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Characterisation of fowl adenovirus (FAdV-8b) strain concerning the geographic analysis and pathological lesions associated with inclusion body hepatitis in broiler flocks in Turkey
2020
Cizmecigil, Utku Yusuf | Umar, Sajid | Yilmaz, Aysun | Bayraktar, Erhan | Turan, Nuri | Tali, Besim | Aydin, Ozge | Tali, Hasan Emre | Yaramanoglu, Mehmetcan | Yilmaz, Semaha Gul | Kolukisa, Ahmet | Sadeyen, Jean-Remy | Munir, Iqbal | Yılmaz, Hüseyin
Fowl adenovirus can cause important diseases in chickens such as inclusion body hepatitis, hepatitis hydropericardium syndrome, and gizzard erosion and ulceration. Inclusion body hepatitis has been regularly reported from many countries. This is the first case report from Turkey, describing an outbreak of inclusion body hepatitis in broiler farms due to fowl adenovirus-8b (FAdV-8b). Broiler flocks with mortality about 10% were visited in Turkey, and necropsy was performed on dead birds. Samples were subjected to PCR assay to detect FAdV and other viral pathogens. After sequencing, phylogenetic analysis was performed and the nucleotide sequences of hexon genes were compared with the FAdV sequences data available in GenBank. Clinical signs such as anorexia, depression, ruffled feathers, huddling, and greenish diarrhoea were observed. Mortality started at the 8ᵗʰ day of age and ranged from 10% to 14%. Necropsy showed severe hepatitis, jaundice, and pancreatitis. The main necropsy findings included a pale, enlarged, haemorrhagic, and friable liver along with swollen and haemorrhagic kidneys and spleen. PCR and sequence analysis revealed the presence of fowl adenovirus serotype 8b (FAdV-E). This is the first report on characterisation and the pathological lesions associated with FAdV in broilers in Turkey. Our findings suggest that FAdV strains could be an emerging pathogen in Turkish broilers and could actively contribute to hepatitis and immunosuppression.
Afficher plus [+] Moins [-]Porcine epidemic diarrhoea virus induces cell-cycle arrest through the DNA damage-signalling pathway
2020
Luo, Yi-Ran | Zhou, Shu-Ting | Yang, Liang | Liu, Yuan-Ping | Jiang, Sheng-Yao | Dawuli, Yeliboli | Hou, Yi-Xuan | Zhou, Tian-Xing | Yang, Zhi-Biao
Porcine epidemic diarrhoea virus (PEDV) infection causes watery diarrhoea, vomiting, anorexia, and weight loss, especially among neonatal piglets, inflicting on them morbidity and mortality potentially reaching 90%–100%. Despite it being known that certain mammalian cell phases are arrested by PEDV, the mechanisms have not been elucidated, and PEDV pathogenesis is poorly understood. This study determined the effect of an epidemic PEDV strain on cell cycle progression. We observed the effect of the PEDV SHpd/2012 strain on an infected Vero cell cycle through flow cytometry and Western blot, investigating the interrelationships of cell-cycle arrest, the DNA damage–signalling pathway caused by PEDV and the phosphorylation levels of the key molecules Chk.2 and H2A.X involved upstream and downstream in this pathway. PEDV induced Vero cell-cycle arrest at the G1/G0 phase. The phosphorylation levels of Chk.2 and H2A.X increased with the prolongation of PEDV infection, and no significant cell-cycle arrest was observed after treatment with ATM or Chk.2 inhibitors. The proliferation of PEDV was also inhibited by treatment with ATM or Chk.2 inhibitors. PEDV-induced cell-cycle arrest is associated with activation of DNA damage–signalling pathways. Our findings elucidate the molecular basis of PEDV replication and provide evidence to support further evaluation of PEDV pathogenesis.
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