Bovine Herpesvirus 5 Glycoprotein E Is Important for Neuroinvasiveness and Neurovirulence in the Olfactory Pathway of the Rabbit

Chowdhury, Shafiqul I.; Lee, B. J.; Özkul, Aykut; Weiss, Mark L.

doi:10.1128/jvi.74.5.2094-2106.2000

Cited by 70 publications

(94 citation statements)

References 57 publications

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“…Infectious virus, viral antigens and DNA were found in limited portions of the CNS of one out of six calves infected with the recombinant (Hübner et al 2005). These results are in contrast with previous experiments performed with different gE and US9 BoHV-5 recombinants (Chowdhury et al 2000(Chowdhury et al , 2002. A BoHV-5 gE -recombinant was able to induce neurological signs in about 10 % of the infected rabbits and no deaths, while the wild type virus caused apparent neurological disease in 70 to 80 % of the infected animals.…”

Section: Discussioncontrasting

confidence: 56%

“…As gI, gE and US9 were previously reported to play a role in neurovirulence of BoHV-5 (Chowdhury et al 2000(Chowdhury et al , 2002, the present study was carried out to examine the neurovirulence and the potential for reactivation of a recombinant BoHV-5 lacking the gI, gE and US9 genes. When the recombinant BoHV-5 gI -/gE -/US9 -was inoculated intranasally in four weeks-old rabbits, it was less virulent than the wild type BoHV-5.…”

Section: Discussionmentioning

confidence: 99%

“…The pathogenicity of BoHV-5 with either gE or US9 negative recombinants has been previously evaluated. In an experimental infection of rabbits with a BoHV-5 gE negative recombinant, the virus dissemination in CNS and induction of neurological signs were significantly impaired (Chowdhury et al 2000). In addition, also for BoHV-5, US9 was shown to play an important role in viral transport from the olfactory receptor neurons to second order neurons within the olfactory bulb of rabbits, and a US9 negative BoHV-5 recombinant was virtually nonpathogenic and failed to invade the CNS (Chowdhury et al 2002).…”

Section: Introductionmentioning

confidence: 99%

“…Several viral proteins seem to contribute to the neurovirulence of alphaherpesviruses (Chowdhury et al 2000, Mettenleiter 2003. Glycoprotein E (gE) is a nonessential glycoprotein which is predominantly found complexed with glycoprotein I (gI) in alphaherpesviruses (Dingwell et al 1995).…”

Section: Introductionmentioning

confidence: 99%

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Experimental infection of rabbits with a recombinant bovine herpesvirus type 5 (BoHV-5) gI, gE and US9-negative

et al. 2009

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Bovine herpesvirus type 5 (BoHV-5) is a major cause of viral meningoencephalitis in cattle. The expression of different viral proteins has been associated with BoHV-5 neuropathogenesis. Among these, gI, gE and US9 have been considered essential for the production of neurological disease in infected animals. To evaluate the role of gI, gE and US9 in neurovirulence, a recombinant from which the respective genes were deleted (BoHV-5 gI-/gE-/US9-) was constructed and inoculated in rabbits of two age groups (four and eight weeks-old). When the recombinant virus was inoculated through the paranasal sinuses of four weeks-old rabbits, neurological disease was observed and death was the outcome in 4 out of 13 (30.7 %) animals, whereas clinical signs and death were observed in 11/13 (84.6%) of rabbits infected with the parental virus. In eight weeks-old rabbits, the BoHV-5 gI-/gE-/US9- did not induce clinically apparent disease and could not be reactivated after dexamethasone administration, whereas wild type BoHV-5 caused disease in 55.5% of the animals and was reactivated. These findings reveal that the simultaneous deletion of gI, gE and US9 genes did reduce but did not completely abolish the neurovirulence of BoHV-5 in rabbits, indicating that other viral genes may also play a role in the induction of neurological disease.

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Section: Discussioncontrasting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Experimental infection of rabbits with a recombinant bovine herpesvirus type 5 (BoHV-5) gI, gE and US9-negative

et al. 2009

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“…However, BoHV-5 gE is not essential for the initial entry into the olfactory pathway [20]. Glycoprotein I is not required for the neurovirulence of gE in BoHV-5 [3], but a glycine-rich BoHV-5 gE-specific epitope is essential for expression of the full virulence potential of BoHV-5 [4].…”

Section: Viral Glycoproteinsmentioning

confidence: 99%

Ruminant alphaherpesviruses related to bovine herpesvirus 1

et al. 2006

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-Herpesviruses have mainly co-evolved with their hosts for millions of years. Consequently, different related host species may have been infected by various genetically related herpesviruses. Illustrating this concept, several ruminant alphaherpesviruses have been shown to form a cluster of viruses closely related to bovine herpesvirus 1 (BoHV-1): namely bovine herpesvirus 5, bubaline herpesvirus 1, caprine herpesvirus 1, cervid herpesviruses 1 and 2 and elk herpesvirus 1. These viruses share common antigenic properties and the serological relationships between them can be considered as a threat to BoHV-1 eradication programmes. BoHV-1 is a herpesvirus responsible for infectious bovine rhinotracheitis, which is a disease of major economic concern. In this article, the genetic properties of these ruminant alphaherpesviruses are reviewed on a comparative basis and the issue of interspecific recombination is assessed. The pathogenesis of these infections is described with emphasis on the host range and crossing of the host species barrier. Indeed, the non bovine ruminant species susceptible to these ruminant alphaherpesviruses may be potential BoHV-1 reservoirs. The differential diagnosis of these related infections is also discussed. In addition, available epidemiological data are used to assess the potential of cross-infection in ruminant populations. A better knowledge of these ruminant alphaherpesvirus infections is essential to successfully control infectious bovine rhinotracheitis.

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Molecular association of herpes simplex virus type 1 glycoprotein E with membrane protein Us9

Awasthi

Friedman

2016

Arch Virol

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Herpes simplex virus type 1 (HSV-1) glycoprotein E (gE), glycoprotein I (gI), and Us9 promote efficient anterograde axonal transport of virus from the neuron cytoplasm to the axon terminus. HSV-1 and PRV gE and gI form a heterodimer that is required for anterograde transport, but an association that includes Us9 has not been demonstrated. NS-gE380 is an HSV-1 mutant that has five amino acids inserted after gE residue 380, rendering it defective in anterograde axonal transport. We demonstrated that gE, gI and Us9 form a trimolecular complex in Vero cells infected with NS-gE380 virus in which gE binds to both Us9 and gI. We detected the complex using immunoprecipitation with anti-gE or anti-gI monoclonal antibodies in the presence of ionic detergents. Under these conditions, Us9 did not associate with gE in cells infected with wild-type HSV-1; however, using a nonionic detergent, TritonX-100, an association between Us9 and gE was detected in immunoprecipitates of both wild-type and NS-gE380-infected cells. The results suggest that the interaction between Us9 and gE is weak and disrupted by ionic detergents in wild-type infected cells. We postulate that the tight interaction between Us9 and gE leads to the antero-grade spread defect in the NS-gE380 virus.

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Bovine Herpesvirus 5 Glycoprotein E Is Important for Neuroinvasiveness and Neurovirulence in the Olfactory Pathway of the Rabbit

Cited by 70 publications

References 57 publications

Experimental infection of rabbits with a recombinant bovine herpesvirus type 5 (BoHV-5) gI, gE and US9-negative

Experimental infection of rabbits with a recombinant bovine herpesvirus type 5 (BoHV-5) gI, gE and US9-negative

Ruminant alphaherpesviruses related to bovine herpesvirus 1

Molecular association of herpes simplex virus type 1 glycoprotein E with membrane protein Us9

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