Pathogenic Pseudorabies Virus, China, 2012

Yu, Xiaofang; Zhou, Zhi; Hu, Dongmei; Zhang, Qian; Han, Tao; Li, Xiaoxia; Gu, Xingfang; Yuan, Lin; Zhang, Shuo; Wang, Baoyue; Qu, Peng; Liu, Jinhua; Zhai, Xinyan; Tian, Kegong

doi:10.3201/eid2001.130531

Cited by 178 publications

(138 citation statements)

References 11 publications

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“…PrV is the etiological agent of Aujeszky's disease, causing neurological, respiratory, and reproductive disease in the pig, its natural host. Despite successful vaccination campaigns and eradication of the virus from various countries, pseudorabies outbreaks still occur in swine populations worldwide, as recently reported from China (3). Because latent infection persists for lifetime after recovery from acute disease, pigs latently infected by PrV are a constant danger for virus reactivation, shedding, and spread in susceptible populations (4)(5)(6).…”

mentioning

confidence: 99%

A 2.5-Kilobase Deletion Containing a Cluster of Nine MicroRNAs in the Latency-Associated-Transcript Locus of the Pseudorabies Virus Affects the Host Response of Porcine Trigeminal Ganglia during Established Latency

Mahjoub

Dhorne–Pollet

Fuchs

et al. 2015

J Virol

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The alphaherpesvirus pseudorabies virus (PrV) establishes latency primarily in neurons of trigeminal ganglia when only the transcription of the latency-associated transcript (LAT) locus is detected. Eleven microRNAs (miRNAs) cluster within the LAT, suggesting a role in establishment and/or maintenance of latency. We generated a mutant (M) PrV deleted of nine miRNA genes which displayed properties that were almost identical to those of the parental PrV wild type (WT) during propagation in vitro. IMPORTANCEThis study provides a thorough reference on the establishment of latency by PrV in its natural host, the pig. Our results corroborate the evidence obtained from the study of several LAT mutants of other alphaherpesviruses encoding miRNAs from their LAT regions. Neither PrV miRNA expression nor high LLT expression levels are essential to achieve latency in trigeminal ganglia. Once latency is established by PrV, the only remarkable differences are found in the pattern of host response. This indicates that, as in herpes simplex virus, LAT functions as an immune evasion locus. P seudorabies virus (PrV) is a porcine alphaherpesvirus. The genome of PrV is more than 142 kb in size and is characterized by the presence of 70 different coding genes plus the latency-associated transcript (LAT) locus (1, 2). PrV is the etiological agent of Aujeszky's disease, causing neurological, respiratory, and reproductive disease in the pig, its natural host. Despite successful vaccination campaigns and eradication of the virus from various countries, pseudorabies outbreaks still occur in swine populations worldwide, as recently reported from China (3). Because latent infection persists for lifetime after recovery from acute disease, pigs latently infected by PrV are a constant danger for virus reactivation, shedding, and spread in susceptible populations (4-6).A particular feature of herpesviruses is their ability to establish and maintain latent infections in which the virus genome circularizes and persists as an episome. As for other alphaherpesviruses, neurons in the trigeminal ganglia are the primary site of PrV latency (7). Over this period, transcription of viral lytic genes is repressed and transcription of the viral genome is restricted to the LAT locus overlapping the internal repeat sequence (IR) (8-10).RNAs of multiple sizes are transcribed from the strand opposite that encoding EP0 and IE180, which can be detected in infected Citation Mahjoub N, Dhorne-Pollet S, Fuchs W, Endale Ahanda M-L, Lange E, Klupp B, Arya A, Loveland JE, Lefevre F, Mettenleiter TC, Giuffra E. 2015. A 2.5-kilobase deletion containing a cluster of nine microRNAs in the latencyassociated-transcript locus of the pseudorabies virus affects the host response of porcine trigeminal ganglia during established latency.

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mentioning

confidence: 99%

A 2.5-Kilobase Deletion Containing a Cluster of Nine MicroRNAs in the Latency-Associated-Transcript Locus of the Pseudorabies Virus Affects the Host Response of Porcine Trigeminal Ganglia during Established Latency

Mahjoub

Dhorne–Pollet

Fuchs

et al. 2015

J Virol

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“…This suggested that the PR vaccine was not effective against wild-type PR infection. According to recent studies, the causative agent of the outbreak was a PRV variant that showed enhanced pathogenicity [3,7,8,10]. In the present study, the PRV strain SH2012 was isolated in 2012 from an infected pig farm in Shanghai, China that used the typical vaccine.…”

Section: Discussionmentioning

confidence: 99%

“…The causative agent of the outbreaks was confirmed to be a PRV variant [3,9]. The PRV variant was shown to be both antigenically different from the classical PRVs and more pathogenic in older pigs [3,7,8,10]. Previous studies on immunological protection in sheep have shown that the Bartha-K61 vaccine does not provide complete protection against the emerging PRV variant, but could offer full protection against infection with PRV strain SC (an earlier virulent strain in China) [3,11].…”

Section: Introductionmentioning

confidence: 99%

“…From the 1990s to 2010, the Bartha-K61 vaccine was widely used in Chinese pig herds and PR was effectively controlled [3,4]. However, in October 2011, a severe PRV outbreak occurred in Bartha-K61-vaccinated pig herds on many Chinese farms, resulting in considerable economic losses [5][6][7][8]. The causative agent of the outbreaks was confirmed to be a PRV variant [3,9].…”

Section: Introductionmentioning

confidence: 99%

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Experimental Infection of Sheep With Pseudorabies Viruses Isolated In Shanghai, China, Between 2010 and 2012

Ju¹,

Yang²,

Wang³

et al. 2017

Eur J Exp Bio

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For many years, pseudorabies has been efficiently controlled in China by vaccination. However, a sudden outbreak occurred on many pig farms during 2012-2013. In this study, phylogenetic analysis was carried out with the aim of understanding the genetic relatedness between strains in both populations and comparing strains in China with those circulating in other countries. To obtain more pathogenetic relevant data regarding two pseudorabies virus (PRV) isolates (SH2010 and SH2012) in sheep, we evaluated samples of PRV isolated in Shanghai, China between 2010 and 2012. Based on clinical signs, body temperature variation, and the maximum amounts of viral DNA in unvaccinated/infected sheep, the emerging PRV variant strain, SH2012 was observed to be more highly virulent than the traditional PRV SH2010 strain. The data of the present study will aid in a better understanding of the differences in pathogenicity between the traditional PRV SH2010 strain and the emerging PRV variant strain SH2012.

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“…18 The variant PRV primarily jeopardized pregnant sows and suckling piglets. Of the pregnant sows at a gestational age of 70-90 days, 5-35% experienced spontaneous abortion, 19 while the surviving piglets mainly exhibited anorexia, hydrostomia, vomiting, diarrhea, tremor, and posterior paralysis. The PRV gE gene was detected in clinical samples obtained from pigs from 15 farms in 6 provinces by specific PCR, and analysis of the gE gene sequence showed that all isolates belonged to a relatively independent cluster and contained 2 amino acid insertions.…”

Section: Research-article2015mentioning

confidence: 99%

Outbreak of variant pseudorabies virus in Bartha-K61–vaccinated piglets in central Shandong Province, China

Zhang

et al. 2015

J VET Diagn Invest

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An epidemic that mainly endangered 3–7-day-old piglets struck many farms in Shandong Province, China in 2013 and caused heavy losses. To identify the pathogenesis, the type of lesions, and the causative agent, systemic examinations were performed. Autopsy showed multiple lesions, including necrotic foci of the spleen and liver, punctate hemorrhage of the renal cortex, and interstitial pneumonia. Histological examinations showed typical nonsuppurative encephalitis, necrotic lymphocytes, and reticuloendothelial cells in lymphatic tissues, as well as eosinophilic inclusion bodies in the nuclei of reticuloendothelial cells, necrotic foci in liver cells, and hemorrhagic glomeruli. The average seroprevalence rate of field pseudorabies virus (PRV; Suid herpesvirus 1) of a representative farm tested by enzyme-linked immunosorbent assay was 46%, indicating that the PRV infectious pressure was quite severe especially among gilts, young multiparous sows, boars, and growing–finishing pigs. The glycoprotein E (gE) gene of PRV was detected in 8 of 10 clinical samples, and the virus in the positive samples induced obvious cytopathic effects. An immunoperoxidase monolayer assay showed that PRV antigens were distributed both in the nucleoli and cytoplasm of infected cells. Sequencing and phylogenetic analysis of the gE gene showed that the strain isolated herein, TaiAn SD 2013, was highly similar to previously isolated strains, especially those isolated in northern China in 2013, and was closely related to other isolates from Asia. Evidence confirmed that the variant PRV was the etiologic agent of this epidemic, suggesting that the Bartha-K61 vaccine does not provide complete protection against PRV infection. Further challenge tests are ongoing to investigate the virulence of variant PRV.

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Pathogenic Pseudorabies Virus, China, 2012

Cited by 178 publications

References 11 publications

A 2.5-Kilobase Deletion Containing a Cluster of Nine MicroRNAs in the Latency-Associated-Transcript Locus of the Pseudorabies Virus Affects the Host Response of Porcine Trigeminal Ganglia during Established Latency

A 2.5-Kilobase Deletion Containing a Cluster of Nine MicroRNAs in the Latency-Associated-Transcript Locus of the Pseudorabies Virus Affects the Host Response of Porcine Trigeminal Ganglia during Established Latency

Experimental Infection of Sheep With Pseudorabies Viruses Isolated In Shanghai, China, Between 2010 and 2012

Outbreak of variant pseudorabies virus in Bartha-K61–vaccinated piglets in central Shandong Province, China

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