Life beyond eradication: veterinary viruses in basic science

Enquist, Lynn W.

doi:10.1007/978-3-7091-6425-9_7

Cited by 16 publications

(15 citation statements)

References 56 publications

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“…Owing to the significant homology between members of the Alphaherpesvirinae, information derived from the study of PRV provides a powerful opportunity for comparative molecular virology (118). Accordingly, research interests in PRV reflect more than the agricultural impact of the disease it causes.…”

Section: Herpesviridae and Alphaherpesvirinaementioning

confidence: 99%

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

Pomeranz

Reynolds

Hengartner

2005

Microbiol Mol Biol Rev

724

657

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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

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Section: Herpesviridae and Alphaherpesvirinaementioning

confidence: 99%

“…While PRV does not infect humans, experimental studies in nonhuman primates indicate that rhesus monkeys and marmosets are susceptible to infection. Other higher-order primates, such as chimpanzees, are not susceptible to infection (118,211).…”

Section: Lethality Of Pseudorabies Infection In Nonnative Hostsmentioning

confidence: 99%

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

Pomeranz

Reynolds

Hengartner

2005

Microbiol Mol Biol Rev

724

657

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“…PRV can infect most mammals, with the exception of higher-order primates and humans, causing lethal central nervous disorders (Enquist, 1999;Wittmann & Rziha, 1989). PRV is a particularly aggressive virus in young animals where infection is frequently fatal (Nauwynck et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Glycoprotein G from pseudorabies virus binds to chemokines with high affinity and inhibits their function

Viejo‐Borbolla

Muñoz

Tabarés

et al. 2009

Journal of General Virology

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Pseudorabies virus (PRV), also known as suid herpesvirus, is the aetiological agent of Aujeszky's disease in swine. In other animals, except higher-order primates, PRV infection is often fatal. The mechanisms of PRV pathogenesis and immune modulation are largely unknown. PRV codes for 11 glycoproteins. Among them, glycoprotein G (gG) is the most abundant PRV protein found in the supernatant of PRV-infected cell cultures. PRV-gG has low amino acid sequence similarity with gG from other animal alphaherpesviruses and its function is unknown. gG from other animal alphaherpesviruses, with the exception of at least equine herpesvirus 4, binds to chemokines. We show here that PRV-gG binds to the human chemokine CL1 and several CC and CXC human chemokines with high affinity. Chemokine-binding activity can be detected in the supernatants of PRV-infected cell cultures, and insertional inactivation of the gene encoding gG from the PRV genome results in loss of chemokine-binding activity. Binding of PRV-gG to chemokines inhibits chemokine-mediated cell migration, suggesting a role for PRV-gG in immune evasion.

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“…Pseudorabies virus (PRV) is an alphaherpesvirus of swine, but it has an exceptionally broad host range to include lethal infection of a variety of mammals and some birds (19,40,48). PRV infections of baby pigs and non-natural hosts invariably involve invasion of the CNS.…”

mentioning

confidence: 99%

Transcriptome Signature of Virulent and Attenuated Pseudorabies Virus-Infected Rodent Brain

Paulus

Sollars

Pickard

et al. 2006

J Virol

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Mammalian alphaherpesviruses normally establish latent infections in ganglia of the peripheral nervous system in their natural hosts. Occasionally, however, these viruses spread to the central nervous system (CNS), where they cause damaging, often fatal, infections. Attenuated alphaherpesvirus derivatives have been used extensively as neuronal circuit tracers in a variety of animal models. Their circuit-specific spread provides a unique paradigm to study the local and global CNS response to infection. Thus, we systematically analyzed the host gene expression profile after acute pseudorabies virus (PRV) infection of the CNS using Affymetrix GeneChip technology. Rats were injected intraocularly with one of three selected virulent and attenuated PRV strains. Relative levels of cellular transcripts were quantified from hypothalamic and cerebellar tissues at various times postinfection. The number of cellular genes responding to infection correlated with the extent of virus dissemination and relative virulence of the PRV strains. A total of 245 out of 8,799 probe sets, corresponding to 182 unique cellular genes, displayed increased expression ranging from 2-to more than 100-fold higher than in uninfected tissue. Over 60% thereof were categorized as immune, proinflammatory, and other cellular defense genes. Additionally, a large fraction of infection-induced transcripts represented cellular stress responses, including glucocorticoid-and redox-related pathways. This is the first comprehensive in vivo analysis of the global transcriptional response of the mammalian CNS to acute alphaherpesvirus infection. The differentially regulated genes reported here are likely to include potential diagnostic and therapeutic targets for viral encephalitides and other neurodegenerative or neuroinflammatory diseases.

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Life beyond eradication: veterinary viruses in basic science

Cited by 16 publications

References 56 publications

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

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

Glycoprotein G from pseudorabies virus binds to chemokines with high affinity and inhibits their function

Transcriptome Signature of Virulent and Attenuated Pseudorabies Virus-Infected Rodent Brain

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