Seasonal outbreaks of airsacculitis in China's poultry cause great economic losses annually. This study tried to unveil the potential role of Avian metopneumovirus (AM PV), Ornithobacterium rhinotrocheale (aRT) a...Seasonal outbreaks of airsacculitis in China's poultry cause great economic losses annually. This study tried to unveil the potential role of Avian metopneumovirus (AM PV), Ornithobacterium rhinotrocheale (aRT) and Chlarnydia psittaci (CPS) in avian airsacculitis. A serological investigation of 673 breeder chickens and a case-controlled study of 430 birds were undertaken. Results showed that infection with AMPV, aRT, and CPS was highly associated with the disease. The correlation between AMPV and CPS were positively robust in both layers and broilers. Finally, we determined the co-infection with AMPV, aRT, and CPS was prevalent in the sampled poultry farms suffering from respiratory diseases and the outbreak of airsacculitis was closely related to simultaneous exposure to all three agents.展开更多
Objective To investigate the mechanisms underlying ozone-induced inactivation of poliovirus type 1(PV1). Methods We used cell culture, long‐overlapping RT‐PCR, and spot hybridization assays to verify and accurately ...Objective To investigate the mechanisms underlying ozone-induced inactivation of poliovirus type 1(PV1). Methods We used cell culture, long‐overlapping RT‐PCR, and spot hybridization assays to verify and accurately locate the sites of action of ozone that cause PV1 inactivation. We also employed recombinant viral genome RNA infection models to confirm our observations. Results Our results indicated that ozone inactivated PV1 primarily by disrupting the 5′-non‐coding region(5′‐NCR) of the PV1 genome. Further study revealed that ozone specifically damaged the 80‐124 nucleotide(nt) region in the 5′-NCR. Recombinant viral genome RNA infection models confirmed that PV1 lacking this region was non‐infectious. Conclusion In this study, we not only elucidated the mechanisms by which ozone induces PV1 inactivation but also determined that the 80‐124 nt region in the 5′‐NCR is targeted by ozone to achieve this inactivation.展开更多
基金supported in part by the Ministry of Science and Technology(MoST),China under Grant No.2016YFE0127100 and 2017YFD0500705-5(HE Cheng)supported by the State Key Laboratory of Veterinary Etiological Biology,Lanzhou Veterinary Research Institute,Chinese Academy of Agricultural Sciences+1 种基金Supported by Beijing Natural Science Foundation[No.6172019]partially funded by Taishan Scholar Project No.ts201511084
文摘Seasonal outbreaks of airsacculitis in China's poultry cause great economic losses annually. This study tried to unveil the potential role of Avian metopneumovirus (AM PV), Ornithobacterium rhinotrocheale (aRT) and Chlarnydia psittaci (CPS) in avian airsacculitis. A serological investigation of 673 breeder chickens and a case-controlled study of 430 birds were undertaken. Results showed that infection with AMPV, aRT, and CPS was highly associated with the disease. The correlation between AMPV and CPS were positively robust in both layers and broilers. Finally, we determined the co-infection with AMPV, aRT, and CPS was prevalent in the sampled poultry farms suffering from respiratory diseases and the outbreak of airsacculitis was closely related to simultaneous exposure to all three agents.
基金supported by the National Key R&D Program of China [2017YFC1601200,2018YFC1602500]Tianjin Science and Technology Support Program [16YFZCSF00340]
文摘Objective To investigate the mechanisms underlying ozone-induced inactivation of poliovirus type 1(PV1). Methods We used cell culture, long‐overlapping RT‐PCR, and spot hybridization assays to verify and accurately locate the sites of action of ozone that cause PV1 inactivation. We also employed recombinant viral genome RNA infection models to confirm our observations. Results Our results indicated that ozone inactivated PV1 primarily by disrupting the 5′-non‐coding region(5′‐NCR) of the PV1 genome. Further study revealed that ozone specifically damaged the 80‐124 nucleotide(nt) region in the 5′-NCR. Recombinant viral genome RNA infection models confirmed that PV1 lacking this region was non‐infectious. Conclusion In this study, we not only elucidated the mechanisms by which ozone induces PV1 inactivation but also determined that the 80‐124 nt region in the 5′‐NCR is targeted by ozone to achieve this inactivation.