Dissemination of wild-type and gC-, gE- and gI-deleted mutants of Aujeszky's disease virus in the maxillary nerve and trigeminal ganglion of pigs after intranasal inoculation

Kritas, Spiridon K.; Nauwynck, Hans; Pensaert, Maurice

doi:10.1099/0022-1317-76-8-2063

Cited by 47 publications

(39 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The correct sorting of HSV-1 to tight junctions is apparently dependent on the cytoplasmic domain of gE (23). Similar to the situation in HSV-1, the PrV gE-gI complex is nonessential for growth in vitro (68), but PrV is impaired in neuropathogenicity after deletion of gE or gI (10,24,61,52,54,56). It has also been shown that deletion of gM in addition to gE and gI results in PrV or equine herpesvirus 1 (EHV-1) progeny that are severely compromised in virus release and cell-to-cell spread of infectivity (6,50).…”

mentioning

confidence: 75%

Glycoproteins E and I of Marek's Disease Virus Serotype 1 Are Essential for Virus Growth in Cultured Cells

Schumacher

Tischer

Reddy

et al. 2001

J Virol

View full text Add to dashboard Cite

mentioning

confidence: 75%

Glycoproteins E and I of Marek's Disease Virus Serotype 1 Are Essential for Virus Growth in Cultured Cells

Schumacher

Tischer

Reddy

et al. 2001

J Virol

View full text Add to dashboard Cite

“…We have further demonstrated that wild-type virus (PRV Becker), but not PRV Bartha, injected into neck musculature of a cat replicates efficiently in DRG neurons serving the inoculated muscles (8). Several laboratories have demonstrated that the absence of the gE and gI genes from PRV Bartha accounts for the restricted spread in neurons in a variety of animal models (1,3,10,12,22,25,26,29,31,45). The PRV Bartha strain carries a large deletion in the unique short region of the genome that removes not only the gE and gI coding sequences but also all of the Us9 gene and part of the Us2 coding sequences (27,29,34).…”

mentioning

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

113

169

View full text Add to dashboard Cite

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...

show abstract

“…These genes encode the envelope glycoproteins E and I (gE and gI, respectively) and an envelope-tegument protein, Us9 (8,10,25,26,31). The gE/gI homologues in alphaherpesviruses are expressed on the infected-cell membrane.…”

mentioning

confidence: 99%

Bovine Herpesvirus 5 (BHV-5) Us9 Is Essential for BHV-5 Neuropathogenesis

Chowdhury

Onderci

Bhattacharjee

et al. 2002

J Virol

View full text Add to dashboard Cite

Bovine herpesvirus 5 (BHV-5) is a neurovirulent alphaherpesvirus that causes fatal encephalitis in calves.In a rabbit model, the virus invades the central nervous system (CNS) anterogradely from the olfactory mucosa following intranasal infection. In addition to glycoproteins E and I (gE and gI, respectively), Us9 and its homologue in alphaherpesviruses are necessary for the viral anterograde spread from the presynaptic to postsynaptic neurons. The BHV-5 Us9 gene sequence was determined, and the predicted amino acid sequence of BHV-5 Us9 was compared with the corresponding Us9 sequences of BHV-1.1. Alignment results showed that they share 77% identity and 83% similarity. BHV-5 Us9 peptide-specific antibody recognized a doublet of 17-and 19-kDa protein bands in BHV-5-infected cell lysates and in purified virions. To determine the role of the BHV-5 Us9 gene in BHV-5 neuropathogenesis, a BHV-5 Us9 deletion recombinant was generated and its neurovirulence and neuroinvasive properties were compared with those of a Us9 rescue mutant of BHV-5 in a rabbit model. Following intranasal infection, the Us9 rescue mutant of BHV-5 displayed a wild-type level of neurovirulence and neural spread in the olfactory pathway, but the Us9 deletion mutant of BHV-5 was virtually avirulent and failed to invade the CNS. In the olfactory mucosa containing the olfactory receptor neurons, the Us9 deletion mutant virus replicated with an efficiency similar to that of the Us9 rescue mutant of BHV-5. However, the Us9 deletion mutant virus was not transported to the bulb. Confocal microscopy of the olfactory epithelium detected similar amounts of virus-specific antigens in the cell bodies of olfactory receptor neuron for both the viruses, but only the Us9 rescue mutant viral proteins were detected in the processes of the olfactory receptor neurons. When injected directly into the bulb, both viruses were equally neurovirulent, and they were transported retrogradely to areas connected to the bulb. Taken together, these results indicate that Us9 is essential for the anterograde spread of the virus from the olfactory mucosa to the bulb.

show abstract

Dissemination of wild-type and gC-, gE- and gI-deleted mutants of Aujeszky's disease virus in the maxillary nerve and trigeminal ganglion of pigs after intranasal inoculation

Cited by 47 publications

References 16 publications

Glycoproteins E and I of Marek's Disease Virus Serotype 1 Are Essential for Virus Growth in Cultured Cells

Glycoproteins E and I of Marek's Disease Virus Serotype 1 Are Essential for Virus Growth in Cultured Cells

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

Bovine Herpesvirus 5 (BHV-5) Us9 Is Essential for BHV-5 Neuropathogenesis

Contact Info

Product

Resources

About