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A live gI/gE-deleted pseudorabies virus (PRV) protects weaned piglets against lethal variant PRV challenge

Virus Genes, 2017
Emerging pseudorabies virus (PRV) variant has led to frequent outbreaks of PRV infection among Bartha-K61-vaccinated swine population in Chinese swine farms and caused high mortality in pigs of all age since late 2011. Here, we generated a gE/gI-deleted PRV (rPRVXJ-delgI/gE-EGFP) based on PRV variant strain (PRV-XJ) through homologous DNA recombination.
Yue, Yin   +8 more
openaire   +2 more sources

Pseudorabies virus (PRV) is protected from complement attack by cellular factors and glycoprotein C (gC)

Virus Research, 2002
Swine kidney derived CPK cells were resistant to swine complement attack in vitro while rabbit kidney derived RK13 cells were destroyed by swine complement. To rabbit complement, RK13 cells were resistant but CPK cells were sensitive. This phenomenon was known as homologous restriction (Proc. Natl. Acad. Sci. USA 78 (1981) 5118). The gC deletion mutant
Kohshi, Maeda   +4 more
openaire   +2 more sources

Expression of pseudorabies virus gE epitopes in Pichia pastoris and its utilization in an indirect PRV gE-ELISA

Journal of Virological Methods, 2003
Pseudorabies virus glycoprotein E (PRV gE) has been recognized as a suitable diagnostic antigen for pseudorabies. In order to produce gE antigen in large quantities and at low cost, a gene fragment encoding PRV gE epitopes was expressed in Pichia pastoris expression system.
Jing-qun, Ao   +4 more
exaly   +3 more sources

Pseudorabies virus (PRV) early protein 0 activates PRV gene transcription in combination with the immediate-early protein IE180 and enhances the infectivity of PRV genomic DNA

Veterinary Microbiology, 1998
Pseudorabies virus (PRV) early protein 0 (EP0) functions as a transactivator of the viral gene promoters. In transient expression assays employing chloramphenicol acetyl transferase (CAT) reporter constructs, EP0 and the immediate-early protein IE180 act in an additive manner to activate transcription from the thymidine kinase (TK) and glycoprotein G ...
E, Ono   +4 more
exaly   +3 more sources

A Study of the Ability of a TK‐Negative and gI/gE‐Negative Pseudorabies Virus (PRV) Mutant Inoculated by Different Routes to Protect Pigs Against PRV Infection

Journal of Veterinary Medicine, Series B, 2000
SummaryThe capacity of a TK‐negative (TK‐) and gI/gE‐negative (gI/gE‐) pseudorabies virus (PRV) mutant to protect pigs against Aujeszky's disease carried out by experimental infection with a virulent PRV strain, was tested. There were three groups, each of four susceptible pigs which were inoculated twice by two different schedules.
Ferrari M.   +9 more
openaire   +3 more sources

A study of two mutant strains of pseudorabies virus (PRV) unable to express thymidine kinase (TK) function

Journal of Veterinary Medicine, Series B, 1995
SummaryTwo mutant strains of pseudorabies virus (PRV) were selected from the virulent 86/27V virus treated with chemical drugs. The viruses, named 6A1 and 6C2, respectively, appeared to be unable to express thymidine kinase function, as demonstrated by the autoradiography test.
M, Ferrari   +5 more
openaire   +2 more sources

[Expression of truncated gE gene of pseudorabies virus (PRV) and primary application in differential diagnosis of PRV vaccination and infection].

Sheng wu gong cheng xue bao = Chinese journal of biotechnology, 2010
With the application of gE gene deleted pseudarabies virus (PRV) vaccine worldwide, a corresponding differential diagnosis based on gE glycoprotein is needed in the project of PRV eradication. In this study, PRV gE gene without signal and transmembrane region was amplified by PCR and cloned into pGEX-6P-1, generated pGEX-gE.
Jian-Qiang, Ni   +5 more
openaire   +1 more source

The first report of Pseudorabies virus (PRV) DNA detection in wild boars in Croatia

2012
The causative agent of Pseudorabies (Aujeszky’s disease) is Pseudorabies virus (PRV) from the Herpesviridae family, genus Alphaherpesvirus. Although the natural host of the virus are swine, most mammals can be infected and develop severe signs of disease, often resulting in high mortality.
Jemeršić, Lorena   +6 more
openaire   +1 more source

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