Herpesvirus (pseudorabies virus) latency in swine: Occurrence and physical state of viral DNA in neural tissues

Rziha, Hanns-Joachim; Mettenleiter, Thomas C.; Ohlinger, Volker; Wittmann, G.

doi:10.1016/0042-6822(86)90220-5

Cited by 98 publications

(74 citation statements)

References 30 publications

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“…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%

“…The major sites of latent infection by human (i.e., herpes simplex virus 1) and animal α-herpesviruses (BHV-5, BHV-1, pseudorabies virus) are the sensory nerve ganglia innervating the site of primary viral replication (2,(9)(10)(11). 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).…”

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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“…CHV belongs to the alphaherpesvirus group, containing feline herpesvirus 1 (FHV-1), equine herpesvirus 1 (EHV-1), bovine herpesvirus 1 (BHV-1) and pseudorabies virus (PRV) [18]. Recent studies demonstrated that the genomes of alphaherpesviruses harbored in the ganglionic neurons [2,13,17,19] as well as in lymphocytes during latent infection [5].…”

Section: 7 and 8)mentioning

confidence: 99%

Detection of Canine Herpesvirus DNA in the Ganglionic Neurons and the Lymph Node Lymphocytes of Latently Infected Dogs.

et al. 1999

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ABSTRACT. To determine the site of latent infection of canine herpesvirus (CHV), tissues from dogs convalescent from acute infection with CHV were examined for the presence of viral genome DNA by the nested polymerase chain reaction. CHV DNA was detected in the trigeminal ganglia and the retropharyngeal lymph nodes. In situ hybridization study of the tissues revealed that CHV genome persisted in the nuclei of ganglionic neurons and lymphocytes.-KEY WORDS: canine herpesvirus, ganglionic neuron, latency, lymphocyte.

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“…In contrast, the nervus trigeminus with all of its branches converges in the trigeminal ganglion leading to the pons and the brain stem. Therefore, after primary replication in the nasal mucosa, these two routes repre-sent the major ways of viral neuroinvasion toward the CNS (20,21,30), and the olfactory bulb and the sensory ganglia are major sites of latent virus (40).…”

mentioning

confidence: 99%

Pseudorabies Virus Expressing Bovine Herpesvirus 1 Glycoprotein B Exhibits Altered Neurotropism and Increased Neurovirulence

Gerdts¹,

Beyer

Lomniczi

et al. 2000

J Virol

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Herpesvirus glycoproteins play dominant roles in the initiation of infection of target cells in culture and thus may also influence viral tropism in vivo. Whereas the relative contribution of several nonessential glycoproteins to neurovirulence and neurotropism of Pseudorabies virus (PrV), an alphaherpesvirus which causes Aujeszky's disease in pigs, has recently been uncovered in studies using viral deletion mutants, the importance of essential glycoproteins is more difficult to assess. We isolated an infectious PrV mutant, PrV-9112C2, which lacks the gene encoding the essential PrV glycoprotein B (gB) but stably carries in its genome and expresses the homologous gene of bovine herpesvirus 1 (BHV-1) (A. Kopp and T. C. Mettenleiter, J. Virol. 66:2754-2762, 1992). Apart from exhibiting a slight delay in penetration kinetics, PrV-9112C2 was similar in its growth characteristics in cell culture to wild-type PrV. To analyze the effect of the exchange of these homologous glycoproteins in PrV's natural host, swine, 4-week-old piglets were intranasally infected with 10 6 PFU of either wild-type PrV strain Kaplan (PrV-Ka), PrV-9112C2, or PrV-9112C2R, in which the PrV gB gene was reinserted instead of the BHV-1 gB gene. Animals infected with PrV-Ka and PrV-9112C2R showed a similar course of disease, i.e., high fever, marked respiratory symptoms but minimal neurological disorders, and excretion of high amounts of virus. All animals survived the infection. In contrast, animals infected with PrV-9112C2 showed no respiratory symptoms and developed only mild fever. However, on day 5 after infection, all piglets developed severe central nervous system (CNS) symptoms leading to death within 48 to 72 h. Detailed histological analyses showed that PrV-9112C2R infected all regions of the nasal mucosa and subsequently spread to the CNS preferentially by the trigeminal route. In contrast, PrV-9112C2 primarily infected the olfactory epithelium and spread via the olfactory route. In the CNS, more viral antigen and significantly more pronounced histological changes resulting in more severe encephalitis were found after PrV-9112C2 infection. Thus, our results demonstrate that replacement of PrV gB by the homologous BHV-1 glycoprotein resulted in a dramatic increase in neurovirulence combined with an alteration in the route of neuroinvasion, indicating that the essential gB is involved in determining neurotropism and neurovirulence of PrV.Pseudorabies virus (PrV) and Bovine herpesvirus 1 (BHV-1) are related alphaherpesviruses of the genus Varicellovirus. PrV, also designated Suid herpesvirus 1, is the causative agent of Aujeszky's disease (AD), a serious illness in domestic and wild animals. PrV has a broad host range and productively infects birds and most mammals, except for horses and higher primates including humans, which are resistant to infection (reviewed in reference 25). Whereas mortality in most infected species regularly amounts to 100%, pigs can survive a productive infection and remain latently infected for life. Thus, pigs a...

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Herpesvirus (pseudorabies virus) latency in swine: Occurrence and physical state of viral DNA in neural tissues

Cited by 98 publications

References 30 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

Detection of Canine Herpesvirus DNA in the Ganglionic Neurons and the Lymph Node Lymphocytes of Latently Infected Dogs.

Pseudorabies Virus Expressing Bovine Herpesvirus 1 Glycoprotein B Exhibits Altered Neurotropism and Increased Neurovirulence

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