Latency of Aujeszky's disease virus

\nAujeszky's Disease Virus (ADV) has the property of \nestablishing reactivatable latency in tissues of pigs that survive an acute infection. The\nlatency is then central to the maintenance of the infections caused \nby this herpesvirus in swine populations. Shortly after Steven's first description of the\nneuronal latency established in murine models by the human \nalphaherpesvirus herpes simplex virus (Science 173 (1971) 843-845), Sabo and Rajcani (Acta\nVirol. 20 (1976) 208-214) reported that ADV is also able to establish\nlatency in sensory ganglia and probably other tissues of the swine host. The molecular\ndetection of the latent ADV, initiated by Rhiza et al. \n(Virology 155 (1986) 600-613), confirmed that central and peripheral nervous system tissues\nare the most consistent sites of latency of ADV. The molecular\nunderstanding of alphaherpesvirus latency has now advanced significantly. It is clear that\nall alphaherpesviruses maintain, during latency, a basic transcriptional \nactivity that is restricted to selected genes, a circumstance that seems to be essential for\nan efficient reactivation from the latent infection. While the knowledge\nspecifically based on the ADV model still remains fragmentary, it is becoming increasingly\nclear, through information collected with other closely-related \nalphaherpesvirus models, that the transcripts expressed during latency may involve the\ntranslation of protein products. These protein(s) may distinctly \nmodulate the survival of the neuron and therefore affect the delicate balance between latency\nand reactivation. The advent of single neuron techniques has \nrecently allowed researchers to reach a more thorough, quantitative understanding of the\nfrequency of latency and reactivation in a same tissue. A \nfascinating point still waiting for a mechanistic explanation is the consistent detection of\nADV DNA in tonsils throughout long time post-infection,\nwhich would be seemingly coupled to the expression of latency transcripts in those tissues.\nThis would suggest the possibility that ADV latency may \nalso be established in non-neuronal, dividing cells. From a clinical standpoint, the\nserological detection of latently infected pigs has been\ncrucial to the success of differential "marker" vaccines. Likewise, the massive application\nof different ADV vaccines has demonstrated that the phenomenon of\nlatency/reactivation can be minimized. Attenuated live vaccine strains can be delivered\nmucosally to block or interfere with the subsequent establishment\nof wild-type latency. Recent advanced techniques that quantitate latent ADV DNA have\nindicated that different vaccine phenotypes vary in their ability \nto prevent latent infection. While vaccines may not completely prevent ADV latency, it has\nbeen amply demonstrated that vaccination can reduce the latency \nlevels in the field to levels compatible with complete eradication of ADV. \n