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Microbiology and Molecular Biology Reviews, September 2005, p. 462-500, Vol. 69, No. 3
1092-2172/05/$08.00+0     doi:10.1128/MMBR.69.3.462-500.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Molecular Biology of Pseudorabies Virus: Impact on Neurovirology and Veterinary Medicine

Lisa E. Pomeranz,* Ashley E. Reynolds, and Christoph J. Hengartner{dagger}

Department of Molecular Biology, Princeton University, Princeton, New Jersey 08540

Pseudorabies virus (PRV) is a herpesvirus of swine, a member of the Alphaherpesvirinae subfamily, and the etiological agent of Aujeszky's disease. This review describes the contributions of PRV research to herpesvirus biology, neurobiology, and viral pathogenesis by focusing on (i) the molecular biology of PRV, (ii) model systems to study PRV pathogenesis and neurovirulence, (iii) PRV transsynaptic tracing of neuronal circuits, and (iv) veterinary aspects of pseudorabies disease. The structure of the enveloped infectious particle, the content of the viral DNA genome, and a step-by-step overview of the viral replication cycle are presented. PRV infection is initiated by binding to cellular receptors to allow penetration into the cell. After reaching the nucleus, the viral genome directs a regulated gene expression cascade that culminates with viral DNA replication and production of new virion constituents. Finally, progeny virions self-assemble and exit the host cells. Animal models and neuronal culture systems developed for the study of PRV pathogenesis and neurovirulence are discussed. PRV serves as a self-perpetuating transsynaptic tracer of neuronal circuitry, and we detail the original studies of PRV circuitry mapping, the biology underlying this application, and the development of the next generation of tracer viruses. The basic veterinary aspects of pseudorabies management and disease in swine are discussed. PRV infection progresses from acute infection of the respiratory epithelium to latent infection in the peripheral nervous system. Sporadic reactivation from latency can transmit PRV to new hosts. The successful management of PRV disease has relied on vaccination, prevention, and testing.

* Corresponding author. Present address: Laboratory of Molecular Genetics, The Rockefeller University, 1230 York Ave., Campus Box 305, New York, NY 10021. Phone: (212) 327-8953. Fax: (212) 327-7420. E-mail: lisa.pomeranz{at}gmail.com.

{dagger} Present address: School of Natural Health and Sciences, Barry University, Miami Shores, FL 33161.

Microbiology and Molecular Biology Reviews, September 2005, p. 462-500, Vol. 69, No. 3
1092-2172/05/$08.00+0     doi:10.1128/MMBR.69.3.462-500.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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