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

Ohishi, Kazue; Suzuki, Hidemi; Yamamoto, Toshiko; Maruyama, Tadashi; Miki, Keizaburo; Ikawa, Yoji; Numakunai, Shigeru; Okada, Kōsuke; Ohshima, Kan-ichi; Sugimoto, Masanobu

doi:10.1099/0022-1317-72-8-1887

Cited by 43 publications

(34 citation statements)

References 12 publications

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“…Thus, production of PGE 2 and the change of macrophage functions contribute to the suppression of CMI responses in the disease-progressed animals. Ohishi et al also supported the critical roles of CMI to eliminate BLV infected cells [41,42,59]. Recombinant vaccinia virus encoding BLVenv gene (rVVenv) was constructed and injected into sheep.…”

Section: Cell-mediated Immunity and Blv Infectionmentioning

confidence: 99%

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Host Immune Responses in the Course of Bovine Leukemia Virus Infection.

Kabeya

Ohashi

Onuma

2001

The Journal of Veterinary Medical Science

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ABSTRACT. Bovine leukemia virus (BLV) is a type C retrovirus infecting bovine B cells and causing enzootic bovine leukosis. Since it takes long periods to develop the disease, it is believed that BLV and host immune responses are closely related. In this review, the accumulated data showing close relationship between BLV and host immune responses are summarized in 4 sections. First, we discuss the role of cell-mediated immunity in protecting hosts from BLV infection. Second, several reports showing the relationship between the disease progression and the change of cytokine profiles are summarized. In the third section, we have focused on tumor necrosis factor α (TNFα) and its two types of receptors, and the possible involvement of TNF α in the BLV-induced leukemogenesis is discussed. The expression of TNF α has been shown to be regulated by major histocompatibility complex (MHC) haplotype. The resistance to BLV infection is supposed to be established by some innate factors, which are closely related to MHC haplotype. Finally, we propose that a breeding strategy based on the MHC haplotype could be a good approach to control BLV infection. This review includes some recent data from us and other groups. KEY WORDS: bovine leukemia virus, cell-mediated immunity, cytokine profile, major histocompatibility complex, tumor necrosis factor α.J. Vet. Med. Sci. 63 (7): [703][704][705][706][707][708] 2001 Bovine leukemia virus (BLV), the causative agent of enzootic bovine leukosis, is an oncogenic B-lymphotropic retrovirus [27]. The disease is divided into three stages; serologically positive, but negative for lymphocytosis (SP); serologically positive and positive for persistent lymphocytosis (PL); and leukemia. Like other members of chronic retrovirus infection, BLV infection results in a prolonged asymptomatic period with a low viral load that persists for 1 to 8 years. Thirty percent of infected animals progress to PL, characterized by a polyclonal expansion of B cells. Only 0.1 to 10 percent develop malignant lymphosarcoma [53]. Usually a long duration is required between these disease stages suggesting that BLV modulate host immune systems [22,23].The purpose of this review is to assemble the results of studies on the host immune responses in the course of BLV infection in an effort to provide a picture towards the control of BLV infection. CELL-MEDIATED IMMUNITY AND BLV INFECTIONBoth humoral and cell-mediated immunity (CMI) are known to be induced in natural BLV-infection, and these play roles in protection of hosts from BLV infection [20,29,41,42,45]. However, their relative roles in protection remain to be elucidated. In this regard, a series of recent studies have postulated that particularly CMI against BLV antigens contributes to the suppression of BLV replication, this leading to the delay of disease progression [42,59]. Orlik and Splitter have shown that CMI responses to BLV antigens were suppressed in correlation to disease progression [46]. The positive effect of indomethacin on the recovery of the suppres...

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Section: Cell-mediated Immunity and Blv Infectionmentioning

confidence: 99%

“…Both humoral and cell-mediated immunity (CMI) are known to be induced in natural BLV-infection, and these play roles in protection of hosts from BLV infection [20,29,41,42,45]. However, their relative roles in protection remain to be elucidated.…”

Section: Cell-mediated Immunity and Blv Infectionmentioning

confidence: 99%

Host Immune Responses in the Course of Bovine Leukemia Virus Infection.

Kabeya

Ohashi

Onuma

2001

The Journal of Veterinary Medical Science

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“…Thus, resistance to BLV challenge after vaccination of sheep with envelope glycoprotein (Env) gp51 antigen and cattle with cells producing BLV envelope-encoded glycoproteins and p24 correlated with the presence of virusspecific antibodies (5,33). In contrast, cell-mediated immunity was the major protective mechanism in sheep inoculated with vaccinia virus expressing gp51 (14,31,32,36), and in which cytotoxic CD8 ϩ T-cell on gp51 were identified (13,16,24). However, the reason(s) why the progression of the disease and immune response in naturally infected animals are different has been unclear.…”

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confidence: 99%

The Influence of Ovine MHC Class IIDRB1Alleles on Immune Response in Bovine Leukemia Virus Infection

Konnai

Takeshima

Tajima

et al. 2003

Microbiology and Immunology

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We have reported previously that the alleles of the ovine leukocyte antigen (OLA)‐DRB1 gene that encode the Arg‐Lys (RK) motif and the Ser‐Arg (SR) motif at positions β70/71 of the OLA‐DRβ1 domain are associated with resistance and susceptibility, respectively, to development of bovine leukemia virus (BLV)‐induced ovine lymphoma. Here, to investigate the different immune response in sheep that carried alleles associated with resistance and susceptible for 30 weeks after infection with BLV, we selected sheep that had the RK/RK or SR/SR genotype among the 52 sheep analyzed by polymerase chain reaction‐restriction fragment length polymorphism and DNA sequencing of PCR product for the OLA‐DRB1 exon 2 and infected them with BLV. Although the number of BLV‐infected cells and virus titer had been maintaining low levels throughout the experimental period, the sheep with the RK/RK genotype could induce expansion of CD5− B‐cells and rapid production of neutralizing antibody in the early phase of infection. The level of incorporation of [3H]thymidine by peripheral blood mononuclear cells from the sheep with RK/RK genotype gave a strong response to BLV virion antigen and synthetic antigenic peptides that corresponded to T‐helper epitope of the BLV envelope glycoprotein gp51. In contrast, the sheep with SR/SR genotype showed a strong response to BLV virion antigen and synthetic antigenic peptides that corresponded to T‐cytotoxic and B‐cell epitopes. In such cases, the animals with the RK/RK strongly expressed IFN‐7, the animals with SR/SR genotype strongly expressed IL‐2. To determine the proliferating cells, we tried a blocking assay with monoclonal antibodies such as anti‐CD4, ‐CD8 and ‐DR molecule. We found that these proliferating cells were MHC‐restricted CD4+ T‐cells.

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“…This effect did not correlate with the presence of the neutralizing or anti-BLV antibody titers observed in these animals, suggesting the stimulation of Th cells, possibly of the type 1, without the induction of a specific humoral immune response. [91][92][93] Vaccination of mice and sheep using the rVV coding for BLV gp51 (BLVgp51-rVV) resulted in protective immunity, with the characteristics of a type 1 response. [94][95][96][97][98] These observations are in agreement with the notion that animals that control the virus express higher levels of interleukin-12 and interferon-gamma and lower levels of interleukin-10.…”

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confidence: 99%

Bovine leukemia virus: current perspectives

Juliarena¹,

Barrios²,

Lützelschwab³

et al. 2017

VAAT

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Enzootic bovine leukosis, caused by bovine leukemia virus (BLV), is the most common neoplasm of dairy cattle. Although beef and dairy cattle are susceptible to BLV infection and BLV-associated lymphosarcoma, the disease is more commonly detected in dairy herds, mostly because of the management practices in dairy farms. The pathogenicity of BLV in its natural host, the bovine, depends mainly on the resistance/susceptibility genetics of the animal. The majority of infected cattle are asymptomatic, promoting the extremely high dissemination rate of BLV in many bovine populations. The important productive losses caused by the BLV, added to the health risk of maintaining populations with a high prevalence of infection with a retrovirus, generates the need to implement control measures. Different strategies to control the virus have been attempted. The most effective approach is to identify and cull the totality of infected cattle in the herd. However, this approach is not suitable for herds with high prevalence of infection. At present, no treatment or vaccine has proven effective for the control of BLV. Thus far, the genetic selection of resistant animals emerges as a natural strategy for the containment of the BLV dissemination. In natural conditions, most of the infected, resistant cattle can control the infection, and therefore do not pass the virus to other animals, gradually decreasing the prevalence of the herd.

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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

Cited by 43 publications

References 12 publications

Host Immune Responses in the Course of Bovine Leukemia Virus Infection.

Host Immune Responses in the Course of Bovine Leukemia Virus Infection.

The Influence of Ovine MHC Class IIDRB1Alleles on Immune Response in Bovine Leukemia Virus Infection

Bovine leukemia virus: current perspectives

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