Aujeszky’s Disease (Pseudorabies) in Pigs

Wittmann, G.; Rziha, Hanns-Joachim

doi:10.1007/978-1-4613-1587-2_7

Cited by 108 publications

(112 citation statements)

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“…Viral spread between adult swine occurs primarily via direct mucosal contact. Common sequelae of wild-type PRV infection include respiratory disease, weight loss, and infertility in pregnant gilts and sows (31). In contrast, PRV infection is lethal in neonatal piglets and in nonnative hosts such as cows, dogs, rodents, and other susceptible animals.…”

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confidence: 99%

Two Modes of Pseudorabies Virus Neuroinvasion and Lethality in Mice

Brittle

Reynolds

Enquist

2004

J Virol

123

142

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We describe two distinct modes of neuroinvasion and lethality after murine flank inoculation with virulent and attenuated strains of pseudorabies virus (PRV). Mice infected with virulent (e.g., PRV-Becker, PRVKaplan, or PRV-NIA3) strains self-mutilate their flank skin in response to virally induced pruritus, die rapidly with no identifiable symptoms of central nervous system (CNS) infection such as behavioral abnormalities, and have little infectious virus or viral antigen in the brain. In distinct contrast, animals infected with an attenuated PRV vaccine strain (PRV-Bartha) survive approximately three times longer than wild-type PRVinfected animals, exhibit severe CNS abnormalities, and have an abundance of infectious virus in the brain at the time of death. Interestingly, these animals have no skin lesions and do not appear pruritic at any time during infection. The severe pruritus and relatively earlier time until death induced by wild-type PRV infection may reflect the peripheral nervous system (PNS) and immune responses to infection rather than a fatal, virally induced CNS pathology. Based on previously characterized afferent (sensory) and efferent (motor) neuronal pathways that innervate the skin, we deduced that wild-type virulent strains transit through the PNS via both afferent and efferent routes, whereas PRV-Bartha travels by only efferent routes in the PNS en route to the brain.Pseudorabies virus (PRV), a swine alphaherpesvirus, is a member of the alphaherpesvirus subfamily, including human and animal pathogens such as varicella-zoster virus, herpes simplex virus type 1 (HSV-1) and HSV-2, bovine herpesvirus types 1 and 5, and equine herpesviruses types 1 and 4 (23). Although the natural hosts of PRV are adult swine, PRV is pantropic, infecting avian embryos and a wide range of mammalian species, with the notable exceptions of humans and other higher-order species of nonhuman primates.PRV routinely establishes a latent infection in PNS ganglia of adult swine and yet rarely invades the central nervous systems (CNS) of these animals (8). Viral spread between adult swine occurs primarily via direct mucosal contact. Common sequelae of wild-type PRV infection include respiratory disease, weight loss, and infertility in pregnant gilts and sows (31). In contrast, PRV infection is lethal in neonatal piglets and in nonnative hosts such as cows, dogs, rodents, and other susceptible animals. In these animals, infection induces severe, uncontrollable pruritus (itchiness), culminating in frantic selfmutilating behavior historically described as "mad itch." Death ensues within days of infection with virulent strains of PRV. The cause of death of these animals has traditionally been ascribed to fatal encephalitis.Adult swine infected with live, attenuated vaccine strains such as PRV-Bartha typically exhibit few, if any, symptoms of infection. In addition, most attenuated PRV strains are significantly less virulent in nonnative hosts such as rodents (8). Despite the attenuated phenotype, PRV-Bartha remains neuroinvas...

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Two Modes of Pseudorabies Virus Neuroinvasion and Lethality in Mice

Brittle

Reynolds

Enquist

2004

J Virol

123

142

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“…HSV-1 and -2 are human pathogens that cause clinical disease involving mucocutaneous surfaces, the central nervous system (CNS) and occasionally visceral organs (Corey, 1991). PRV is a natural pathogen of swine that causes a contagious, epidemic disease characterized by CNS and upper respiratory tract infection (Wittman & Rziha, 1988). PRV is also neurotropic and disease in infant pigs results in high mortality.…”

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“…To explore infectivity in vivo, 3-day-old pigs were inoculated intranasally with HSV-1, HSV-2 or PRV and examined over 3 weeks for evidence of clinical infection. Piglets less than 2 weeks of age are most susceptible to infection by PRV (Wittman & Rziha, 1988). By the natural route of infection through intranasal mucosal surfaces, which also allows neuronal invasion and spread, less than 103 p.f.u, of virus results in 100% mortality in piglets (Wittman & Rziha, 1988).…”

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confidence: 99%

“…Piglets less than 2 weeks of age are most susceptible to infection by PRV (Wittman & Rziha, 1988). By the natural route of infection through intranasal mucosal surfaces, which also allows neuronal invasion and spread, less than 103 p.f.u, of virus results in 100% mortality in piglets (Wittman & Rziha, 1988). Three-day-old piglets from four litters were inoculated intranasally with HSV-1 (1.2x 106p.f.u.)…”

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Defective entry of herpes simplex virus types 1 and 2 into porcine cells and lack of infection in infant pigs indicate species tropism

Subramanian¹,

LeBlanc

Wardley

et al. 1995

Journal of General Virology

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We have determined if a defect at entry of the human pathogen herpes simplex virus type 1 (HSV-1) into cultured porcine cells extends to Herpes simplex virus (HSV) and pseudorabies virus (PRV) are related alphaherpesviruses that have a broad cell host range, many collinear genes and similar replicative cycles and clinical outcome in their natural hosts (Roizman & Sears, 1990;Wittman & Rziha, 1988). HSV-1 and -2 are human pathogens that cause clinical disease involving mucocutaneous surfaces, the central nervous system (CNS) and occasionally visceral organs (Corey, 1991). PRV is a natural pathogen of swine that causes a contagious, epidemic disease characterized by CNS and upper respiratory tract infection (Wittman & Rziha, 1988). PRV is also neurotropic and disease in infant pigs results in high mortality. PRV does not cause clinical infection in humans and infection has not been proven virologically or serologically in suspected cases (Hussell et al., 1963; Jenzsch & Apostoloff, 1970;Mbravak et al., 1987).The outcome of virus infection is determined by the interactions between the virus and host cell constituents. The cellular or molecular basis for the broad host range and the natural mammalian hosts for these herpesviruses is not understood. Recent studies indicate that determinants of tropism occur in the cell surface receptors used for HSV-1 entry into porcine cells (Subramanian et al., 1994) and at replication post-entry for PRV into some human cells (G. Subramanian et al., unpublished results). The major obstacles to understanding HSV * Author for correspondence. Fax +1 313 764 3562. e-mail fullerao@umich.edu infection, pathogenesis and tropism have been the unavailability of a cell line that lacks the surface component(s) required for virus entry and the lack of a non-susceptible animal model for HSV infection. In this report we show that the poor susceptibility of cultured porcine cells extends to HSV-2, also because of a defect in entry. Furthermore, the in vitro restriction to HSV correlates with lack of HSV replication and no clinical infection of infant pigs in vivo, indicating that cellular receptor(s) contribute to HSV species tropism.Yields of infectious HSV-1 and HSV-2 from swine testis (ST) cells were three to four orders of magnitude lower over time than from human embryonic lung (HEL) cells (Fig. l a). Exposure to either HSV-1 or HSV-2 produced extensive CPE by 36 h post-infection in HEL cells but minimal CPE in ST cells (data not shown). PRV-infected ST cells also showed extensive CPE and produced approximately l0 s p.f.u., comparable to the high virus yields observed from HSV-infected HEL cells. Even at a 300-fold higher HSV input (Fig. 1 a), few foci of infection were observed in ST cells. Virus yields increased, but titres were still two orders of magnitude below the yields from low input virus into human cells.Infectious cell centres of ST and HEL cells were compared to determine the number of cells that became infected with HSV (Fig. 1 b). The number of HSV-1-or HSV-2-infected ST ce...

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Reactions of oligodendrocyte precursor cells to alpha herpesvirus infection of the central nervous system

Levine

Enquist

Card

1998

Glia

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Adult animals harbor an abundant population of oligodendrocyte precursor cells (OPCs) whose functions, other than providing a pool of precursors for oligodendrocytes, are unknown. Previous studies have demonstrated that these unusual glial cells, which can be identified by virtue of their expression of the NG2 chondroitin sulfate proteoglycan, react to traumatic brain injury. To determine the generality of the ability of OPCs to react to neuropathological insults, we have examined the reactions of OPCs to infection of the brainstem with virulent and attenuated strains pseudorabies virus (PRV). When motor neurons within the dorsal vagal complex are infected with PRV, OPCs immediately adjacent to the infected neurons display dramatic reactive changes. These changes are characterized by (1) cell bodies that stain more heavily with antibodies against NG2 than do non‐reactive OPCs, (2) an increased density of processes, and (3) the appearance of fine filopodia on the cell body and processes. The onset of these morphological changes was rapid, and they occurred simultaneously with the appearance of viral antigens in motor neurons. At late stages of infection, the soma of OPCs elaborated fewer processes. A small number of the reactive OPCs contain viral antigens. These findings extend the range of neuropathological situations to which OPCs react indicating that this cell population is extremely dynamic. They also suggest that the reaction of OPCs and the consequences of these reactions to brain function must be considered in any procedure, either experimental or clinical, in which viruses are introduced into the central nervous system. GLIA 23:316–328, 1998. © 1998 Wiley‐Liss, Inc.

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Aujeszky’s Disease (Pseudorabies) in Pigs

Cited by 108 publications

References 172 publications

Two Modes of Pseudorabies Virus Neuroinvasion and Lethality in Mice

Two Modes of Pseudorabies Virus Neuroinvasion and Lethality in Mice

Defective entry of herpes simplex virus types 1 and 2 into porcine cells and lack of infection in infant pigs indicate species tropism

Reactions of oligodendrocyte precursor cells to alpha herpesvirus infection of the central nervous system

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