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.

Aujeszky's disease virus (ADV) is a well known neurotropic virus in pigs. In the present study the mechanism of spread of ADV along the maxillary nerve and the role of the viral envelope glycoproteins gC, gE and gI in this process was examined in pigs. The Ka parental strain of ADV and its gC-, gE-and gI-deleted mutants were inoculated intranasally in pigs, after which virus dissemination in the maxillary nerve and the trigeminal ganglion was monitored at time intervals by means of virus isolation. The parental strain was isolated from both the nasal mucosa and the trigeminal ganglion at 21 h post-inoculation (p.i.), whereas the middle part of the connecting maxillary nerve was positive only after 48 h p.i. It appears, therefore, that ADV travels from the nasal mucosa via the nerve towards the ganglion in a non-infectious form, and then replicates in the neuronal somas, after which infectious virus is transported towards the nasal mucosa. Although all mutants were present at 48h p.i. in the nasal mucosa and the trigeminal ganglion, the appearance of infectious virus in the maxillary nerve was clearly delayed with the gE-and gI mutants. It is suggested that glycoproteins gE and gI are involved in the axonal transport of infectious ADV away from neuronal cell bodies, also called anterograde transport.