Enquist Lab Research

Pseudorabies Virus (PRV)

Pseudorabies Virus (PRV) as a Model System

Our a-herpesvirus of choice is PRV, a broad host range herpesvirus that causes fatal encephalitis in a wide variety of animal species except its natural host, the adult pig. PRV is not a human pathogen and grows well in the lab. Using rodent and chick embryo models and defined mutations in specific PRV genes, we are studying mechanisms of spread from site of primary infection, evasion of innate and acquired immune defense, and cell/tissue damage. We have identified several PRV gene products that affect the extent of PRV pathogenesis in both model systems affecting cell to cell spread, direction of spread, and host response to infection. We have constructed infectious bacterial artificial chromosomes carrying the entire PRV genome and are using E. coli mutagenesis and recombination techniques for genetic analysis of PRV. cDNA analyses coupled with gene array technology are being developed to understand the role of virus and host genes in virus replications in various cell types and tissues of infected animals.

The Alphaherpesvirus Subfamily



Subfamily: alphaherpesvirinae

Human herpes simplex virus types 1 and 2, varicella-zoster virus.  Agricultural pathogens include pseudorabies virus, bovine herpes virus type 1, equine herpesvirus type 1, and Marek's disease virus types 1 and 2.

Subfamily: betaherpesvirinae

Human cytomegalovirus; murine cytomegalovirus; herpesvirus 6 and 7.

Subfamily: gammaherpesvirinae

Epstein-Barr virus and human herpesvirus 8.
Other primate viruses include herpesvirus saimiri and herpesvirus ateles, Rhesus rhadinovirus; murine herpesvirus 68; bovine herpesvirus 4 and equine herpesvirus 2.

Undefined Subfamily:

Channel catfish virus; oyster herpesvirus.


The family Herpesviridae comprises over 120 viruses that infect a wide range of vertebrates and at least one invertebrate (the oyster). While some herpesviruses have broad host ranges, most are restricted to infection of a single species and spread in the population by direct contact or aerosols. The hallmark of herpesvirus infections is the establishment of a lifelong, latent infection that can reactivate to cause one or more rounds of disease. Many herpesvirus infections are inapparent, but if the immune defenses are compromised, infections can be devastating. Eight different herpesviruses have humans as their natural hosts: herpes simplex virus type 1, herpes simplex virus type 2, varicella-zoster virus, Epstein-Barr virus, human cytomegalovirus, human herpesvirus 6, human herpesvirus 7, human herpesvirus 8 (also known as Kaposi's sarcoma-associated herpesvirus).

Alpha herpesviruses:

There are four genera in the alphaherpesvirinae subfamily: simplexvirus, varicellovirus, Marek's disease-like viruses, and infectious laryngotracheitis-like viruses. There are eight known members of the simplexvirus genus and human herpes simplex virus type 1 is the type species. There are 18 members of the varicellovirus genus and human varicella-zoster virus is the type species. There are three members of the Marek's disease-like virus genus and Gallid herpesvirus 2 is the type species. There is one member of the infectious laryngotracheitis-like viruses and Gallid herpesvirus 1 is the type species. There are at least three unassigned members of teh alphaherpesvirinae subfamily (two wallaby herpesviruses and one parrot herpesvirus).

Most alpha herpesviruses follow a common pathway of infection. They establish a primary infection at mucosal or epithelial surfaces and then leave that site by invading the peripheral nervous system (PNS) where they establish a reactivatable latent infection, or by infecting lymphoid cells and entering the circulation (viremia). Normally, these events are relatively benign promoting survival of both virus and host. However, aberrations in this pathway give rise to the set of common diseases caused by these viruses. Invasion of the central nervous system (CNS; the brain and spinal cord) is a rare, but exceedingly serious possibility. The directional spread of a herpes infection from epithelial surfaces to PNS neurons (where latency is established), and then, upon reactivation, spread back to epithelial surfaces constitutes the virus survival strategy.