GLYCOPROTEIN-I OF PSEUDORABIES VIRUS (AUJESZKYS-DISEASE VIRUS) DETERMINES VIRULENCE AND FACILITATES PENETRATION OF THE VIRUS INTO THE CENTRAL-NERVOUS-SYSTEM OF PIGS

In the present study we investigated the virulence and neural spread o f pseudorabies virus (PRV) strains with mutations in the gene encoding glycoprotein I (gI) in 3-week-old pigs which were intranasally infect ed. Mutant M303 (A 125, 126) lacks amino acids valine-125 and cysteine -126 in an immunodominant antigenic region of gI which contains 2 disc ontinuous antigenic domains, whereas mutant virus M304 (Lambda 59, 60) lacks amino acids glycine-59 and aspartic acid-60 in a continuous ant igenic domain. Mutant M301 contains a frame shift mutation. Both mutan ts M301 (gI-) and M303 (Lambda 125, 126) were not virulent for pigs, w hereas mutant M304 (Lambda 59, 60) was as virulent as wild-type PRV. A ll gI mutant viruses replicated in the oropharyngeal mucosa, although M304 (Lambda 59, 60) and wild-type PRV replicated to higher titres tha n M303 (Lambda 125, 126) and M301 (gI-). In contrast to M304 (Lambda 5 9, 60) and wild-type PRV, both mutant viruses M301 (gI-) and M303 (Lam bda 125, 126) were not recovered from any part of the central nervous system at day 6 after infection. To study the spread of M301 (gI-) in the central nervous system in more detail, a second experiment was don e in which 100-fold more virus was intranasally administered and virus was recovered from various tissues at day 4 after infection. Again, n o gI-negative virus was isolated from the central nervous system. We c oncluded that deleting the amino acids valine-125 and cysteine-126 dec reases virulence and reduces neurotropism to the same degree as deleti ng the gI protein. In addition, gI-negative virus does not spread in t he central nervous system of pigs, probably because the transport of t he virus across the synapse is hampered.