Latency of Aujeszky's disease virus

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