Glycoprotein C of bovine herpesvirus 5 (BHV-5) confers a distinct heparin-binding phenotype to BHV-1

Liman, Anne; Engels, Monika; Meyer, Gilles; Ackermann, Mathias

doi:10.1007/s007050070039

Cited by 13 publications

(12 citation statements)

References 26 publications

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“…As alphaherpesvirus gC mediates primary attachment of virus to target cells via binding to surface glycans, variability in the heparin binding sites of BHV-5 gC (gC5) and BHV-1 gC (gC1) likely account for differences in their heparin-binding phenotypes (60). Although gC5 and gC1 are 75% identical, the ami- c Names for viruses: EHV-1, equine herpesvirus 1; PRV, pseudorabies virus; EHV-4, equine herpesvirus 4; CaHV-1, caprine herpesvirus 1; HSV-2, herpes simplex virus type 2; FHV-1, feline herpesvirus 1; HHV-6b, human herpesvirus 6B; CeHV-1, cervid herpesvirus 1.…”

Section: Resultsmentioning

confidence: 99%

Genome of Bovine Herpesvirus 5

Delhon

Moraes

et al. 2003

J Virol

143

114

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Here we present the complete genomic sequence of bovine herpesvirus 5 (BHV-5), an alphaherpesvirus responsible for fatal meningoencephalitis in cattle. The 138,390-bp genome encodes 70 putative proteins and resembles the ␣2 subgroup of herpesviruses in genomic organization and gene content. BHV-5 is very similar to BHV-1, the etiological agent of infectious bovine rhinotracheitis, as reflected by the high level of amino acid identity in their protein repertoires (average, 82%). The highest similarity to BHV-1 products (>95% amino acid identity) is found in proteins involved in viral DNA replication and processing (UL5, UL15, UL29, and UL39) and in virion proteins (UL14, UL19, UL48, and US6). Among the least conserved (<75%) are the homologues of immediate-early (IE) proteins BICP0, BICP4, and BICP22, the three proteins being longer in BHV-5 than in BHV-1. The structure of the BHV-5 latency-related (LR) region departs markedly from that of BHV-1 in both coding and transcriptional regulatory regions. Given the potential significance of IE genes and the LR region in virus-neuron interactions, it is likely these differences contribute to BHV-5 neuropathogenicity.

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Section: Resultsmentioning

confidence: 99%

Genome of Bovine Herpesvirus 5

Delhon

Moraes

et al. 2003

J Virol

143

114

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“…Thereafter, sections were fixed with 50 l of 0.4% paraformaldehyde for 5 min at 4°C. Twenty microliters of the probe cocktail, containing a randomly digoxigenin-dUTP-labeled BHV-1 or BHV-5 glycoprotein C probe (31), was added to each section (DIG DNA labeling and detection kit; Roche Diagnostics GmbH, Mannheim, Germany). The samples were denatured by placing the slides on a 95°C heating plate for 6 min.…”

Section: Methodsmentioning

confidence: 99%

“…The virus has only rarely been associated with central nervous disorders (4,5,21,37). In contrast, BHV-5 causes severe encephalitis in calves and, upon experimental infection, in rabbits (31)(32)(33)(34)39).…”

mentioning

confidence: 99%

Both Viral and Host Factors Contribute to Neurovirulence of Bovine Herpesviruses 1 and 5 in Interferon Receptor-Deficient Mice

Abril

Engels

Liman

et al. 2004

J Virol

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Herpes simplex virus (HSV) type 1 and bovine herpesviruses 1 and 5 (BHV-1 and BHV-5) can use the same cellular receptor for entry, but only HSV is known to cause disease in mice. We hypothesized that components of either the innate or the adaptive immune system, or a combination of both, were responsible for curbing replication of BHVs in mice. Therefore, wild-type mice as well as mice with various combined genetic deficiencies in the alpha/beta interferon receptor or gamma interferon receptor and in the ability to produce mature B and T lymphocytes (RAG-2 deletion) were infected with BHV-1 and BHV-5 and monitored clinically, serologically, histopathologically, and virologically. A functional immune system protected the mice from disease and death due to BHV infection, and the immune response was Th1 like. BHV-5 was transported to the central nervous system by the axonal pathway, whereas viremia was required for this outcome with BHV-1. The alpha/beta interferon system was able to obstruct quantitative spread of the viruses in the infected organism. The gamma interferon system had a protective effect against BHV-1, even in mice with the RAG-2 deletion. In contrast, the same mice succumbed to neurological disease and death upon infection with BHV-5. Productively infected neurons were detected only in BHV-5-infected mice with an intact gamma interferon system. We conclude that the alpha/beta interferon system had a protective effect, while an intact gamma interferon system was required for efficient replication of BHV-5 in mouse neurons and for the development of neurological disease.

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“…BoHV-5 gC, although not essential, regulates neurotropism in some areas of the olfactory pathway and is important for BoHV-5 neurovirulence in rabbits [21]. This glycoprotein is also able to transfer the heparin binding phenotype of BoHV-5 to a recombinant BoHV-1 [71].…”

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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Glycoprotein C of bovine herpesvirus 5 (BHV-5) confers a distinct heparin-binding phenotype to BHV-1

Cited by 13 publications

References 26 publications

Genome of Bovine Herpesvirus 5

Genome of Bovine Herpesvirus 5

Both Viral and Host Factors Contribute to Neurovirulence of Bovine Herpesviruses 1 and 5 in Interferon Receptor-Deficient Mice

Ruminant alphaherpesviruses related to bovine herpesvirus 1

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