Contradictory data have recently been reported on the role of the unique long-internal repeat junction area of pseudorabies (Aujeszky's disease) virus (PrV) genome in the virulence of the virus. To investigate the basis of the difference, four recombinant PrVs mutated at the outer region of inverted repeats that involved a putative latency promoter (P(LAT2)) were constructed in this study. Propagation characteristics of mutant viruses in cultured cells were similar to those of the wild-type virus. However, a 757 bp deletion at this location caused significant reduction in the virulence of PrV after intraperitoneal inoculation of mice and a moderate decrease in the virulence after intracranial inoculation. These results indicate that the P(LAT2) region is an important virulence determinant that may be implicated in the neuroinvasive capability of the virus.
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