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Pathogenesis of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus

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Authors

도두이티엔

Advisor
Chanhee Chae, DVM, PhD
Major
수의과대학 수의학과
Issue Date
2015-08
Publisher
서울대학교 대학원
Keywords
PhD dissertattion
Description
학위논문 (박사)-- 서울대학교 대학원 : 수의학과(수의병리학전공), 2015. 8. 채찬희.
Abstract
Porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV) is the causative agent of PRRS. A new disease syndrome known as high fever disease was first reported in China in 2006, since then spreading rapidly in neighboring Asian countries such as Vietnam, Laos, Cambodia, Myanmar, Philippines, and Russia. Currently, infection of HP-PRRSV causes very huge economic loss for the Asian swine industry. This high fever disease was recognized as an atypical form of PRRS and the causative virus was named as highly pathogenic PRRSV (HP-PRRSV). In Vietnam, HP-PRRSV lead to the death of thousands of pigs as the virus spread from northern through central and to southern Vietnam within 3 months of the first outbreaks in 2007.

The first study aimed to compare the virulence of northern and southern Vietnamese strains of highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) as assessed by the level of viral replication, gross and microscopical lung lesions and virus distribution in experimentally infected pigs. The northern and southern Vietnamese HP-PRRSV strains share 96.7% (non-structural protein 2) and 99.3% (open reading frame 5) nucleotide identity. On experimental challenge, approximately 50% of pigs infected with northern Vietnamese HP-PRRSV died, while death was not observed in any pigs infected with southern Vietnamese HP-PRRSV. Mean viral titres (expressed as log10TCID50/mL) were significantly (P <0.05) higher in sera and lungs from pigs infected with the northern Vietnamese HP-PRRSV than from those infected with the southern Vietnamese strain at multiple time points. Lung lesion scores and PRRSV antigen within pulmonary and lymphoid lesions were significantly (P <0.05) higher in pigs infected with northern Vietnamese HP-PRRSV than in those receiving southern Vietnamese HP-PRRSV at multiple time points. PRRSV antigens were observed in cardiac myocytes, gastric and renal tubular epithelial cells, and astrocytes and microglia of white matter in the brain from pigs infected with the northern Vietnamese HP-PRRSV strain only. Thus, genetic similarity did not predict the degree of virulence of these strains. Northern Vietnamese HP-PRRSV was more virulent and had extended tissue tropism when compared with southern Vietnamese HP-PRRSV.

The objective of the second study was to compare the pathogenicity of highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) infection between wild and domestic pigs based on clinical, immunological, and pathological evaluation. Upon challenge with HP-PRRSV, five wild pigs died compared to none of the domestic. Anti-PRRSV antibody titers were significantly (P < 0.05) higher in wild HP-PRRSV-infected pigs versus the domestic HP-PRRSV-infected pigs at 21 days post inoculation (dpi). Lung lesion scores at 7 dpi were also significantly (P < 0.01) higher in domestic infected pigs than wild infected pigs. The most striking difference was the viral tissue distribution between the wild and domestic HP-PRRSV-infected pigs. HP-PRRSV-positive cells were observed in bronchiolar, gastric, and renal tubular epithelial cells from wild HP-PRRSV-infected pigs only. The results in this study demonstrated a genetic difference exists between wild and domestic pigs, which could results in different clinical signs, immunological responses, and pathological outcomes to HP-PRRSV infection.

In the last study, a total of 34 highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) strains isolated from Vietnam during 2013?2014 were sequenced and analyzed. Partial sequence of nonstructural protein 2 (Nsp2) gene and full sequence of open reading frame 5 (ORF5) gene was used for the analysis. The HP-PRRSV strains were isolated from pig herds that had never been vaccinated for PRRSV. The nucleotide homology of Nsp2 and ORF5 ranged between 96.4 to 100% and 83.2 to 100%, respectively. All of the 34 Vietnamese HP-PRRSV strains showed two discontinuous 30 amino acids deletions in the Nsp2 gene as a genetic marker of prototypic Chinese HP-PRRSV. Amino acids at position 13 and 151 in ORF5 are arginine (R) in 29 out of 34 Vietnamese HP-PRRSV isolates as those in prototypic Chinese HP-PRRSV. Genomic analysis of ORF5 from all Vietnamese HP-PRRSVs revealed six subgroups
Viet 1 to 4, JXA1-like, and VR-2332-like. Nucleotide and amino acid sequence analysis of 34 Vietnamese HP-PRRSV isolated during 2013?2014 indicate that Vietnamese HP-PRRSV has undergone rapid evolutionary changes in recent years when compared with Vietnamese HP-PRRSV isolated before 2012.

Conclusively, genetic similarity did not predict the degree of virulence of these strains. Northern Vietnamese HP-PRRSV was more virulent and had extended tissue tropism when compared with southern Vietnamese HP-PRRSV. The genetic difference exists between wild and domestic pigs, which could results in different clinical signs, immunological responses, and pathological outcomes to HP-PRRSV infection


Keywords: highly pathogenic porcine reproductive and respiratory syndrome virus
pathogenicity
respiratory disease
genetic difference
pig
wild pig.

Student number: 2013-31339
Language
English
URI
https://hdl.handle.net/10371/120216
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