Pseudorabies virus infections in explants of porcine nasal mucosa

Pol, J.M.A.; Quint, Wim; Kok, G. L.; Broekhuysen-Davies, J.

doi:10.1016/0034-5288(91)90052-p

Cited by 15 publications

(16 citation statements)

References 19 publications

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“…To obtain more information about the role of UL21 gene products in the natural host, we studied all strains in porcine nasal mucosa explant cultures, because they closely mimic the in vivo situation [16,25].…”

Section: Discussionmentioning

confidence: 99%

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Deletion of the UL21 gene in Pseudorabies virus results in the formation of DNA-deprived capsids: an electron microscopy study

Wagenaar¹,

Pol²,

Wind

et al. 2001

Vet. Res.

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-We studied the morphogenesis of three pseudorabies virus mutants lacking parts of the gene homologous to the UL21 gene of the herpes simplex virus type 1. The mutants were examined in an SK-6 cell-line, in an SK-6 cell-line expressing the UL21 gene product, in porcine lung alveolar macrophages (PLAM) and in porcine nasal mucosa explants. Although on SK-6 cells and PLAM, the virus-assembly and egress of mutant virus M155, lacking almost the entire UL21 gene, was similar to that of the rescued PRV mutant, M155 producing virions containing little or no DNA (Atype particles). Virus mutants M133 and M134 (lacking 23 and 232 amino acids respectively) produced more C-type particles. In SK-6 cells stably expressing the UL21-encoded protein, all mutants produced C-type particles. All mutants produced C-type particles in nasal mucosa explants, indicating that the UL 21-gene product is not essential for virus production in porcine tissue. These results support and extend previous work that indicated a role for the UL21 encoded protein in the packaging of newly replicated viral DNA. electron microscopy / morphology / pseudorabies virus / UL21 gene Résumé -La délétion du gène UL21 du virus de la maladie d'Aujeszky résulte dans la formation de capsides dépourvues d'ADN : étude en microscopie électronique. Nous avons étudié la morphogenèse de trois mutants du virus de la maladie d'Aujeszky (VMA) comportant des délétions dans l'homologue du gène UL21 du virus de l'herpes simplex de type 1. Les mutants ont été examinés dans une lignée cellulaire SK-6, dans une lignée SK-6 exprimant le produit du gène UL21, dans des Vet. Res. 32 (2001) 47-54 47

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Section: Discussionmentioning

confidence: 99%

“…During packaging, concatameric viral DNA is cleaved and subsequently packaged into the preformed capsids [20,26] yielding capsids with electron dense cores [16,17,20,22,25,28]. According to Booy et al [5] viral DNA is packed as locally ordered, liquid-crystalline, parallel packings of DNA duplexes.…”

Section: Introductionmentioning

confidence: 99%

Deletion of the UL21 gene in Pseudorabies virus results in the formation of DNA-deprived capsids: an electron microscopy study

Wagenaar¹,

Pol²,

Wind

et al. 2001

Vet. Res.

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“…Tissue specimens of lung and nasal mucosa were fixed and processed as described elsewhere (10) and were examined by transmission electron microscopy.…”

Section: Transmission Electron Microscopical Examinationmentioning

confidence: 99%

Pathological, ultrastructural, and immunohistochemical changes caused by Lelystad virus in experimentally induced infections of mystery swine disease (synonym: Porcine epidemic abortion and respiratory syndrome (PEARS))

Pol¹,

Dijk²,

Wensvoort³

et al. 1991

Veterinary Quarterly

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133

104

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“…While the phenotypes of individual null mutants of gE, gI, and Us2 have been analyzed, the phenotype of a PRV Us9 null virus in an otherwise wildtype background has never been reported. All previously char-acterized Us9 mutant viruses contained additional mutations, especially in the neighboring genes, the gI and gE genes (30,32,(35)(36)(37)43). Therefore, to determine the Us9 null phenotype in vitro and in vivo, we constructed two isogenic strains of PRV Becker containing defined mutations in the Us9 gene.…”

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confidence: 99%

Role of Pseudorabies Virus Us9, a Type II Membrane Protein, in Infection of Tissue Culture Cells and the Rat Nervous System

Brideau

Card

Enquist

2000

J Virol

114

169

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The protein product of the pseudorabies virus (PRV) Us9 gene is a phosphorylated, type II membrane protein that is inserted into virion envelopes and accumulates in the trans-Golgi network. It is among a linked group of three envelope protein genes in the unique short region of the PRV genome which are absent from the attenuated Bartha strain. We found that two different Us9 null mutants exhibited no obvious phenotype after infection of PK15 cells in culture. Unlike those of gE and gI null mutants, the plaque size of Us9 null mutants on Madin-Darby bovine kidney cells was indistinguishable from that of wild-type virus. However, both of the Us9 null mutants exhibited a defect in anterograde spread in the visual and cortical circuitry of the rat. The visual system defect was characterized by restricted infection of a functionally distinct subset of visual projections involved in the temporal organization of behavior, whereas decreased anterograde spread of virus to the cortical projection targets was characteristic of animals receiving direct injections of virus into the cortex. Spread of virus through retrograde pathways in the brain was not compromised by a Us9 deletion. The virulence of the Us9 null mutants, as measured by time to death and appearance of symptoms of infection, also was reduced after their injection into the eye, but not after cortical injection. Through sequence analysis, construction of revertants, measurement of gE and gI protein synthesis in the Us9 null mutants, and mixedinfection studies of rats, we conclude that the restricted-spread phenotype after infection of the rat nervous system reflects the loss of Us9 and is not an indirect effect of the Us9 mutations on expression of glycoproteins gE and gI. Therefore, at least three viral envelope proteins, Us9, gE, and gI, function together to promote efficient anterograde transneuronal infection by PRV in the rat central nervous system.Pseudorabies virus (PRV) is a neurotropic alphaherpesvirus of the Herpesviridae family that is able to infect neurons of both the peripheral and central nervous systems of a wide variety of mammals and birds (4, 39). When PRV replicates and spreads in the nervous system, it acts as a self-amplifying tracer of synaptically connected neurons (10, 16). Integral to this process is the demonstrated ability of the virus to exploit the polarized cellular architecture of neurons and move throughout the brain of a host organism. Thus, assays of the spread of virus through the brain naturally incorporate a determination of the direction of viral transport through a circuit. Direction in the nervous system is defined by the terms "anterograde" and "retrograde," which can be used to describe directional movement of virus inside a cell as well as the spread of virus between synaptically connected neurons. We use the terms anterograde spread and retrograde spread in this report to describe movement of virus between synaptically connected neurons. Spread from the primary infected neuron to the second-order uninfected neuron in...

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Pseudorabies virus infections in explants of porcine nasal mucosa

Cited by 15 publications

References 19 publications

Deletion of the UL21 gene in Pseudorabies virus results in the formation of DNA-deprived capsids: an electron microscopy study

Deletion of the UL21 gene in Pseudorabies virus results in the formation of DNA-deprived capsids: an electron microscopy study

Pathological, ultrastructural, and immunohistochemical changes caused by Lelystad virus in experimentally induced infections of mystery swine disease (synonym: Porcine epidemic abortion and respiratory syndrome (PEARS))

Role of Pseudorabies Virus Us9, a Type II Membrane Protein, in Infection of Tissue Culture Cells and the Rat Nervous System

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