Role of envelope glycoproteins gI, gp63 and gIII in the invasion and spread of Aujeszky's disease virus in the olfactory nervous pathway of the pig

Abstract

One-week-old pigs were infected intranasally with the Ka strain of Aujeszky's disease virus (ADV) or with mutants that were lacking the non-essential envelope glycoproteins gI, gp63 or glII. The invasion and spread of these strains in the olfactory nervous pathway were examined by assessing virus levels and by localizing viral antigens in the olfactory mucosa representing the first neuronal level, in the olfactory bulb representing the second neuronal level and in the lateral olfactory gyrus, the rostral perforated substance and the piriform lobe, all representing the third neuronal level. The Ka parental strain invaded and spread up to the third neuronal level. The extent of invasion and spread of the gill-mutant were similar to those of the parental strain. The gp63-mutant replicated normally in the olfactory mucosa, but its spread to all the other levels was limited as compared with that of the parental strain. The gl-mutant showed a defect in infection at all neuronal levels. These results indicate that, of the non-essential envelope glycoproteins, gI plays the major role in neural invasion and spread of ADV in its natural host. The pattern of invasion and spread of these mutants in the olfactory pathway of pigs was similar to that previously observed in the trigeminal pathway. The type of nervous pathway therefore appears not to influence the neuropathogenesis of ADV or mutants deleted in non-essential envelope glycoproteins in the pig.

Glycoprotein gH of Pseudorabies Virus is Essential for Penetration and Propagation in Cell Culture and in the Nervous System of Mice

“…the olfactory, trigeminal, sympathetic and parasympathetic pathways (Babic et al, 1996). These results confirm and extend observations from other laboratories that PrV or HSV-1 gE is implicated in transneuronal transfer rather than in penetration and multiplication in first order neurons (Card et aL, 1992;Ba[an et aI., 1994;Kritas et al, 1994, Mulder et a]., 1994Dingwell et al, 1995;Standish et al, 1994).…”

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

“…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).…”

Cell biological and molecular characteristics of pseudorabies virus infections in cell cultures and in pigs with emphasis on the respiratory tract

“…In naïve pigs, PrV replicates first in the respiratory tract, mainly in the upper part, consisting of the nasal cavity, tonsils and the oropharynx upon intranasal/peroral inoculation. It infects primarily the epithelial cells and within 24 h it crosses the basement membrane in order to infect all cell types in the underlying tissues in a plaquewise fashion (fibrocytes, endothelial cells, mononuclear cells) [31,32,39,56,57,72]. How the virus penetrates easily through the mucus layer barrier on top of the epithelial cells and crosses the basement membrane barrier is not known and deserves more indepth studies.…”

“…PrV gC and gI negative mutants behaved like the wild type virus with respect to the number and size of the foci of infected cells in the mucosa/submucosa. In contrast, the absence of gE and gD resulted in a reduced number of infected cells and gave foci with smaller dimensions [31,32,40]. Concerning the enzymes, it was demonstrated that the absence of viral ribonucleotide reductase, dUTPase and US3-encoded protein kinase was reducing virus excretion in pigs, indicating that the replication was clearly affected [9,20,23].…”