Efficacy of Various Non‐Oily Adjuvants in Immunization Against the Aujeszky's Disease (Pseudorabies) Virus

Vázquez

Journal of Veterinary Medicine Series A

et al. 1995

Summary Blue foxes were inoculated orally with Aujeszky's disease virus. Several foxes were killed at the onset of clinical signs and other animals spontaneously died. The incubation period ranged from 3 to 6 days and was followed by a short illness characterized by anorexia, depression and coma. At autopsy, no specific gross findings were observed. Microscopically, lesions included a non‐suppurative meningoencephalitis with neuronal necrosis, gliosis, neuronophagia and mononuclear cell cuffing. Viral antigen was detected by immunoperoxidase technique.

Section: Methodsmentioning

confidence: 99%

Experimental Aujeszky's Disease in Blue Foxes (Alopex lagopus

Vázquez

Journal of Veterinary Medicine Series A

et al. 1995

“…The E-974 strain is a high-virulence field strain of PRV which was isolated in northwestern Spain from the brain tissue of naturally infected pigs and adapted to cell culture. Information about the preparation, characterization, and use of this strain has been published previously (2,10,29,30,31). The titer of the virus suspension, determined on BHK-21 cells, was 10 6.5 50% tissue culture infective doses of PRV-E-974 per ml.…”

Section: Animalsmentioning

confidence: 99%

L-Particle Production during Primary Replication of Pseudorabies Virus in the Nasal Mucosa of Swine

Alemañ¹,

et al. 2003

J Virol

Different tissue culture cell lines infected with a number of alphaherpesviruses produce, in addition to virions, light particles (L particles). L particles are composed of the envelope and tegument components of the virion but totally lack the proteins of the capsid and the virus genome; therefore, they are noninfectious. In this electron microscopy report, we show that L particles are produced during primary replication of the alphaherpesvirus pseudorabies virus (PRV) in the nasal mucosa of experimentally infected swine, its natural host. Although PRV infected different types of cells of the respiratory and olfactory mucosae, PRV L particles were found to be produced exclusively by epithelial cells and fibroblasts. We observed that formation of noninfectious particles occurred by budding of condensed tegument at the inner nuclear membrane and at membranes of cytoplasmic vesicles, resulting in intracisternal and intravesicular L particles, respectively. Both forms of capsidless particles were clearly distinguishable by the presence of prominent surface projections on the envelope and the higher electron density of the tegument, morphological features which were only observed in intravesicular L particles. Moreover, intravesicular but not intracisternal L particles were found to be released by exocytosis and were also identified extracellularly. Comparative analysis between PRV virion and L-particle morphogenesis indicates that both types of virus particles share a common intracellular pathway of assembly and egress but that they show different production patterns during the replication cycle of PRV.The only purpose of a virus is to perpetuate its genome, and this objective is achieved through parasitization of a host cell and subsequent production of infectious progeny. In the case of alphaherpesviruses, virions released from infected cells are the sole product of virus replication with the capacity to infect new cells and thus to maintain the virus in nature. Alphaherpesvirus virions consist of four distinct morphological components, each of them playing an important role in the infectious process: (i) an external lipid bilayer envelope that contains virus-encoded proteins essential for the attachment and fusion of the virus envelope with the plasma membrane of target cells (11,25,36); (ii) a characteristic layer (known as the tegument) consisting of proteins that are transferred into the cytosol immediately after virus entry and that enhance the ability of virions to initiate the process of infection (7,8,32); and (iii) an icosahedral capsid (consisting of 162 capsomers) that contains and transports (iv) a double-stranded linear DNA molecule up to the nuclear envelope, where the capsid interacts with the nuclear pore complexes to release the virus genome into the nucleus (15, 27, 32). After virus gene expression and DNA replication, progeny nucleocapsids assemble in the nucleus and reach the cytoplasm by envelopment followed by deenvelopment at the nuclear membranes. Recent data indicate that the definitive v...

“…Eight pigs were infected intranasally with a virulent strain of PRV isolated in northwestern Spain (INIA reference no. E-974) from brain tissue of naturally infected pigs and adapted to cell culture according to the method described by Puentes et al (36). Each inoculated animal was given 2 ml of suspension containing 10 6.5 50% tissue culture infective doses of PRV per ml, 1 ml per nostril.…”

Section: Animals and Virusmentioning

confidence: 99%

Induction and Inhibition of Apoptosis by Pseudorabies Virus in the Trigeminal Ganglion during Acute Infection of Swine

Alemañ¹,

et al. 2001

J Virol

We examined the ability of pseudorabies virus (PRV) to induce and suppress apoptosis in the trigeminal ganglion during acute infection of its natural host. Eight pigs were intranasally inoculated with a virulent field strain of PRV, and at various early times after inoculation, the trigeminal ganglia were assessed histologically. PRV-infected cells were detected by use of immunohistochemistry and in situ hybridization, and apoptosis was identified by in situ terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling. Light and electron microscopy was also used for morphological studies. Apoptosis was readily detected among infiltrating immune cells that were located surrounding PRV-infected neurons. The majority of PRV-infected neurons did not show morphological or histochemical evidence of apoptosis, even including those neurons that were surrounded by numerous inflammatory cells and exhibited profound pathological changes. However, neuronal virus-induced apoptosis also occurred but at a sporadic low level. These findings suggest that PRV is able to block apoptosis of infected trigeminal ganglionic neurons during acute infection of swine. Furthermore, our results also suggest that apoptosis of infiltrating inflammatory cells may represent an important viral mechanism of immune evasion.