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Conference Paper: PRRSV– A Role In The “high Fever” Pandemic Swine Disease In China?

TitlePRRSV– A Role In The “high Fever” Pandemic Swine Disease In China?
Authors
Issue Date2007
Citation
2007 International PRRS Symposium, Chicago, IL, December 2007 How to Cite?
AbstractA large-scale outbreak of an unknown porcine disease associated with high fever emerged in mainland China from mid 2006 to early 2007. Recent study has reported that the causative factor for this disease outbreak is probably a mutated strain of PRRSV. In Hong Kong, a similar high fever disease outbreak also occurred in early 2007. Lung tissues were collected from deceased animals showing fever and PRRS symptoms and RT-PCR was performed amplifying ORF5 and nsp2 genes for genetic analysis. Phylogenetic analysis of ORF5 nucleotide sequences revealed that the strain (P385) isolated in this outbreak was different from those isolated in mainland China (JXA1, HUB2 and HEB1), with 80.1 to 80.8% nucleotide identity. On the other hand, these mainland-isolates showed high homology to the samples collected locally in typical PRRSV-infected animals in 2004 to 2005 (98.9 to 99.1 % similarity). Identical amino acid sequences were observed in the hypervarible region I and II. Therefore, it is seemed that the outbreak of the high fever disease may not be directly related to the variations in this major neutralizing epitope. Besides, study on the nsp2 protein indicated that the P385 strain contained two discontinuous deletions with the sizes of 125 and 5 amino acids. When compared with the VR-2332 strain, these deletions occurred in positions 315-440 and 483-487 respectively, which were downstream to the cysteine protease (PL2) domain of the nsp2 protein. The P385 strain was inoculated into MARC-145 cells in parallel with strains possessed similar ORF5 sequence but no deletion in nsp2. Preliminary result showed that such discontinuous deletions did not confer a higher virulence in vitro than those of the wild type PRRSV. Therefore, it was believed that such deletion event did not necessarily contribute to the increase in PRRSV virulence, and thus lead to outbreak of the high fever disease. Further characterization and in vivo studies are to be carried out to clarify the role of PRRSV and its nsp2 protein in this epidemic. In summary, deletion occurred in nsp2 of PRRSV may not completely account for the outbreak of the high fever disease. Some other factors, for example, co-infection with PCV2, may probably be involved in exerting selective pressure to the virus and affecting the pathogenic process. PRRSV – a role in the “High fever” pandemic swine disease in China? | Request PDF. Available from: https://www.researchgate.net/publication/279824357_PRRSV_-_a_role_in_the_High_fever_pandemic_swine_disease_in_China?ev=auth_pub [accessed Aug 17 2018].
DescriptionNational Pork Board
Persistent Identifierhttp://hdl.handle.net/10722/257916

 

DC FieldValueLanguage
dc.contributor.authorHui, RKH-
dc.contributor.authorWong, TWL-
dc.contributor.authorLeung, FCC-
dc.date.accessioned2018-08-17T02:56:36Z-
dc.date.available2018-08-17T02:56:36Z-
dc.date.issued2007-
dc.identifier.citation2007 International PRRS Symposium, Chicago, IL, December 2007-
dc.identifier.urihttp://hdl.handle.net/10722/257916-
dc.descriptionNational Pork Board-
dc.description.abstractA large-scale outbreak of an unknown porcine disease associated with high fever emerged in mainland China from mid 2006 to early 2007. Recent study has reported that the causative factor for this disease outbreak is probably a mutated strain of PRRSV. In Hong Kong, a similar high fever disease outbreak also occurred in early 2007. Lung tissues were collected from deceased animals showing fever and PRRS symptoms and RT-PCR was performed amplifying ORF5 and nsp2 genes for genetic analysis. Phylogenetic analysis of ORF5 nucleotide sequences revealed that the strain (P385) isolated in this outbreak was different from those isolated in mainland China (JXA1, HUB2 and HEB1), with 80.1 to 80.8% nucleotide identity. On the other hand, these mainland-isolates showed high homology to the samples collected locally in typical PRRSV-infected animals in 2004 to 2005 (98.9 to 99.1 % similarity). Identical amino acid sequences were observed in the hypervarible region I and II. Therefore, it is seemed that the outbreak of the high fever disease may not be directly related to the variations in this major neutralizing epitope. Besides, study on the nsp2 protein indicated that the P385 strain contained two discontinuous deletions with the sizes of 125 and 5 amino acids. When compared with the VR-2332 strain, these deletions occurred in positions 315-440 and 483-487 respectively, which were downstream to the cysteine protease (PL2) domain of the nsp2 protein. The P385 strain was inoculated into MARC-145 cells in parallel with strains possessed similar ORF5 sequence but no deletion in nsp2. Preliminary result showed that such discontinuous deletions did not confer a higher virulence in vitro than those of the wild type PRRSV. Therefore, it was believed that such deletion event did not necessarily contribute to the increase in PRRSV virulence, and thus lead to outbreak of the high fever disease. Further characterization and in vivo studies are to be carried out to clarify the role of PRRSV and its nsp2 protein in this epidemic. In summary, deletion occurred in nsp2 of PRRSV may not completely account for the outbreak of the high fever disease. Some other factors, for example, co-infection with PCV2, may probably be involved in exerting selective pressure to the virus and affecting the pathogenic process. PRRSV – a role in the “High fever” pandemic swine disease in China? | Request PDF. Available from: https://www.researchgate.net/publication/279824357_PRRSV_-_a_role_in_the_High_fever_pandemic_swine_disease_in_China?ev=auth_pub [accessed Aug 17 2018].-
dc.languageeng-
dc.relation.ispartofInternational PRRS Symposium-
dc.titlePRRSV– A Role In The “high Fever” Pandemic Swine Disease In China?-
dc.typeConference_Paper-
dc.identifier.emailHui, RKH: rkhhui@hkucc.hku.hk-
dc.identifier.emailLeung, FCC: fcleung@hkucc.hku.hk-
dc.identifier.authorityHui, RKH=rp00711-
dc.identifier.authorityLeung, FCC=rp00731-
dc.identifier.hkuros167643-
dc.publisher.placeChicago, United States-

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