Life beyond eradication: veterinary viruses in basic science
To some, the focus of research in virology entails the search for solutions of practical problems. By definition then, attention is limited to those viruses that cause disease or to exploitation of some aspect of virology to a practical end (e.g., antivir
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w. Enquist
Department of Molecular Biology, Princeton University, Princeton, New Jersey, U.S.A.
Summary. To some, the focus of research in virology entails the search for solutions of practical problems. By definition then, attention is limited to those viruses that cause disease or to exploitation of some aspect of virology to a practical end (e.g., antiviral drugs or vaccines). Once a disease is cured, or the agent eradicated, it is time to move on to something else. To others, virology offers the opportunity to study fundamental problems in biology. Work on these problems may offer no obvious practical justification; it is an affliction of the terminally curious, perhaps with the outside hope that something "useful" will come of it. To do this so-called "basic science", one must find the most tractable system to solve the problem, not the system that has "relevance" to disease. I have found that veterinary viruses offer a variety of opportunities to study relevant problems at the fundamental level. To illustrate this point, I describe some recent experiments in my laboratory using pseudorabies virus (PRV), a swine herpesvirus.
Introduction Research in my laboratory centers on the molecular biology of neurotropic alphaherpesviruses, a subfamily in the Herpesviridae family [51]. The human viruses are well known - herpes simplex virus types 1 and 2 (HSV-l, HSV-2) and varicellazoster virus (VZV) [58]. Common domestic animals have their own unique alphaherpesviruses as well, e.g., bovine herpes virus type I (BHV-I) in cattle, equine herpes virus type 1 (EHV-l) in horses, Marek's disease virus (MDV) in chickens, and pseudorabies virus (PRV) of pigs [59]. Despite having the ability to infect many cell types, these viruses invariably infect neurons in the periphery and travel inside neurons to sensory ganglia where they establish either a productive or nonproductive (latent) infection (Fig. 1). The latent infection ensures longterm survival of virus in the host population. Viral replication usually occurs first in non-neuronal cells, followed by spread of virus into afferent (e.g., sensory) or efferent (e.g., motor) nerve fibers innervating the infected tissue. Under some circumstances, virus may enter neurons directly with no prior replication in
C. H. Calisher et al. (eds.), 100 Years of Virology © Springer-Verlag Wien 1999
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L. W. Enquist
Spread of PRV to the Nervous System After Peripheral Infection
Virus Infection at Mucosal Surface
Anows Indicate direction of nerv" impulse
Fig. 1 Routes of spread to the nervous system after infection of a peripheral site. The cartoon illustrates virus infection at a generalized mucosal surface (left) where virus spreads among polarized epithelial cells. Depending on the surface, different cells can be found below the epithelial cell layer. Four types of neurons whose processes or cell bodies are in the periphery are illustrated. Any of these may be infected after, or concurrent with, epithelial cell infection, depending on the mucosal surface. The direction of the nerv
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