Serological and phylogenetic analysis indicating prevalence of fowl adenovirus in China
Fowl adenoviruses (FAdVs), which belong to the genus  Aviadenovirus  in the Adenoviridae family, are grouped into five species named Fowl adenovirus A–E ( FAdV-A to FAdV - E ) and 12 serotypes (1–11, 8a, 8b) based on genome sequencing and virus neutralisation, respectively. FAdVs are responsible for a wide range of clinical signs, including hydropericardium-hepatitis syndrome (HHS), inclusion body hepatitis (IBH) and gizzard erosion (GE).1 HHS is primarily caused by the FAdV-4 serotype and causes more than 30 per cent mortality.2 3 IBH is related to the multiserotype of FAdVs and leads to 10–30 per cent mortality in chickens. Some FAdV-1 strains are responsible for GE.1 3

Cases of IBH or HHS have been increasing rapidly, resulting in great economic losses worldwide.3–8 In the present study, we determined the prevalence of FAdV infections in chicken flocks in China by serological analysis and characterised the genotypic distribution among the FAdV strains previously reported in China in GenBank database by phylogenetic analysis. Our findings could provide implications for a promising control measure and vaccination strategy for FAdV infection in the poultry industry.

To evaluate the prevalence of FAdV infections in China, a total of 4544 serum samples were collected from 119 different non-vaccinated chicken flocks in 2014–2016. These samples were localised in 13 provinces or cities in …
Fiber2 and hexon genes are closely associated with the virulence of the emerging and highly pathogenic fowl adenovirus 4
Since May 2015, outbreaks of hydropericardium-hepatitis syndrome (HHS) caused by fowl adenovirus 4 (FAdV-4) with a novel genotype have been reported in China, causing significant economic losses to the poultry industry. A previous comparative analysis revealed that highly virulent FAdV-4 isolates contain various genomic deletions and multiple distinct mutations in the major structural genes fiber2 and hexon. To identify the genes responsible for the virulence of HHS-associated novel FAdV-4 isolates, FAdV-4 infectious clones were constructed by directly cloning the whole genome of a highly pathogenic FAdV-4 isolate (CH/HNJZ/2015) and that of a nonpathogenic strain (ON1) into a p15A-cm vector using the ExoCET method. Subsequently, the fiber2, hexon, and 1966-bp fragment-replaced mutant/recombinant viruses were constructed using Redαβ recombineering and ccdB counter-selection techniques. The pathogenicity of the rescued viruses was compared with that of the rescued parent viruses rHNJZ and rON1 in 3-week-old SPF chickens. Chickens infected with the rescued viruses carrying the fiber2 and/or hexon gene of the HNJZ strain developed similar clinical signs to the natural infection, with distinctive gross lesions and characteristic histological signs indicative of HHS observed in sick/dead chickens. Our results clearly demonstrated that the virulence of the novel highly pathogenic FAdV-4 strain was independent of the 1966-bp deletion and that the fiber2 and hexon genes have crucial roles in FAdV-4 pathogenicity. The data presented in this report will provide further insights into the crucial factors determining the pathogenicity of FAdV strains. Furthermore, the infectious clones generated based on the FAdV-4 genome can be used as a platform for studies of gene function and for the development of recombinant vaccines.
Adrenocorticotropin insensitivity syndromes.
I. Introduction II. Familial Glucocorticoid Deficiency A. Clinical presentation B. Investigation C. Treatment D. Pathogenesis III. Triple A Syndrome A. Clinical features B. Treatment C. Pathogenesis D. Mapping of triple A syndrome gene E. Candidate genes IV. Acquired ACTH Resistance V. Conclusions