Intrapreputial infection of young bulls with bovine herpesvirus type 1.2 (BHV-1.2): acute balanoposthitis, latent infection and detection of viral DNA in regional neural and non-neural tissues 50 days after experimental reactivation

Vogel, Fernanda Silveira Flôres; Flores, Eduardo Furtado; Weiblen, Rudi; Winkelmann, E.; Moraes, Mauro Pires; Bragança, José Francisco Manta

doi:10.1016/j.vetmic.2003.09.020

Cited by 21 publications

(26 citation statements)

References 37 publications

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“…In addition, BHV-1 DNA has been detected in tonsils, in CD 4 + T lymphocytes and in peripheral blood mononuclear cells of latently infected animals (16,17). After experimental genital infection, latent BHV-1 DNA was consistently found in sacral ganglia of heifers (18) and in sacral and other nerve ganglia and in regional lymph nodes of bulls (12). The biological significance of latent infection in non-neural sites and neural sites other than sensory nerve ganglia remains obscure since reactivation from these sites has not been unequivocally demonstrated.…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, oronasal infection results in the establishment of latency mainly in trigeminal ganglia (TG) and genital infection ensues, with colonization of sacral ganglia with latent viral DNA (2,(9)(10)(11)(12). However, other possible neural and nonneural sites of latent infection by, or persistence of, these viruses have also been described (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

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Dexamethasone-induced reactivation of bovine herpesvirus type 5 latent infection in experimentally infected rabbits results in a broader distribution of latent viral DNA in the brain

Mayer

Quadros

Vogel

et al. 2006

Braz J Med Biol Res

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Bovine herpesvirus type 5 (BHV-5) is a major agent of meningoencephalitis in cattle and establishes latent infections mainly in sensory nerve ganglia. The distribution of latent BHV-5 DNA in the brain of rabbits prior to and after virus reactivation was studied using a nested PCR. Fifteen rabbits inoculated intranasally with BHV-5 were euthanized 60 days post-inoculation (group A, N = 8) or submitted to dexamethasone treatment (2.6 mg kg -1 day -1 , im, for 5 days) and euthanized 60 days later (group B, N = 7) for tissue examination. Two groups of BHV-1-infected rabbits (C, N = 3 and D, N = 3) submitted to each treatment were used as controls. Viral DNA of group A rabbits was consistently detected in trigeminal ganglia (8/8), frequently in cerebellum (5/8), anterior cerebral cortex and pons-medulla (3/8) and occasionally in dorsolateral (2/8), ventrolateral and posterior cerebral cortices, midbrain and thalamus (1/8). Viral DNA of group B rabbits showed a broader distribution, being detected at higher frequency in ventrolateral (6/7) and posterior cerebral cortices (5/7), pons-medulla (6/7), thalamus (4/7), and midbrain (3/7). In contrast, rabbits inoculated with BHV-1 harbored viral DNA almost completely restricted to trigeminal ganglia and the distribution did not change post-reactivation. These results demonstrate that latency by BHV-5 is established in several areas of the rabbit's brain and that virus reactivation leads to a broader distribution of latent viral DNA. Spread of virus from trigeminal ganglia and other areas of the brain likely contributes to this dissemination and may contribute to the recrudescence of neurological disease frequently observed upon BHV-5 reactivation.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dexamethasone-induced reactivation of bovine herpesvirus type 5 latent infection in experimentally infected rabbits results in a broader distribution of latent viral DNA in the brain

Mayer

Quadros

Vogel

et al. 2006

Braz J Med Biol Res

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“…The challenge used in the present study has been designed as to really evaluate the protection conferred by immunization. For this, we used a heterologous BoHV-1.2 isolate previously shown to be highly virulent for bulls (Vogel et al 2004) and heifers (Henzel et al 2008), in a titer unlikely to be found in raw semen of infected bulls (Vogel et al 2004) or in semen used for artificial insemination (AI) (Van Engelenburg et al 1995). Furthermore, the virus suspension was applied by vigorous swabbing against the mucosa to assure efficient infection.…”

Section: Discussionmentioning

confidence: 99%

“…The virus used for challenge (SV-56/ 90) was isolated from an outbreak of balanoposthitis in bulls in Southern Brazil (Weiblen et al 1992) and subsequently characterized as belonging to BoHV-1.2 subtype (D'Arce et al 2002). The virulence of this isolate has been demonstrated after intrapreputial inoculation of bulls (Vogel et al 2004) and following intravaginal inoculation of heifers (Henzel et al 2008).…”

Section: Cells and Virusesmentioning

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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“…Em um estudo anterior, foi relatada a reprodução de balanopostite clínica em touros jovens inoculados pela via intraprepucial com o isolado SV-56/90 (Vogel et al 2004). O SV-56/90 é uma amostra de BoHV-1.2 isolada de um surto de balanopostite em touros de uma central de inseminação no Rio Grande do Sul, Brasil (Weiblen et al 1992).…”

Section: Introductionunclassified

Aspectos virológicos e clínico-patológicos da infecção genital aguda e latente pelo herpesvírus bovino tipo 1.2 em bezerras infectadas experimentalmente

et al. 2008

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2) may result in vulvovaginitis and transient infertility. The acute infection is followed by the establishment of latent infection which can be periodically reactivated. We herein describe the virology and clinico-pathological aspects of acute and recrudescent vulvovaginitis in heifers inoculated with a Brazilian BoHV-1.2 isolate recovered from an outbreak of balanoposthitis. Genital inoculation of isolate SV-56/90 (10 8.1 TCID 50 / animal) in four eight-months-old heifers resulted in efficient virus replication in the genital mucosa and the development of moderate to severe vulvovaginitis. The inoculated heifers shed virus in genital secretions in titers up to 10 7.3 TCID 50 /mL until day 10 pi and developed genital congestion, swelling, vesicles and pustules. The vesicles and pustules increased in size eventually coalesced and became covered with a yellowish exsudate. These signs appeared at day 2 pi, increased in severity up to days 5 -8 pi and progressively subsided thereafter. Dexamethasone administration at day 55 pi resulted in virus shedding in vaginal secretions for up to 10 days. Virus reactivation in all animals was accompanied by clinical recrudescence of the disease, yet less severe than during acute infection. Examination of sacral ganglia and lymph nodes by PCR at day 36 postreactivation revealed the presence of latent viral DNA in the pudendal (4/4), genitofemoral, sciatic and rectal caudal (3/4) and obturator nerve ganglia (1/4); in addition to several regional lymph nodes. These results demonstrate the virulence of isolate SV-56/90 for heifers and pave the way for its use in further pathogenesis studies and vaccine-challenge trials.

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Intrapreputial infection of young bulls with bovine herpesvirus type 1.2 (BHV-1.2): acute balanoposthitis, latent infection and detection of viral DNA in regional neural and non-neural tissues 50 days after experimental reactivation

Cited by 21 publications

References 37 publications

Dexamethasone-induced reactivation of bovine herpesvirus type 5 latent infection in experimentally infected rabbits results in a broader distribution of latent viral DNA in the brain

Dexamethasone-induced reactivation of bovine herpesvirus type 5 latent infection in experimentally infected rabbits results in a broader distribution of latent viral DNA in the brain

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

Aspectos virológicos e clínico-patológicos da infecção genital aguda e latente pelo herpesvírus bovino tipo 1.2 em bezerras infectadas experimentalmente

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