Immunology of bovine herpesvirus 1 infection

Babiuk, Lorne A.; Hurk, Sylvia van Drunen Littel‐van den; Tikoo, Suresh K.

doi:10.1016/s0378-1135(96)01232-1

Cited by 113 publications

(96 citation statements)

References 40 publications

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“…It generally coincides with the recovery of clinical manifestations [5]. Specific T helper lymphocytes mediate the lysis of BoHV-1 infected cells by activating macrophage and NK cells through IFNγ and IL2 secretion, and by recruiting and promoting the proliferation of specific cytotoxic T lymphocytes (Tab.…”

Section: Immune Response and Immune Evasion Strategiesmentioning

confidence: 81%

“…These effectors enhance the first antiviral wave by secreting cytokines in the infected epithelium and killing virus infected cells [23,24]. The non specific activated immune cells are also essential in initiating and regulating the specific immune response to BoHV-1 [5,34].…”

Section: Immune Response and Immune Evasion Strategiesmentioning

confidence: 99%

“…Even if antibodies seem to be less important in the recovery of primary infection, they probably participate in BoHV-1 infection clearance by neutralizing cell free virus particles thus preventing the extracellular spread of infection and by mediating the antibody-dependent cell cytotoxicity. In return the antibody response is of critical importance in preventing secondary infections and limiting the consequences of reactivation [5]. Moreover the passive immunity afforded by colostral antibodies from BoHV-1 immune cows is fully efficacious at protecting the neonate against systemic and lethal disease [123].…”

Section: Immune Response and Immune Evasion Strategiesmentioning

confidence: 99%

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Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

et al. 2007

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-Bovine herpesvirus 1 (BoHV-1), classified as an alphaherpesvirus, is a major pathogen of cattle. Primary infection is accompanied by various clinical manifestations such as infectious bovine rhinotracheitis, abortion, infectious pustular vulvovaginitis, and systemic infection in neonates. When animals survive, a life-long latent infection is established in nervous sensory ganglia. Several reactivation stimuli can lead to viral re-excretion, which is responsible for the maintenance of BoHV-1 within a cattle herd. This paper focuses on an updated pathogenesis based on a molecular characterization of BoHV-1 and the description of the virus cycle. Special emphasis is accorded to the impact of the latency and reactivation cycle on the epidemiology and the control of BoHV-1. Several European countries have initiated BoHV-1 eradication schemes because of the significant losses incurred by disease and trading restrictions. The vaccines used against BoHV-1 are described in this context where the differentiation of infected from vaccinated animals is of critical importance to achieve BoHV-1 eradication.

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Section: Immune Response and Immune Evasion Strategiesmentioning

confidence: 81%

Section: Immune Response and Immune Evasion Strategiesmentioning

confidence: 99%

Section: Immune Response and Immune Evasion Strategiesmentioning

confidence: 99%

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Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

et al. 2007

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“…The exact role of BoHV-1 antibodies in protection remains undetermined. Whereas neutralizing antibodies appear not to play a critical role in recovering from primary BoHV-1 infection, systemic (and likely locally secreted) neutralizing antibodies are believed play a relevant role in protecting and/ or limiting virus replication and spread upon reinfection (Babiuk et al 1996). Thus, it is reasonable to assume that locally secreted antibodies (IgA, IgG) might have contributed to limit viral replication and spread following challenge, thereby contributing for the reduction of severity and duration of genital disease in IV vaccinated heifers.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, control animals responded serologically with in primary response kinetics (Fig.3). It is reasonable to consider that, in addition to locally secreted antibodies, other humoral and cell-mediated immune mechanismssuch as lysis of infected cells by virus-specific cytotoxic T lymphocytes, antibody-dependent cellular cytotoxicity (ADCC) by NK cells (Babiuk et al 1996, Tikoo et al 1995 -triggered within the genital mucosa-associated lymphoid tissue, may have also contributed to restrict virus replication and reduce the severity of clinical disease after challenge. The reduction or virus replication and shedding in the IV vaccinated heifers (thereby reducing the severity and duration of clinical signs) is consistent with a local, virus replication restrictive immune response.…”

Section: Discussionmentioning

confidence: 99%

Genital immunization of heifers with a glycoprotein Edeleted, recombinant bovine herpesvirus 1 strain confers protection upon challenge with a virulent isolate

et al. 2010

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ABSTRACT.-Weiss M., Vogel F.S.F., Martins M., Weiblen R., Roehe P.M., Franco A.C. & Flores E.F. 2010. Genital immunization of heifers with a glycoprotein E-deleted, recombinant bovine herpesvirus 1 strain confers protection upon challenge with a virulent isolate. Pesquisa Veterinária Brasileira 30(1):42-50. Departamento de Medicina Veterinária Preventiva, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: eduardofurtadoflores@gmail.com Venereal infection of seronegative heifers and cows with bovine herpesvirus type 1.2 (BoHV-1.2) frequently results in vulvovaginitis and transient infertility. Parenteral immunization with inactivated or modified live BoHV-1 vaccines often fails in conferring protection upon genital challenge. We herein report an evaluation of the immune response and protection conferred by genital vaccination of heifers with a glycoprotein E-deleted recombinant virus (SV265gE-). A group of six seronegative heifers was vaccinated with SV265gE-(0,2mL containing 10 6.9 TCID 50 ) in the vulva submucosa (group IV); four heifers were vaccinated intramuscularly (group IM, 1mL containing 10 7.6 TCID 50 ) and four heifers remained as non-vaccinated controls. Heifers vaccinated IV developed mild, transient local edema and hyperemia and shed low amounts of virus for a few days after vaccination, yet a sentinel heifer maintained in close contact did not seroconvert. Attempts to reactivate the vaccine virus in two IV vaccinated heifers by intravenous administration of dexamethasone (0.5mg/kg) at day 70 pv failed since no virus shedding, recrudescence of genital signs or seroconversion were observed. At day 70 pv, all vaccinated and control heifers were challenged by genital inoculation of a highly virulent BoHV-1.2 isolate (SV-56/90, 10 7.1 TCID 50 /animal). After challenge, virus shedding was detected in genital secretions of control animals for 8.2 days (8-9); in the IM group for 6.2 days (4-8 days) and during 5.2 days (5-6 days) in the IV group. Control non-vaccinated heifers developed moderate (2/4) or severe (2/4) vulvovaginitis lasting 9 to 13 days (x: 10.7 days). The disease was characterized by vulvar edema, vulvo-vestibular congestion, vesicles progressing to coalescence and erosions, fibrino-necrotic plaques and fibrinopurulent exudate. IM vaccinated heifers developed mild (1/3) or moderate (3/4) genital lesions, lasting 10 to 12 days (x: 10.7 days); and IV vaccinated heifers developed mild and transient vulvovaginitis (3/4) or mild to moderate genital lesions (1/4). In the IV group, the clinical signs lasted 4 to 8 days (x: 5.5 days). Clinical examination of the animals after challenge revealed that vaccination by both routes conferred some degree of protection, yet IV vaccination was clearly more effective in reducing the severity and duration of clinical 2) pode resultar em vulvovaginite e infertilidade temporária. As vacinas atenuadas ou inativadas administradas pela via parenteral freqüente-mente conferem proteção incompleta frente a desafio pela via genital. Este...

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Effect of stress on viral–bacterial synergy in bovine respiratory disease: novel mechanisms to regulate inflammation

et al. 2005

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The severity of bovine respiratory infections has been linked to a variety of factors, including environmental and nutritional changes, transportation, and social reorganization of weaned calves. Fatal respiratory infections, however, usually occur when a primary viral infection compromises host defences and enhances the severity of a secondary bacterial infection. This viral–bacterial synergy can occur by a number of different mechanisms and disease challenge models have been developed to analyse host responses during these respiratory infections. A primary bovine herpesvirus-1 (BHV-1) respiratory infection followed by a secondary challenge with Mannheimia haemolytica results in fatal bovine respiratory disease (BRD) and host responses to these two pathogens have been studied extensively. We used this disease model to demonstrate that stress significantly altered the viral–bacterial synergy resulting in fatal BRD. Functional genomic analysis revealed that BHV-1 infection enhanced toll-like receptors (TLR) expression and increased pro-inflammatory responses which contribute to the severity of a Mannheimia haemolytica infection. TLRs play a critical role in detecting bacterial infections and inducing pro-inflammatory responses. It is difficult to understand, however, how stress-induced corticosteroids could enhance this form of viral–bacterial synergy. Nuclear translocation of the glucocorticoid receptor activates cell signalling pathways which inhibit both TLR signalling and pro-inflammatory responses. The apparent conundrum between stress-induced corticosteroids and enhanced BRD susceptibility is discussed in terms of present data and previous investigations of stress and respiratory disease.

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Immunology of bovine herpesvirus 1 infection

Cited by 113 publications

References 40 publications

Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

Genital immunization of heifers with a glycoprotein Edeleted, recombinant bovine herpesvirus 1 strain confers protection upon challenge with a virulent isolate

Effect of stress on viral–bacterial synergy in bovine respiratory disease: novel mechanisms to regulate inflammation

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