 gene distinguished by PCR-RFLP. Anim Genet. 1992;23:483-496.
Not in our library10.1111/j.1365-2052.1992.tb00168.x
123.
Burke MG, Stone RT, Muggli-Cockett NE. Nucleotide sequence and northern analysis of a bovine major histocompatibility class II DR beta-like cDNA. Anim Genet. 1991;22:343-352.
Not in our library10.1111/j.1365-2052.1991.tb00688.x
124.
Mirsky ML, Olmstead C, Da Y, Lewin HA. Reduced bovine leukaemia virus proviral load in genetically resistant cattle. Anim Genet. 1998;29:245-252.
Not in our library10.1046/j.1365-2052.1998.00320.x
125.
Zanotti M, Poli G, Ponti W, Polli M, Rocchi M, Bolzani E, Longeri M, Russo S, Lewin HA, van Eijk MJ. Association of BoLA class II haplotypes with subclinical progression of bovine leukaemia virus infection in Holstein-Friesian cattle. Anim Genet. 1996;27:337-341.
Not in our library
126.
Udina IG, Karamysheva EE, Turkova SO, Orlova AR, Sulimova GE. Genetic mechanisms of resistance and susceptibility to leukemia in Ayrshire and black pied cattle breeds determined by allelic distribution of gene Bola-DRB3. Genetika. 2003;39:383-396.
Not in our library
127.
Juliarena MA, Poli M, Sala L, Ceriani C, Gutierrez S, Dolcini G, Rodriguez EM, Marino B, Rodriguez-Dubra C, Esteban EN. Association of BLV infection profiles with alleles of the BoLA-DRB3.2 gene. Anim Genet. 2008;39:432-438.
Not in our library10.1111/j.1365-2052.2008.01750.x
128.
Takashima I, Olson C. Histocompatibility antigens in bovine lymphosarcoma. A preliminary study. Ann Rech Vet. 1978;9:821-823.
Not in our library
129.
Aida Y. Influence of host genetic diffences on leukemogenesis induced bovine leukaemia virus. AIDS Res Hum Retroviruses. 2001;17:12.
Not in our library
130.
Nagaoka Y, Kabeya H, Onuma M, Kasai N, Okada K, Aida Y. Ovine MHC class II DRB1 alleles associated with resistance or susceptibility to development of bovine leukemia virus-induced ovine lymphoma. Cancer Res. 1999;59:975-981.
Not in our library
131.
Kabeya H, Ohashi K, Oyunbileg N, Nagaoka Y, Aida Y, Sugimoto C, Yokomizo Y, Onuma M. Up-regulation of tumor necrosis factor alpha mRNA is associated with bovine-leukemia virus (BLV) elimination in the early phase of infection. Vet Immunol Immunopathol. 1999;68:255-265.
Not in our library10.1016/s0165-2427(99)00029-x
132.
Konnai S, Usui T, Ikeda M, Kohara J, Hirata T, Okada K, Ohashi K, Onuma M. Tumor necrosis factor-alpha genetic polymorphism may contribute to progression of bovine leukemia virus-infection. Microbes Infect. 2006;8:2163-2171.
Not in our library10.1016/j.micinf.2006.04.017
133.
Bojarojc-Nosowicz B, Kaczmarczyk E. Somatic cell count and chemical composition of milk in naturally BLV-infected cows with different phenotypes of blood leukocyte acid phosphatase. Archiv für Tierzucht. 2006;49:17-28.
Not in our library
134.
Lewin HA. Disease resistance and immune response genes in cattle: Strategies for their detection and evidence of their existence. J Dairy Sci. 1989;72:1334-1348.
Not in our library10.3168/jds.s0022-0302(89)79241-9
135.
Lander ES, Schork NJ. Genetic dissection of complex traits. Science. 1994;265:2037-2048.
Not in our library10.1126/science.8091226
136.
Kramnik I, Boyartchuk V. Immunity to intracellular pathogens as a complex genetic trait. Curr Opin Microbiol. 2002;5:111-117.
Not in our library10.1016/s1369-5274(02)00295-3
137.
Glass EJ, Baxter R, Leach R, Taylor G, Bishop SC, Axford RFE, Owen J, Nicholas F. Bovine viral diseases: The role of host genetics. Breeding for Disease Resistance in Farm Animals. 2011;88-140.
Not in our library
138.
Williams JL. The use of marker-assisted selection in animal breeding and biotechnology. Rev Sci Tech Off Int Epiz. 2005;24:379-391.
Not in our library
139.
Juliarena MA, Poli M, Ceriani C, Sala L, Rodriguez E, Gutierrez S, Dolcini G, Odeon A, Esteban EN. Antibody response against three widespread bovine viruses is not impaired in Holstein cattle carrying bovine leukocyte antigen DRB3.2 alleles associated with bovine leukemia virus resistance. J Dairy Sci. 2009;92:375-381.
Not in our library10.3168/jds.2008-1143
140.
Ng HH, Bird A. Histone deacetylases: Silencers for hire. Trends Biochem Sci. 2000;25:121-126.
Not in our library10.1016/s0968-0004(00)01551-6
141.
Graessle S, Loidl P, Brosch G. Histone acetylation: Plants and fungi as model systems for the investigation of histone deacetylases. Cell Mol Life Sci. 2001;58:704-720.
Not in our library10.1007/pl00000894
142.
Czermin B, Imhof A. The sounds of silence-histone deacetylation meets histone methylation. Genetica. 2003;117:159-164.
Not in our library10.1023/a:1022927725945
143.
Yoo CB, Jones PA. Epigenetic therapy of cancer: Past, present and future. Nat Rev Drug Discov. 2006;5:37-50.
Not in our library10.1038/nrd1930
144.
Papait R, Monti E, Bonapace IM. Novel approaches on epigenetics. Curr Opin Drug Discov Devel. 2009;12:264-275.
Not in our library
145.
Wanczyk M, Roszczenko K, Marcinkiewicz K, Bojarczuk K, Kowara M, Winiarska M. HDACi-going through the mechanisms. Front Biosci. 2011;16:340-359.
Not in our library10.2741/3691
146.
de Ruijter AJ, van Gennip AH, Caron HN, Kemp S, van Kuilenburg AB. Histone deacetylases (HDACs): Characterization of the classical HDAC family. Biochem J. 2003;370:737-749.
Not in our library10.1042/bj20021321
147.
Kettmann R, Marbaix G, Cleuter Y, Portetelle D, Mammerickx M, Burny A. Genomic integration of bovine leukemia provirus and lack of viral RNA expression in the target cells of cattle with different responses to BLV infection. Leuk Res. 1980;4:509-519.
Not in our library10.1016/0145-2126(80)90062-4
148.
Gupta P, Ferrer JF. Expression of bovine leukemia virus genome is blocked by a nonimmunoglobulin protein in plasma from infected cattle. Science. 1982;215-407.
Not in our library10.1126/science.6276975
149.
Kashmiri SV, Mehdi R, Gupta P, Ferrer JF. Methylation and expression of bovine leukemia proviral DNA. Biochem Biophys Res Commun. 1985;129:126-133.
Not in our library10.1016/0006-291x(85)91412-3
150.
Van den Broeke A, Cleuter Y, Chen G, Portetelle D, Mammerickx M, Zagury D, Fouchard M, Coulombel L, Kettmann R, Burny A. Even transcriptionally competent proviruses are silent in bovine leukemia virus-induced sheep tumor cells. Proc Natl Acad Sci U S A. 1988;85:9263-3267.
Not in our library10.1073/pnas.85.23.9263
151.
Lagarias DM, Radke K. Transcriptional activation of bovine leukemia virus in blood cells from experimentally infected, asymptomatic sheep with latent infections. J Virol. 1989;63:2099-2107.
Not in our library10.1128/jvi.63.5.2099-2107.1989
152.
Merimi M, Klener P, Szynal M, Cleuter Y, Bagnis C, Kerkhofs P, Burny A, Martiat P, Van den Broeke A. Complete suppression of viral gene expression is associated with the onset and progression of lymphoid malignancy: Observations in Bovine Leukemia Virus-infected sheep. Retrovirology. 2007;4:51.
Not in our library10.1186/1742-4690-4-51
153.
Merimi M, Klener P, Szynal M, Cleuter Y, Kerkhofs P, Burny A, Martiat P, Van den Broeke A. Suppression of viral gene expression in bovine leukemia virus-associated B-cell malignancy: interplay of epigenetic modifications leading to chromatin with a repressive histone code. J Virol. 2007;81:5929-5939.
Not in our library10.1128/jvi.02606-06
154.
Kerkhofs P, Adam E, Droogmans L, Portetelle D, Mammerickx M, Burny A, Kettmann R, Willems L. Cellular pathways involved in the ex vivo expression of bovine leukemia virus. J Virol. 1996;70:2170-2177.
Not in our library10.1128/jvi.70.4.2170-2177.1996
155.
Merezak C, Reichert M, Van Lint C, Kerkhofs P, Portetelle D, Willems L, Kettmann R. Inhibition of histone deacetylases induces bovine leukemia virus expression in vitro and in vivo. J Virol. 2002;76:5034-5042.
Not in our library10.1128/jvi.76.10.5034-5042.2002
156.
Tajima S, Tsukamoto M, Aida Y. 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. 2003;77:4423-4430.
Not in our library10.1128/jvi.77.7.4423-4430.2003
157.
Calomme C, Dekoninck A, Nizet S, Adam E, Nguyen TL, Van Den Broeke A, Willems L, Kettmann R, Burny A, Van Lint C. Overlapping CRE and E box motifs in the enhancer sequences of the bovine leukemia virus 5′ long terminal repeat are critical for basal and acetylation-dependent transcriptional activity of the viral promoter: implications for viral latency. J Virol. 2004;78:13848-13864.
Not in our library10.1128/jvi.78.24.13848-13864.2004
158.
Nguyen TL, Calomme C, Wijmeersch G, Nizet S, Veithen E, Portetelle D, de Launoit Y, Burny A, Van Lint C. Deacetylase inhibitors and the viral transactivator TaxBLV synergistically activate bovine leukemia virus gene expression via a cAMP-responsive element-and cAMP-responsive element-binding protein-dependent mechanism. J Biol Chem. 2004;279:35025-35036.
Not in our library10.1074/jbc.m404081200
159.
Achachi A, Florins A, Gillet N, Debacq C, Urbain P, Foutsop GM, Vandermeers F, Jasik A, Reichert M, Kerkhofs P, et al. Valproate activates bovine leukemia virus gene expression, triggers apoptosis, and induces leukemia/lymphoma regression in vivo. Proc Natl Acad Sci U S A. 2005;102:10309-10314.
Not in our library10.1073/pnas.0504248102
160.
Pierard V, Guiguen A, Colin L, Wijmeersch G, Vanhulle C, Van Driessche B, Dekoninck A, Blazkova J, Cardona C, Merimi M, et al. DNA cytosine methylation in the bovine leukemia virus promoter is associated with latency in a lymphoma-derived B-cell line: potential involvement of direct inhibition of cAMP-responsive element (CRE)-binding protein/CRE modulator/activation transcription factor binding. J Biol Chem. 2010;285:19434-19449.
Not in our library10.1074/jbc.m110.107607
161.
Merezak C, Pierreux C, Adam E, Lemaigre F, Rousseau GG, Calomme C, Van Lint C, Christophe D, Kerkhofs P, Burny A, et al. Suboptimal enhancer sequences are required for efficient bovine leukemia virus propagation in vivo: Implications for viral latency. J Virol. 2001;75:6977-6988.
Not in our library10.1128/jvi.75.15.6977-6988.2001
162.
Mechanisms of leukemogenesis induced by bovine leukemia virus: prospects for novel anti-retroviral therapies in human · 2007
No notice
163.
Lezin A, Gillet N, Olindo S, Signate A, Grandvaux N, Verlaeten O, Belrose G, de Carvalho Bittencourt M, Hiscott J, Asquith B, et al. Histone deacetylase mediated transcriptional activation reduces proviral loads in HTLV-1 associated myelopathy/tropical spastic paraparesis patients. Blood. 2007;110:3722-3728.
Not in our library10.1182/blood-2007-04-085076
164.
Bouzar AB, Boxus M, Defoiche J, Berchem G, Macallan D, Pettengell R, Willis F, Burny A, Lagneaux L, Bron D, et al. Valproate synergizes with purine nucleoside analogues to induce apoptosis of B-chronic lymphocytic leukaemia cells. Br J Haematol. 2009;144:41-52.
Not in our library10.1111/j.1365-2141.2008.07426.x
165.
Ramos JC, Toomey N, Diaz L, Ruiz P, Barber G, Harrington W. Targeting HTLV-I latency in Adult T-cell Leukemia/Lymphoma. Retrovirology. 2011;8:A48.
Not in our library
166.
Olindo S, Belrose G, Gillet N, Rodríguez SM, Asquith B, Bangham C, Signaté A, Smadja D, Lezin A, Césaire R, et al. Safety of long-term treatment of HAM/TSP patients with valproic acid. Blood. 2011.
Not in our library10.1182/blood-2011-04-349910
167.
Afonso PV, Mekaouche M, Mortreux F, Toulza F, Moriceau A, Wattel E, Gessain A, Bangham CR, Dubreuil G, Plumelle Y, et al. Highly active antiretroviral treatment against STLV-1 infection combining reverse transcriptase and HDAC inhibitors. Blood. 2010;116:3802-3808.
Not in our library10.1182/blood-2010-02-270751
168.
Willems L, Portetelle D, Kerkhofs P, Chen G, Burny A, Mammerickx M, Kettmann R. In vivo transfection of bovine leukemia provirus into sheep. Virology. 1992;189:775-7.
Not in our library10.1016/0042-6822(92)90604-n
169.
Willems L, Kettmann R, Dequiedt F, Portetelle D, Voneche V, Cornil I, Kerkhofs P, Burny A, Mammerickx M. In vivo infection of sheep by bovine leukemia virus mutants. J Virol. 1993;67:4078-4085.
Not in our library10.1128/jvi.67.7.4078-4085.1993
170.
Willems L, Burny A, Collete D, Dangoisse O, Dequiedt F, Gatot JS, Kerkhofs P, Lefebvre L, Merezak C, Peremans T, et al. Genetic determinants of bovine leukemia virus pathogenesis. AIDS Res Hum Retroviruses. 2000;16:1787-1795.
Not in our library10.1089/08892220050193326
171.
Miller JM, Van Der Maaten MJ. Evaluation of an inactivated bovine leukemia virus preparation as an immunogen in cattle. Ann Rech Vet. 1978;9:871-877.
Not in our library
172.
Patrascu IV, Coman S, Sandu I, Stiube P, Munteanu I, Coman T, Ionescu M, Popescu D, Mihailescu D. Specific protection against bovine leukemia virus infection conferred on cattle by the Romanian inactivated vaccine BL-VACC-RO. Virologie. 1980;31:95-102.
Not in our library
173.
Parfanovich MI, Zhdanov VM, Lazarenko AA, Nomm EM, Simovart Yu A, Parakin VK, Lemesh VM. The possibility of specific protection against bovine leukaemia virus infection and bovine leukaemia with inactivated BLV. Br Vet J. 1983;139:137-146.
Not in our library10.1016/s0007-1935(17)30537-7
174.
Miller JM, Van der Maaten MJ, Schmerr MJ. Vaccination of cattle with binary ethylenimine-treated bovine leukemia virus. Am J Vet Res. 1983;44:64-67.
Not in our library
175.
Fukuyama S, Kodama K, Hirahara T, Nakajima N, Takamura K, Sasaki O, Imanishi J. Protection against bovine leukemia virus infection by use of inactivated vaccines in cattle. J Vet Med Sci. 1993;55:99-106.
Not in our library10.1292/jvms.55.99
176.
Ristau E, Beier D, Wittmann W. The course of infection with bovine leukosis virus (BLV) in calves after the administration of cell extract from lymph node tumors of BLV-infected cattle. Arch Exp Veterinarmed. 1987;41:323-331.
Not in our library
177.
Ristau E, Beier D, Wittmann W, Klima F. Protection of sheep against infection with bovine leukemia virus by vaccination with tumor cells or tumor cell preparations from lymph nodes of leukemic cattle. Arch Exp Veterinarmed. 1987;41:185-196.
Not in our library
178.
Onuma M, Hodatsu T, Yamamoto S, Higashihara M, Masu S, Mikami T, Izawa H. Protection by vaccination against bovine leukemia virus infection in sheep. Am J Vet Res. 1984;45:1212-1215.
Not in our library
179.
Altaner C, Altanerova V, Ban J, Janik V, Volejnicek V, Frajs Z, Cerny L. Cell-derived vaccine against bovine leukaemia virus infection. Zentralbl Veterinarmed B. 1988;35:736-746.
Not in our library10.1111/j.1439-0450.1988.tb00553.x
180.
Altaner C, Ban J, Altanerova V, Janik V. Protective vaccination against bovine leukaemia virus infection by means of cell-derived vaccine. Vaccine. 1991;9:889-895.
Not in our library10.1016/0264-410x(91)90009-u
181.
Miller JM, Van der Maaten MJ, Schmerr MJF, Straub OC. Vaccination with glycosidase-treated glycoprotein antigen does not prevent bovine leukosis virus infection in cattle. 1984.
Not in our library
182.
Burkhardt H, Rosenthal S, Wittmann W, Starick E, Scholz D, Rosenthal HA, Kluge KH. Immunization of young cattle with gp51 of the bovine leukosis virus and the subsequent experimental infection. Arch Exp Veterinarmed. 1989;43:933-942.
Not in our library
183.
Merza M, Sober J, Sundquist B, Toots I, Morein B. Characterization of purified gp 51 from bovine leukemia virus integrated into iscom. Physicochemical properties and serum antibody response to the integrated gp51. Arch Virol. 1991;120:219-231.
Not in our library10.1007/bf01310477
184.
Kabeya H, Ohashi K, Ohishi K, Sugimoto C, Amanuma H, Onuma M. An effective peptide vaccine to eliminate bovine leukaemia virus (BLV) infected cells in carrier sheep. Vaccine. 1996;14:1118-1122.
Not in our library10.1016/0264-410x(96)00047-3
185.
Mamoun RZ, Morisson M, Rebeyrotte N, Busetta B, Couez D, Kettmann R, Hospital M, Guillemain B. Sequence variability of bovine leukemia virus env gene and its relevance to the structure and antigenicity of the glycoproteins. J Virol. 1990;64:4180-4188.
Not in our library10.1128/jvi.64.9.4180-4188.1990
186.
Willems L, Thienpont E, Kerkhofs P, Burny A, Mammerickx M, Kettmann R. Bovine leukemia virus, an animal model for the study of intrastrain variability. J Virol. 1993;67:1086-1089.
Not in our library10.1128/jvi.67.2.1086-1089.1993
187.
Fechner H, Blankenstein P, Looman AC, Elwert J, Geue L, Albrecht C, Kurg A, Beier D, Marquardt O, Ebner D. Provirus variants of the bovine leukemia virus and their relation to the serological status of naturally infected cattle. Virology. 1997;237:261-269.
Not in our library10.1006/viro.1997.8784
188.
Beier D, Blankenstein P, Marquardt O, Kuzmak J. Identification of different BLV provirus isolates by PCR, RFLPA and DNA sequencing. Berl Munch Tierarztl Wochenschr. 2001;114:252-256.
Not in our library
189.
Camargos MF, Pereda A, Stancek D, Rocha MA, dos Reis JK, Greiser-Wilke I, Leite RC. Molecular characterization of the env gene from Brazilian field isolates of Bovine leukemia virus. Virus Genes. 2007;34:343-350.
Not in our library10.1007/s11262-006-0011-x
190.
Licursi M, Inoshima Y, Wu D, Yokoyama T, González ET, Sentsui H. Provirus variants of bovine leukemia virus in naturally infected cattle from Argentina and Japan. Vet Microbiol. 2003;96:17-23.
Not in our library10.1016/s0378-1135(03)00202-5
191.
Felmer R, Munoz G, Zuniga J, Recabal M. Molecular analysis of a 444 bp fragment of the bovine leukaemia virus gp51 env gene reveals a high frequency of non-silent point mutations and suggests the presence of two subgroups of BLV in Chile. Vet Microbiol. 2005;108:39-47.
Not in our library10.1016/j.vetmic.2005.04.005
192.
Hemmatzadeh F. Sequencing and phylogenetic analysis of gp51 gene of bovine leukaemia virus in Iranian isolates. Vet Res Commun. 2007;31:783-789.
Not in our library10.1007/s11259-007-0012-9
193.
Zhao X, Buehring GC. Natural genetic variations in bovine leukemia virus envelope gene: possible effects of selection and escape. Virology. 2007;366:150-165.
Not in our library10.1016/j.virol.2007.03.058
194.
Rodríguez SM, Golemba MD, Campos RH, Trono K, Jones LR. Bovine leukemia virus can be classified into seven genotypes: evidence for the existence of two novel clades. J Gen Virol. 2009;90:2788-2797.
Not in our library10.1099/vir.0.011791-0
195.
Moratorio G, Obal G, Dubra A, Correa A, Bianchi S, Buschiazzo A, Cristina J, Pritsch O. Phylogenetic analysis of bovine leukemia viruses isolated in South America reveals diversification in seven distinct genotypes. Arch Virol. 2010;155:481-489.
Not in our library10.1007/s00705-010-0606-3
196.
Matsumura K, Inoue E, Osawa Y, Okazaki K. Molecular epidemiology of bovine leukemia virus associated with enzootic bovine leukosis in Japan. Virus Res. 2011;155:343-348.
Not in our library10.1016/j.virusres.2010.11.005
197.
Bruck C, Mathot S, Portetelle D, Berte C, Franssen JD, Herion P, Burny A. Monoclonal antibodies define eight independent antigenic regions on the bovine leukemia virus (BLV) envelope glycoprotein gp51. Virology. 1982;122:342-352.
Not in our library10.1016/0042-6822(82)90234-3
198.
Bruck C, Portetelle D, Burny A, Zavada J. Topographical analysis by monoclonal antibodies of BLV-gp51 epitopes involved in viral functions. Virology. 1982;122:353-362.
Not in our library10.1016/0042-6822(82)90235-5
199.
Bruck C, Portetelle D, Mammerickx M, Mathot S, Burny A. Epitopes of bovine leukemia virus glycoprotein gp51 recognized by sera of infected cattle and sheep. Leuk Res. 1984;8:315-321.
Not in our library10.1016/0145-2126(84)90070-5
200.
Bruck C, Rensonnet N, Portetelle D, Cleuter Y, Mammerickx M, Burny A, Mamoun R, Guillemain B, van der Maaten MJ, Ghysdael J. Biologically active epitopes of bovine leukemia virus glycoprotein gp51: Their dependence on protein glycosylation and genetic variability. Virology. 1984;136:20-31.
Not in our library10.1016/0042-6822(84)90244-7
201.
Portetelle D, Bruck C, Mammerickx M, Burny A. In animals infected by bovine leukemia virus (BLV) antibodies to envelope glycoprotein gp51 are directed against the carbohydrate moiety. Virology. 1980;105:223-233.
Not in our library10.1016/0042-6822(80)90169-5
202.
Portetelle D, Couez D, Bruck C, Kettmann R, Mammerickx M, Van der Maaten M, Brasseur R, Burny A. Antigenic variants of bovine leukemia virus (BLV) are defined by amino acid substitutions in the NH2 part of the envelope glycoprotein gp51. Virology. 1989;169-33.
Not in our library10.1016/0042-6822(89)90037-8
203.
Portetelle D, Dandoy C, Burny A, Zavada J, Siakkou H, Gras-Masse H, Drobecq H, Tartar A. Synthetic peptides approach to identification of epitopes on bovine leukemia virus envelope glycoprotein gp51. Virology. 1989;169:34-41.
Not in our library10.1016/0042-6822(89)90038-x
204.
Thurmond MC, Carter RL, Puhr DM, Burridge MJ. Decay of colostral antibodies to bovine leukemia virus with application to detection of calfhood infection. Am J Vet Res. 1982;43:1152-1155.
Not in our library
205.
Jacobsen KL, Bull RW, Miller JM, Herdt TH, Kaneene JB. Transmission of bovine leukemia virus: prevalence of antibodies in precolostral calves. Prev Vet Med. 1983;1:265-272.
Not in our library10.1016/0167-5877(83)90031-4
206.
Lassauzet ML, Johnson WO, Thurmond MC, Stevens F. Factors associated with decay of colostral antibodies to bovine leukemia virus infection. Prev Vet Med. 1990;9:45-58.
Not in our library
207.
Nagy DW, Tyler JW, Kleiboeker SB. Decreased periparturient transmission of bovine leukosis virus in colostrum-fed calves. J Vet Intern Med. 2007;21:1104-1107.
Not in our library10.1892/0891-6640(2007)21[1104:dptobl]2.0.co;2
208.
Kono Y, Arai K, Sentsui H, Matsukawa S, Itohara S. Protection against bovine leukemia virus infection in sheep by active and passive immunization. Nippon Juigaku Zasshi. 1986;48:117-125.
Not in our library10.1292/jvms1939.48.117
209.
Portetelle D, Limbach K, Burny A, Mammerickx M, Desmettre P, Riviere M, Zavada J, Paoletti E. Recombinant vaccinia virus expression of the bovine leukaemia virus envelope gene and protection of immunized sheep against infection. Vaccine. 1991;9:194-200.
Not in our library10.1016/0264-410x(91)90153-w
210.
Gatei MH, Naif HM, Kumar S, Boyle DB, Daniel RC, Good MF, Lavin MF. Protection of sheep against bovine leukemia virus (BLV) infection by vaccination with recombinant vaccinia viruses expressing BLV envelope glycoproteins: Correlation of protection with CD4 T-cell response to gp51 peptide 51–70. J Virol. 1993;67:1803-1810.
Not in our library10.1128/jvi.67.4.1803-1810.1993
211.
Burny A. Comparative approach to retroviral vaccines. AIDS Res Hum Retroviruses. 1996;12:389-392.
Not in our library10.1089/aid.1996.12.389
212.
Kumar S, Andrew ME, Boyle DB, Brandon RB, Lavin MF, Daniel RC. Expression of bovine leukaemia virus envelope gene by recombinant vaccinia viruses. Virus Res. 1990;17:131-142.
Not in our library10.1016/0168-1702(90)90074-l
213.
Ohishi K, Suzuki H, Maruyama T, Yamamoto T, Funahashi S, Miki K, Ikawa Y, Sugimoto M. Induction of neutralizing antibodies against bovine leukosis virus in rabbits by vaccination with recombinant vaccinia virus expressing bovine leukosis virus envelope glycoprotein. Am J Vet Res. 1990;51:1170-1173.
Not in our library
214.
Ohishi K, Suzuki H, Yamamoto T, Maruyama T, Miki K, Ikawa Y, Numakunai S, Okada K, Ohshima K, Sugimoto M. Protective immunity against bovine leukaemia virus (BLV) induced in carrier sheep by inoculation with a vaccinia virus-BLV env recombinant: association with cell-mediated immunity. J Gen Virol. 1991;72:1887-1892.
Not in our library10.1099/0022-1317-72-8-1887
215.
Okada K, Ikeyama S, Ohishi K, Suzuki H, Sugimoto M, Numakunai S, Chiba T, Murakami K, Davis WC, Ohshima K, et al. Involvement of CD8+ T cells in delayed-type hypersensitivity responses against bovine leukemia virus (BLV) induced in sheep vaccinated with recombinant vaccinia virus expressing BLV envelope glycoprotein. Vet Pathol. 1993;30:104-110.
Not in our library10.1177/030098589303000202
216.
Ohishi K, Ikawa Y. T cell-mediated destruction of bovine leukemia virus-infected peripheral lymphocytes by bovine leukemia virus env-vaccinia recombinant vaccine. AIDS Res Hum Retroviruses. 1996;12:393-398.
Not in our library10.1089/aid.1996.12.393
217.
Ohishi K, Suzuki H, Yasutomi Y, Onuma M, Okada K, Numakunai S, Ohshima K, Ikawa Y, Sugimoto M. Augmentation of bovine leukemia virus (BLV)-specific lymphocyte proliferation responses in ruminants by inoculation with BLV envrecombinant vaccinia virus: their role in the suppression of BLV replication. Microbiol Immunol. 1992;36:1317-1323.
Not in our library10.1111/j.1348-0421.1992.tb02133.x
218.
Cherney TM, Schultz RD. Viral status and antibody response in cattle inoculated with recombinant bovine leukemia virus-vaccinia virus vaccines after challenge exposure with bovine leukemia virus-infected lymphocytes. Am J Vet Res. 1996;57:812-818.
Not in our library
219.
Von Beust BR, Brown WC, Estes DM, Zarlenga DS, McElwain TF, Palmer GH. Development and in vitro characterization of recombinant vaccinia viruses expressing bovine leukemia virus gp51 in combination with bovine IL4 or IL12. Vaccine. 1999;17:384-395.
Not in our library10.1016/s0264-410x(98)00208-4
220.
Callebaut I, Mornon JP, Burny A, Portetelle D. The bovine leukemia virus (BLV) envelope glycoprotein gp51 as a general model for the design of a subunit vaccine against retroviral infection: Mapping of functional sites through immunological and structural data. Leukemia. 1994;8:218-221.
Not in our library
221.
Ohishi K, Kabeya H, Amanuma H, Onuma M. Induction of bovine leukaemia virus Env-specific Th-1 type immunity in mice by vaccination with short synthesized peptide-liposome. Vaccine. 1996;14:1143-1148.
Not in our library10.1016/0264-410x(96)00033-3
222.
Ohishi K, Kabeya H, Amanuma H, Onuma M. Peptide-based bovine leukemia virus (BLV) vaccine that induces BLV-Env specific Th-1 type immunity. Leukemia. 1997;11:223-226.
Not in our library
223.
Okada K, Sonoda K, Koyama M, Yin S, Ikeda M, Goryo M, Chen SL, Kabeya H, Ohishi K, Onuma M. Delayed-type hypersensitivity in sheep induced by synthetic peptides of bovine leukemia virus encapsulated in mannan-coated liposome. J Vet Med Sci. 2003;65:515-518.
Not in our library10.1292/jvms.65.515
224.
Hislop AD, Good MF, Mateo L, Gardner J, Gatei MH, Daniel RC, Meyers BV, Lavin MF, Suhrbier A. Vaccine-induced cytotoxic T lymphocytes protect against retroviral challenge. Nat Med. 1998;4:1193-1196.
Not in our library10.1038/2690
225.
Mateo L, Gardner J, Suhrbier A. Delayed emergence of bovine leukemia virus after vaccination with a protective cytotoxic T cell-based vaccine. AIDS Res Hum Retroviruses. 2001;17:1447-1453.
Not in our library10.1089/088922201753197114
226.
Brillowska A, Dabrowski S, Rulka J, Kubis P, Buzala E, Kur J. Protection of cattle against bovine leukemia virus (BLV) infection could be attained by DNA vaccination. Acta Biochim Pol. 1999;46:971-976.
Not in our library
227.
Usui T, Konnai S, Tajima S, Watarai S, Aida Y, Ohashi K, Onuma M. Protective effects of vaccination with bovine leukemia virus (BLV) Tax DNA against BLV infection in sheep. J Vet Med Sci. 2003;65:1201-1205.
Not in our library10.1292/jvms.65.1201
228.
Sakakibara N, Kabeya H, Ohashi K, Sugimoto C, Onuma M. Epitope mapping of bovine leukemia virus transactivator protein tax. J Vet Med Sci. 1998;60:599-605.
Not in our library10.1292/jvms.60.599
229.
Van den Broeke A, Oumouna M, Beskorwayne T, Szynal M, Cleuter Y, Babiuk S, Bagnis C, Martiat P, Burny A, Griebel P. Cytotoxic responses to BLV tax oncoprotein do not prevent leukemogenesis in sheep. Leuk Res. 2010;34:1663-1669.
Not in our library10.1016/j.leukres.2010.06.003
230.
Boris-Lawrie K, Temin HM. Genetically simpler bovine leukemia virus derivatives can replicate independently of Tax and Rex. J Virol. 1995;69:1920-1924.
Not in our library10.1128/jvi.69.3.1920-1924.1995
231.
Boris-Lawrie K, Altanerova V, Altaner C, Kucerova L, Temin HM. In vivo study of genetically simplified bovine leukemia virus derivatives that lack tax and rex. J Virol. 1997;71:1514-1520.
Not in our library10.1128/jvi.71.2.1514-1520.1997
232.
Kucerova L, Altanerova V, Altaner C, Boris-Lawrie K. Bovine leukemia virus structural gene vectors are immunogenic and lack pathogenicity in a rabbit model. J Virol. 1999;73:8160-8166.
Not in our library10.1128/jvi.73.10.8160-8166.1999
233.
Kerkhofs P, Gatot JS, Knapen K, Mammerickx M, Burny A, Portetelle D, Willems L, Kettmann R. Long-term protection against bovine leukaemia virus replication in cattle and sheep. J Gen Virol. 2000;81:957-963.
Not in our library10.1099/0022-1317-81-4-957
234.
Reichert M, Cantor GH, Willems L, Kettmann R. Protective effects of a live attenuated bovine leukaemia virus vaccine with deletion in the R3 and G4 genes. J Gen Virol. 2000;81:965-969.
Not in our library10.1099/0022-1317-81-4-965
235.
Altanerova V, Holicova D, Kucerova L, Altaner C, Lairmore MD, Boris-Lawrie K. Long-term infection with retroviral structural gene vector provides protection against bovine leukemia virus disease in rabbits. Virology. 2004;329:434-439.
Not in our library10.1016/j.virol.2004.09.001
236.
Debacq C, Sanchez Alcaraz MT, Mortreux F, Kerkhofs P, Kettmann R, Willems L. Reduced proviral loads during primo-infection of sheep by Bovine Leukemia virus attenuated mutants. Retrovirology. 2004;1:31.
Not in our library10.1186/1742-4690-1-31
237.
Florins A, Gillet N, Boxus M, Kerkhofs P, Kettmann R, Willems L. Even attenuated bovine leukemia virus proviruses can be pathogenic in sheep. J Virol. 2007;81:10195-10200.
Not in our library10.1128/jvi.01058-07
238.
Willems L, Kerkhofs P, Attenelle L, Burny A, Portetelle D, Kettmann R. The major homology region of bovine leukaemia virus p24gag is required for virus infectivity in vivo. J Gen Virol. 1997;78:637-640.
Not in our library10.1099/0022-1317-78-3-637
239.
Willems L, Gatot JS, Mammerickx M, Portetelle D, Burny A, Kerkhofs P, Kettmann R. 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. 1995;69:4137-4141.
Not in our library10.1128/jvi.69.7.4137-4141.1995
240.
Willems L, Kerkhofs P, Dequiedt F, Portetelle D, Mammerickx M, Burny A, Kettmann R. Attenuation of bovine leukemia virus by deletion of R3 and G4 open reading frames. Proc Natl Acad Sci U S A. 1994;91:11532-11536.
Not in our library10.1073/pnas.91.24.11532
241.
Bartoe JT, Albrecht B, Collins ND, Robek MD, Ratner L, Green PL, Lairmore MD. Functional role of pX open reading frame II of human T-lymphotropic virus type 1 in maintenance of viral loads in vivo. J Virol. 2000;74:1094-1100.
Not in our library10.1128/jvi.74.3.1094-1100.2000
242.
Collins ND, Newbound GC, Albrecht B, Beard JL, Ratner L, Lairmore MD. Selective ablation of human T-cell lymphotropic virus type 1 p12I reduces viral infectivity in vivo. Blood. 1998;91:4701-4707.
Not in our library
243.
Silverman LR, Phipps AJ, Montgomery A, Ratner L, Lairmore MD. Human T-cell lymphotropic virus type 1 open reading frame II-encoded p30II is required for in vivo replication: evidence of in vivo reversion. J Virol. 2004;78:3837-3845.
Not in our library10.1128/jvi.78.8.3837-3845.2004
244.
Seiki M, Hattori S, Hirayama Y, Yoshida M. Human adult T-cell leukemia virus: complete nucleotide sequence of the provirus genome integrated in leukemia cell DNA. Proc Natl Acad Sci U S A. 1983;80:3618-3622.
Not in our library10.1073/pnas.80.12.3618
245.
Sagata N, Yasunaga T, Tsuzuku-Kawamura J, Ohishi K, Ogawa Y, Ikawa Y. Complete nucleotide sequence of the genome of bovine leukemia virus: its evolutionary relationship to other retroviruses. Proc Natl Acad Sci U S A. 1985;82:677-681.
Not in our library10.1073/pnas.82.3.677
246.
Matsuoka M, Jeang KT. Human T-cell leukaemia virus type 1 (HTLV-1) infectivity and cellular transformation. Nat Rev Cancer. 2007;7:270-280.
Not in our library10.1038/nrc2111
247.
Silencing of human T-cell leukemia virus type I gene transcription by epigenetic mechanisms · 2005
No notice
248.
Wattel E, Cavrois M, Gessain A, Wain-Hobson S. Clonal expansion of infected cells: a way of life for HTLV-I. J Acquir Immune Defic Syndr Hum Retrovirol. 1996;13:92-99.
Not in our library10.1097/00042560-199600001-00016
249.
Mortreux F, Leclercq I, Gabet AS, Leroy A, Westhof E, Gessain A, Wain-Hobson S, Wattel E. Somatic mutation in human T-cell leukemia virus type 1 provirus and flanking cellular sequences during clonal expansion in vivo. J Natl Cancer Inst. 2001;93:367-377.
Not in our library10.1093/jnci/93.5.367
250.
Sibon D, Gabet AS, Zandecki M, Pinatel C, Thete J, Delfau-Larue MH, Rabaaoui S, Gessain A, Gout O, Jacobson S, Mortreux F, Wattel E. HTLV-1 propels untransformed CD4 lymphocytes into the cell cycle while protecting CD8 cells from death. J Clin Invest. 2006;116:974-983.
Not in our library10.1172/jci27198
251.
Willems L, Gegonne A, Chen G, Burny A, Kettmann R, Ghysdael J. The bovine leukemia virus p34 is a transactivator protein. EMBO J. 1987;6:3385-3389.
Not in our library10.1002/j.1460-2075.1987.tb02661.x
252.
Willems L, Heremans H, Chen G, Portetelle D, Billiau A, Burny A, Kettmann R. Cooperation between bovine leukaemia virus transactivator protein and Haras oncogene product in cellular transformation. EMBO J. 1990;9:1577-1581.
Not in our library10.1002/j.1460-2075.1990.tb08277.x
253.
Burny A, Cleuter Y, Couez D, Dandoy C, Gras-Masse H, Gregoire D, Kettmann R, Mammerickx M, Marbaix G, Portetelle D, et al. Bovine leukemia Virus (BLV) as a model system for human lymphotropic virus (HTLV) and HTLV as a model for BLV. 336-348.
Not in our library
254.
Willems L, Burny A, Dangoisse O, Dequiedt F, Gatot JS, Kerkhofs P, Lefebvre L, Merezak C, Portatelle D, Twizere JC, Kettmann R. Bovine leukemia virus as a model for the human T-cell leukemia. Curr Top Virol. 1999;16:1787-1795.
Not in our library10.1089/08892220050193326
255.
Willems L. Bovine leukemia virus as a model for studying human leukemias. Bull Mem Acad R Med Belg. 2004;159:473-478.
Not in our library
256.
Lezin A, Olindo S, Belrose G, Signate A, Cesaire R, Smadja D, Macallan D, Asquith B, Bangham C, Bouzar A, et al. Gene activation therapy: from the BLV model to HAM/TSP patients. Front Biosci. 2009;1:205-215.
Not in our library10.2741/s20
257.
Boxus M, Willems L. Mechanisms of HTLV-1 persistence and transformation. Br J Cancer. 2009;101:1497-1501.
Not in our library10.1038/sj.bjc.6605345
258.
Diamond GA, Denton TA. Alternative perspectives on the biased foundations of medical technology assessment. Ann Intern Med. 1993;118:455-464.
Not in our library10.7326/0003-4819-118-6-199303150-00010
259.
Nakano S, Ando Y, Saito K, Moriyama I, Ichijo M, Toyama T, Sugamura K, Imai J, Hinuma Y. Primary infection of Japanese infants with adult T-cell leukaemia-associated retrovirus (ATLV): evidence for viral transmission from mothers to children. J Infect. 1986;12:205-212.
Not in our library10.1016/s0163-4453(86)94086-7
260.
Hino S, Yamaguchi K, Katamine S, Sugiyama H, Amagasaki T, Kinoshita K, Yoshida Y, Doi H, Tsuji Y, Miyamoto T. Mother-to-child transmission of human T-cell leukemia virus type-I. Jpn J Cancer Res. 1985;76:474-480.
Not in our library
261.
Ando Y, Nakano S, Saito K, Shimamoto I, Ichijo M, Toyama T, Hinuma Y. Transmission of adult T-cell leukemia retrovirus (HTLV-I) from mother to child: Comparison of bottle- with breast-fed babies. Jpn J Cancer Res. 1987;78:322-324.
Not in our library
262.
Kusuhara K, Sonoda S, Takahashi K, Tokugawa K, Fukushige J, Ueda K. Mother-to-child transmission of human T-cell leukemia virus type I (HTLV-I): A fifteen-year follow-up study in Okinawa, Japan. Int J Cancer. 1987;40:755-757.
Not in our library10.1002/ijc.2910400607
263.
Kinoshita K, Hino S, Amagaski T, Ikeda S, Yamada Y, Suzuyama J, Momita S, Toriya K, Kamihira S, Ichimaru M. Demonstration of adult T-cell leukemia virus antigen in milk from three sero-positive mothers. Gann. 1984;75:103-105.
Not in our library
264.
Takeuchi H, Takahashi M, Norose Y, Takeshita T, Fukunaga Y, Takahashi H. Transformation of breast milk macrophages by HTLV-I: Implications for HTLV-I transmission via breastfeeding. Biomed Res. 2010;31:53-61.
Not in our library10.2220/biomedres.31.53
265.
Takahashi K, Takezaki T, Oki T, Kawakami K, Yashiki S, Fujiyoshi T, Usuku K, Mueller N, Osame M, Miyata K, et al. Inhibitory effect of maternal antibody on mother-to-child transmission of human T-lymphotropic virus type I. The Mother-to-Child Transmission Study Group. Int J Cancer. 1991;49:673-677.
Not in our library10.1002/ijc.2910490508
266.
Takezaki T, Tajima K, Ito M, Ito S, Kinoshita K, Tachibana K, Matsushita Y. Short-term breast-feeding may reduce the risk of vertical transmission of HTLV-I. The Tsushima ATL Study Group. Leukemia. 1997;11:60-62.
Not in our library
267.
Wiktor SZ, Pate EJ, Rosenberg PS, Barnett M, Palmer P, Medeiros D, Maloney EM, Blattner WA. Mother-to-child transmission of human T-cell lymphotropic virus type I associated with prolonged breast-feeding. J Hum Virol. 1997;1:37-44.
Not in our library
268.
Ando Y, Nakano S, Saito K, Shimamoto I, Ichijo M, Toyama T, Hinuma Y. Prevention of HTLV-I transmission through the breast milk by a freeze-thawing process. Jpn J Cancer Res. 1986;77:974-977.
Not in our library
269.
Ando Y, Kakimoto K, Tanigawa T, Furuki K, Saito K, Nakano S, Hashimoto H, Moriyama I, Ichijo M, Toyama T. Effect of freeze-thawing breast milk on vertical HTLV-I transmission from seropositive mothers to children. Jpn J Cancer Res. 1989;80:405-407.
Not in our library10.1111/j.1349-7006.1989.tb02327.x
270.
Yamato K, Taguchi H, Yoshimoto S, Fujishita M, Yamashita M, Ohtsuki Y, Hoshino H, Miyoshi I. Inactivation of lymphocyte-transforming activity of human T-cell leukemia virus type I by heat. Jpn J Cancer Res. 1986;77:13-15.
Not in our library
271.
Saito S, Furuki K, Ando Y, Tanigawa T, Kakimoto K, Moriyama I, Ichijo M. Identification of HTLV-I sequence in cord blood mononuclear cells of neonates born to HTLV-I antigen/antibody-positive mothers by polymerase chain reaction. Jpn J Cancer Res. 1990;81:890-895.
Not in our library10.1111/j.1349-7006.1990.tb02663.x
272.
Tajima K, Tominaga S, Suchi T, Kawagoe T, Komoda H, Hinuma Y, Oda T, Fujita K. Epidemiological analysis of the distribution of antibody to adult T-cell leukemia-virus-associated antigen: Possible horizontal transmission of adult T-cell leukemia virus. Gann. 1982;73:893-901.
Not in our library
273.
Kajiyama W, Kashiwagi S, Ikematsu H, Hayashi J, Nomura H, Okochi K. Intrafamilial transmission of adult T cell leukemia virus. J Infect Dis. 1986;154:851-857.
Not in our library10.1093/infdis/154.5.851
274.
Murphy EL, Figueroa JP, Gibbs WN, Brathwaite A, Holding-Cobham M, Waters D, Cranston B, Hanchard B, Blattner WA. Sexual transmission of human T-lymphotropic virus type I (HTLV-I). Ann Intern Med. 1989;111:555-560.
Not in our library10.7326/0003-4819-111-7-555
275.
Stuver SO, Tachibana N, Okayama A, Shioiri S, Tsunetoshi Y, Tsuda K, Mueller NE. Heterosexual transmission of human T cell leukemia/lymphoma virus type I among married couples in southwestern Japan: an initial report from the Miyazaki Cohort Study. J Infect Dis. 1993;167:57-65.
Not in our library10.1093/infdis/167.1.57
276.
Okochi K, Sato H, Hinuma Y. A retrospective study on transmission of adult T cell leukemia virus by blood transfusion: Seroconversion in recipients. Vox Sang. 1984;46:245-253.
Not in our library10.1111/j.1423-0410.1984.tb00083.x
277.
Sato H, Okochi K. Transmission of human T-cell leukemia virus (HTLV-I) by blood transfusion: demonstration of proviral DNA in recipients’ blood lymphocytes. Int J Cancer. 1986;37:395-400.
Not in our library10.1002/ijc.2910370311
278.
Larson CJ, Taswell HF. Human T-cell leukemia virus type I (HTLV-I) and blood transfusion. Mayo Clin Proc. 1988;63:869-875.
Not in our library10.1016/s0025-6196(12)62689-5
279.
Lee H, Swanson P, Shorty VS, Zack JA, Rosenblatt JD, Chen IS. High rate of HTLV-II infection in seropositive i.v. drug abusers in New Orleans. Science. 1989;244:471-475.
Not in our library10.1126/science.2655084
280.
Kwok S, Gallo D, Hanson C, McKinney N, Poiesz B, Sninsky JJ. High prevalence of HTLV-II among intravenous drug abusers: PCR confirmation and typing. AIDS Res Hum Retroviruses. 1990;6:561-565.
Not in our library10.1089/aid.1990.6.561
281.
Zella D, Mori L, Sala M, Ferrante P, Casoli C, Magnani G, Achilli G, Cattaneo E, Lori F, Bertazzoni U. HTLV-II infection in Italian drug abusers. Lancet. 1990;336:575-576.
Not in our library10.1016/0140-6736(90)92140-d
282.
Khabbaz RF, Hartel D, Lairmore M, Horsburgh CR, Schoenbaum EE, Roberts B, Hartley TM, Friedland G. Human T lymphotropic virus type II (HTLV-II) infection in a cohort of New York intravenous drug users: An old infection. J Infect Dis. 1991;163:252-256.
Not in our library10.1093/infdis/163.2.252
283.
Pepin J, Labbe AC, Mamadou-Yaya F, Mbelesso P, Mbadingai S, Deslandes S, Locas MC, Frost E. Iatrogenic transmission of human T cell lymphotropic virus type 1 and hepatitis C virus through parenteral treatment and chemoprophylaxis of sleeping sickness in colonial Equatorial Africa. Clin Infect Dis. 2010;51:777-784.
Not in our library10.1086/656232
284.
Morikawa K, Kuroda M, Tofuku Y, Uehara H, Akizawa T, Kitaoka T, Koshikawa S, Sugimoto H, Hashimoto K. Prevalence of HTLV-1 antibodies in hemodialysis patients in Japan. Am J Kidney Dis. 1988;12:185-193.
Not in our library10.1016/s0272-6386(88)80120-3
285.
Kauffman HM, Taranto SE. Human T-cell lymphotrophic virus type-1 and organ donors. Transplantation. 2003;76:745-746.
Not in our library10.1097/01.tp.0000071847.36786.c1
286.
González-Pérez MP, Munoz-Juárez L, Cárdenas FC, Zarranz Imirizaldu JJ, Carranceja JC, García-Saiz A. Human T-cell leukemia virus type I infection in various recipients of transplants from the same donor. Transplantation. 2003;75:1006-1011.
Not in our library10.1097/01.tp.0000058470.15921.ca
287.
Zarranz Imirizaldu JJ, Gomez Esteban JC, Rouco Axpe I, Perez Concha T, Velasco Juanes F, Allue Susaeta I, Corral Carranceja JM. Post-transplantation HTLV-1 myelopathy in three recipients from a single donor. J Neurol Neurosurg Psychiatry. 2003;74:1080-1084.
Not in our library10.1136/jnnp.74.8.1080
288.
Arjmand B, Aghayan SH, Goodarzi P, Farzanehkhah M, Mortazavi SM, Niknam MH, Jafarian A, Arjmand F, Jebellyfar S. Seroprevalence of human T lymphtropic virus (HTLV) among tissue donors in Iranian tissue bank. Cell Tissue Bank. 2009;10:247-252.
Not in our library10.1007/s10561-008-9117-9
289.
Khameneh ZR, Sepehrvand N, Masudi S, Taghizade-Afshari A. Seroprevalence of HTLV-1 among kidney graft recipients: A single-center study. Exp Clin Transplant. 2010;8:146-149.
Not in our library
290.
Clark J, Saxinger C, Gibbs WN, Lofters W, Lagranade L, Deceulaer K, Ensroth A, Robert-Guroff M, Gallo RC, Blattner WA. Seroepidemiologic studies of human T-cell leukemia/lymphoma virus type I in Jamaica. Int J Cancer. 1985;36:37-41.
Not in our library10.1002/ijc.2910360107
291.
de The G, Gessain A. Seroepidemiologic data on viral infections (HTLV-I and LAV/HTLV-III) in the Caribbean region and intertropical Africa. Ann Pathol. 1986;6:261-264.
Not in our library
292.
Iwanaga M, Chiyoda S, Kusaba E, Kamihira S. Trends in the seroprevalence of HTLV-1 in Japanese blood donors in Nagasaki Prefecture, 2000–2006. Int J Hematol. 2009;90:186-190.
Not in our library10.1007/s12185-009-0366-6
293.
Galvao-Castro B, Loures L, Rodriques LG, Sereno A, Ferreira Junior OC, Franco LG, Muller M, Sampaio DA, Santana A, Passos LM, et al. Distribution of human T-lymphotropic virus type I among blood donors: A nationwide Brazilian study. Transfusion. 1997;37:242-243.
Not in our library10.1046/j.1537-2995.1997.37297203532.x
294.
Kazanji M, Gessain A. Human T-cell Lymphotropic Virus types I and II (HTLV-I/II) in French Guiana: Clinical and molecular epidemiology. Cad Saude Publica. 2003;19:1227-1240.
Not in our library10.1590/s0102-311x2003000500002
295.
Leon G, Quiros AM, Lopez JL, Hung M, Diaz AM, Goncalves J, Da Costa O, Hernandez T, Chirinos M, Gomez R. Seropositivity for human T-lymphotropic virus types I and II among donors at the Municipal Blood Bank of Caracas and associated risk factors. Rev Panam Salud Publica. 2003;13:117-123.
Not in our library10.1590/s1020-49892003000200012
296.
Sanchez-Palacios C, Gotuzzo E, Vandamme AM, Maldonado Y. Seroprevalence and risk factors for human T-cell lymphotropic virus (HTLV-I) infection among ethnically and geographically diverse Peruvian women. Int J Infect Dis. 2003;7:132-137.
Not in our library10.1016/s1201-9712(03)90009-9
297.
Gastaldello R, Hall WW, Gallego S. Seroepidemiology of HTLV-I/II in Argentina: an overview. J Acquir Immune Defic Syndr. 2004;35:301-308.
Not in our library10.1097/00126334-200403010-00012
298.
Biglione MM, Astarloa L, Salomon HE. High prevalence of HTLV-I and HTLV-II among blood donors in Argentina: A South American health concern. AIDS Res Hum Retroviruses. 2005;21:1-4.
Not in our library10.1089/aid.2005.21.1
299.
Chandia L, Sotomayor C, Ordenes S, Salas P, Navarrete M, Lopez M, Otth C. Seroprevalence of human T-cell lymphotropic virus type 1 and 2 in blood donors from the regional hospital of Valdivia, Chile. Med Microbiol Immunol. 2010;199:341-344.
Not in our library10.1007/s00430-010-0166-x
300.
Osame M, Janssen R, Kubota H, Nishitani H, Igata A, Nagataki S, Mori M, Goto I, Shimabukuro H, Khabbaz R, et al. Nationwide survey of HTLV-I-associated myelopathy in Japan: association with blood transfusion. Ann Neurol. 1990;28:50-56.
Not in our library10.1002/ana.410280110
301.
Inaba S, Okochi K, Sato H, Fukada K, Kinukawa N, Nakata H, Kinjyo K, Fujii F, Maeda Y. Efficacy of donor screening for HTLV-I and the natural history of transfusion-transmitted infection. Transfusion. 1999;39:1104-1110.
Not in our library10.1046/j.1537-2995.1999.39101104.x
302.
Polizzotto MN, Wood EM, Ingham H, Keller AJ. Reducing the risk of transfusiontransmissible viral infection through blood donor selection: The Australian experience 2000 through 2006. Transfusion. 2008;48:55-63.
Not in our library10.1111/j.1537-2995.2007.01482.x
303.
Berini CA, Gendler SA, Pascuccio S, Eirin ME, McFarland W, Page K, Carnevali L, Murphy E, Biglione MM. Decreasing trends in HTLV-1/2 but stable HIV-1 infection among replacement donors in Argentina. J Med Virol. 2010;82:873-877.
Not in our library10.1002/jmv.21728
304.
Declínio da prevalência do HTLV-1/2 em doadores de sangue do Hemocentro Regional da Cidade de Uberaba, Estado de Minas Gerais, 1995 a 2008 Decline in the prevalence of HTLV-1/2 among blood donors at the Regional Blood Center of the City of Uberaba, State of Minas Gerais, from 1995 to 2008 · 2010
Not checked
305.
Bitar N, Hajj HE, Houmani Z, Sabbah A, Otrock ZK, Mahfouz R, Zaatari G, Bazarbachi A. Adult T-cell leukemia/lymphoma in the Middle East: first report of two cases from Lebanon. Transfusion. 2009;49:1859-1864.
Not in our library10.1111/j.1537-2995.2009.02223.x
306.
Stienlauf S, Yahalom V, Schwartz E, Shinar E, Segal G, Sidi Y. Epidemiology of human T-cell lymphotropic virus type 1 infection in blood donors, Israel. Emerg Infect Dis. 2009;15:1116-1118.
Not in our library10.3201/eid1507.080796
307.
de The G, Bomford R. An HTLV-I vaccine: Why, how, for whom. AIDS Res Hum Retroviruses. 1993;9:381-386.
Not in our library10.1089/aid.1993.9.381
308.
Bomford R, Kazanji M, De The G. Vaccine against human T cell leukemia-lymphoma virus type I: progress and prospects. AIDS Res Hum Retroviruses. 1996;12:403-405.
Not in our library10.1089/aid.1996.12.403
309.
Takehara N, Iwahara Y, Uemura Y, Sawada T, Ohtsuki Y, Iwai H, Hoshino H, Miyoshi I. Effect of immunization on HTLV-I infection in rabbits. Int J Cancer. 1989;44:332-336.
Not in our library10.1002/ijc.2910440224
310.
Nakamura H, Hayami M, Ohta Y, Ishikawa K, Tsujimoto H, Kiyokawa T, Yoshida M, Sasagawa A, Honjo S. Protection of cynomolgus monkeys against infection by human T-cell leukemia virus type-I by immunization with viral env gene products produced in Escherichia coli. Int J Cancer. 1987;40:403-407.
Not in our library10.1002/ijc.2910400320
311.
Ohashi T, Hanabuchi S, Kato H, Tateno H, Takemura F, Tsukahara T, Koya Y, Hasegawa A, Masuda T, Kannagi M. Prevention of adult T-cell leukemia-like lymphoproliferative disease in rats by adoptively transferred T cells from a donor immunized with human T-cell leukemia virus type 1 Tax-coding DNA vaccine. J Virol. 2000;74:9610-9616.
Not in our library10.1128/jvi.74.20.9610-9616.2000
312.
Kazanji M, Tartaglia J, Franchini G, de Thoisy B, Talarmin A, Contamin H, Gessain A, de The G. Immunogenicity and protective efficacy of recombinant human T-cell leukemia/lymphoma virus type 1 NYVAC and naked DNA vaccine candidates in squirrel monkeys (Saimiri sciureus). J Virol. 2001;75:5939-5948.
Not in our library10.1128/jvi.75.13.5939-5948.2001
313.
Baba E, Nakamura M, Ohkuma K, Kira J, Tanaka Y, Nakano S, Niho Y. A peptide-based human T cell leukemia virus type I vaccine containing T and B cell epitopes that induces high titers of neutralizing antibodies. J Immunol. 1995;154:399-412.
Not in our library
314.
Tanaka Y, Tanaka R, Terada E, Koyanagi Y, Miyano-Kurosaki N, Yamamoto N, Baba E, Nakamura M, Shida H. Induction of antibody responses that neutralize human T-cell leukemia virus type I infection in vitro and in vivo by peptide immunization. J Virol. 1994;68:6323-6331.
Not in our library10.1128/jvi.68.10.6323-6331.1994
315.
Hanabuchi S, Ohashi T, Koya Y, Kato H, Hasegawa A, Takemura F, Masuda T, Kannagi M. Regression of human T-cell leukemia virus type I (HTLV-I)-associated lymphomas in a rat model: Peptide-induced T-cell immunity. J Natl Cancer Inst. 2001;93:1775-1783.
Not in our library10.1093/jnci/93.23.1775
316.
Sundaram R, Lynch MP, Rawale S, Dakappagari N, Young D, Walker CM, Lemonnier F, Jacobson S, Kaumaya PT. Protective efficacy of multiepitope human leukocyte antigen-A*0201 restricted cytotoxic T-lymphocyte peptide construct against challenge with human T-cell lymphotropic virus type 1 Tax recombinant vaccinia virus. J Acquir Immune Defic Syndr. 2004;37:1329-1339.
Not in our library10.1097/00126334-200411010-00001
317.
Sundaram R, Sun Y, Walker CM, Lemonnier FA, Jacobson S, Kaumaya PT. A novel multivalent human CTL peptide construct elicits robust cellular immune responses in HLAA*0201 transgenic mice: implications for HTLV-1 vaccine design. Vaccine. 2003;21:2767-2781.
Not in our library10.1016/s0264-410x(03)00179-8
318.
Kobayashi H, Ngato T, Sato K, Aoki N, Kimura S, Tanaka Y, Aizawa H, Tateno M, Celis E. In vitro peptide immunization of target tax protein human T-cell leukemia virus type 1-specific CD4+ helper T lymphocytes. Clin Cancer Res. 2006;12:3814-3822.
Not in our library10.1158/1078-0432.ccr-06-0384
319.
Kozako T, Hirata S, Shimizu Y, Satoh Y, Yoshimitsu M, White Y, Lemonnier F, Shimeno H, Soeda S, Arima N. Oligomannose-coated liposomes efficiently induce human T-cell leukemia virus-1-specific cytotoxic T lymphocytes without adjuvant. FEBS J. 2011;278:1358-1366.
Not in our library10.1111/j.1742-4658.2011.08055.x
320.
Kozako T, Fukada K, Hirata S, White Y, Harao M, Nishimura Y, Kino Y, Soeda S, Shimeno H, Lemonnier F, Sonoda S, Arima N. Efficient induction of human T-cell leukemia virus-1-specific CTL by chimeric particle without adjuvant as a prophylactic for adult T-cell leukemia. Mol Immunol. 2009;47:606-613.
Not in our library10.1016/j.molimm.2009.09.006
321.
Conrad SF, Byeon IJ, DiGeorge AM, Lairmore MD, Tsai MD, Kaumaya PT. Immunogenicity and conformational properties of an N-linked glycosylated peptide epitope of human T-lymphotropic virus type 1 (HTLV-I). Biomed Pept Proteins Nucleic Acids. 1995;1:83-92.
Not in our library
322.
Frangione-Beebe M, Albrecht B, Dakappagari N, Rose RT, Brooks CL, Schwendeman SP, Lairmore MD, Kaumaya PT. Enhanced immunogenicity of a conformational epitope of human T-lymphotropic virus type 1 using a novel chimeric peptide. Vaccine. 2000;19:1068-1081.
Not in our library10.1016/s0264-410x(00)00340-6
323.
Kazanji M, Heraud JM, Merien F, Pique C, de The G, Gessain A, Jacobson S. Chimeric peptide vaccine composed of B- and T-cell epitopes of human T-cell leukemia virus type 1 induces humoral and cellular immune responses and reduces the proviral load in immunized squirrel monkeys (Saimiri sciureus). J Gen Virol. 2006;87:1331-1337.
Not in our library10.1099/vir.0.81582-0
324.
Shida H, Tochikura T, Sato T, Konno T, Hirayoshi K, Seki M, Ito Y, Hatanaka M, Hinuma Y, Sugimoto M, et al. Effect of the recombinant vaccinia viruses that express HTLV-I envelope gene on HTLV-I infection. EMBO J. 1987;6:3379-3384.
Not in our library10.1002/j.1460-2075.1987.tb02660.x
325.
Hakoda E, Machida H, Tanaka Y, Morishita N, Sawada T, Shida H, Hoshino H, Miyoshi I. Vaccination of rabbits with recombinant vaccinia virus carrying the envelope gene of human T-cell lymphotropic virus type I. Int J Cancer. 1995;60:567-570.
Not in our library10.1002/ijc.2910600423
326.
Franchini G, Benson J, Gallo R, Paoletti E, Tartaglia J. Attenuated poxvirus vectors as carriers in vaccines against human T cell leukemia-lymphoma virus type I. AIDS Res Hum Retroviruses. 1996;12:407-408.
Not in our library10.1089/aid.1996.12.407
327.
Franchini G, Tartaglia J, Markham P, Benson J, Fullen J, Wills M, Arp J, Dekaban G, Paoletti E, Gallo RC. Highly attenuated HTLV type Ienv poxvirus vaccines induce protection against a cell-associated HTLV type I challenge in rabbits. AIDS Res Hum Retroviruses. 1995;11:307-313.
Not in our library10.1089/aid.1995.11.307
328.
Ibuki K, Funahashi SI, Yamamoto H, Nakamura M, Igarashi T, Miura T, Ido E, Hayami M, Shida H. Long-term persistence of protective immunity in cynomolgus monkeys immunized with a recombinant vaccinia virus expressing the human T cell leukaemia virus type I envelope gene. J Gen Virol. 1997;78:147-152.
Not in our library10.1099/0022-1317-78-1-147
329.
Kazanji M, Bomford R, Bessereau JL, Schulz T, de The G. Expression and immunogenicity in rats of recombinant adenovirus 5 DNA plasmids and vaccinia virus containing the HTLV-I env gene. Int J Cancer. 1997;71:300-307.
Not in our library10.1002/(sici)1097-0215(19970410)71:2<300::aid-ijc27>3.0.co;2-j
330.
Kchour G, Makhoul NJ, Mahmoudi M, Kooshyar MM, Shirdel A, Rastin M, Rafatpanah H, Tarhini M, Zalloua PA, Hermine O, Farid R, Bazarbachi A. Zidovudine and interferon-alpha treatment induces a high response rate and reduces HTLV-1 proviral load and VEGF plasma levels in patients with adult T-cell leukemia from North East Iran. Leuk Lymphoma. 2007;48:330-336.
Not in our library10.1080/10428190601071717
331.
Tsukasaki K, Hermine O, Bazarbachi A, Ratner L, Ramos JC, Harrington W, O’Mahony D, Janik JE, Bittencourt AL, Taylor GP, et al. Definition, prognostic factors, treatment, and response criteria of adult T-cell leukemia-lymphoma: A proposal from an international consensus meeting. J Clin Oncol. 2009;27:453-459.
Not in our library10.1200/jco.2008.18.2428

Cited by papers we hold 3

Expression Profiles and Interaction of MicroRNA and Transcripts in Response to Bovine Leukemia Virus Exposure · 2022
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How Does HTLV-1 Undergo Oncogene-Dependent Replication Despite a Strong Immune Response? · 2018
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Epidemiology and genetic diversity of bovine leukemia virus · 2017
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