Submitted to: Archives of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/15/1997
Publication Date: N/A
Citation: Interpretive Summary: Pseudorabies virus causes Aujeszky's disease in pigs which results in large economic losses annually in the swine industry. While there is an eradication program being implemented in the United States today, outbreaks of this disease still occur. One of the reasons the disease continues to exist is due to the ability of this virus to establish a latent infection in pigs. During latency, the virus goes into "hiding" in the animal, and the animal appears healthy. However, the virus can be brought out of hiding during a process called reactivation. Reactivation of the virus results in shedding of infectious virus causing its spread to uninfected animals. At this time, it is unclear how reactivation occurs. We are studying reactivation from latency so that we can develop better methods for preventing transmission of pseudorabies virus between animals. In this study, we have shown that a single viral gene product can stimulate reactivation of pseudorabies virus. Our work differs from work previously done by others, because the latent infection was established naturally in pigs rather than in an artificial system. This type of information is critical in allowing us to gain a better understanding of reactivation which is necessary for improved control of pseudorabies virus.
Technical Abstract: Pseudorabies virus (PrV), like other alphaherpesviruses, is a neurotropic virus which can establish a latent infection in swine. Reactivation of PrV from latency may occur spontaneously or after induction with corticosteroids. The mechanisms involved in the establishment of latency and reactivation are currently unknown. Here, we examined gene-specific reactivation of PrV by herpes simplex virus type 1 (HSV-1) immediate early protein, ICP-0. Primary neuronal cell cultures established from the trigeminal ganglia of latently infected swine were superinfected with recombinant adenoviruses expressing ICP-0. Reactivation of PrV occurred in cultures that were superinfected with two different ICP-0-expressing adenovirus recombinants, but not in cultures that were either mock-infected, or superinfected with wild-type adenovirus, or recombinant adenoviruses not expressing ICP-0. Infectious PrV was detected between 4 and 7 days postinfection, regardless of the promoter driving expression of ICP-0. Results from these experiments show that HSV-1 ICP-0, a homolog of PrV EPO, can induce PrV reactivation from trigeminal ganglia of latently infected swine.