Serosurvey of Avian metapneumovirus, Orithobacterium rhinotracheale, and Chlamydia psittaci and Their Potential Association with Avian Airsacculitis

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.

Inactivation of Poliovirus by Ozone and the Impact of Ozone on the Viral Genome

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.