Duck adenoviruses ( DAdVs ) include serotype 1 ( DAdV-1 ) in the genus Atadenovirus and serotypes 2-4 (DAdV-2, 3, and 4) in the genus Aviadenovirus. DAdV-3 was initially isolated from Chinese Muscovy ducks in 2014, whereby the infected ducks exhibited yellowing and hemorrhaging in the liver, along with slight pericardial effusion, swelling, and hemorrhaging in the kidneys. In recent years, duck adenovirus infections have appeared in Muscovy duck farms in Fujian, Zhejiang, Anhui, Guangdong, and other places in China. They have an incidence rate of 40 to 55% and a mortality rate of 35 to 43%, resulting in great losses to the duck breeding industry. In this study, 7 DAdV-3 strains, designated as TZ193, FJPT20161124, GX20170519, FJZZ, GDMM, AHAQ, and GDHS were isolated from Muscovy ducks in different provinces of China during 2016–2019, and their complete genomics were sequenced. Their genomes all exhibited significant deletions in ORF67 , which also had G to A transitions at the 41st and 977th nt positions, resulting in a stop codon. The pathogenicity of TZ193, a novel isolate of DAdV-3, was investigated in Muscovy ducks. TZ193 caused characteristic lesions of swelling as well as hemorrhagic liver and kidney in the infected ducklings. Moreover, the mortality rate of TZ193 in 5-day-old domestic ducks was 100%. Our data provide concrete evidence for the identification of the DAdV-3 novel variant mutant in China, which effects increased mortality in ducks. This highlights the necessity for monitoring the specific molecular epidemiology of novel DAdV-3 mutants and the development of new vaccines in the future.
Fowl adenoviruses (FAdVs), which are distributed worldwide, have caused considerable economic losses to poultry farms. Co-infection with FAdVs and other avian pathogens has been reported previously. However, the pathogenicity of different serotypes of FAdVs causing co-infection remains unclear. Herein, strain HN from FAdV species C serotype 4 (FAdV-4) and strain AH720 from species E serotype 8a (FAdV-8a) were used to assess the pathogenicity of their co-infection in specific-pathogen-free (SPF) chickens. Compared with chickens infected with FAdV-4 alone, those co-infected with FAdV-4 and FAdV-8a showed similar clinical symptoms, mortality rates and degree of tissue lesions, and notably decreased viral loads of HN. Conversely, the viral loads of AH720 increased markedly in the co-infection group compared with that in chickens infected with AH720 strain alone. Increased viral loads of AH720 in the liver were suspected to contribute to the pathogenicity of chickens co-infected with the HN and AH720 strains. This was further investigated by histopathology and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining analyses. Collectively, these data indicated that co-infection with FAdV-4 and FAdV-8a suppresses the replication and proliferation of FAdV-4 but enhances the replication and proliferation of FAdV-8a in chicken liver. This study will provide valuable information for the further investigation of the interactions between FAdV-4 and FAdV-8a during co-infection.
Fowl adenovirus serotype 4 (FAdV-4), the causative agent of hepatitis-hydropericardium syndrome (HHS), distributed widely in the poultry farms in China. Hexon is one of the major capsid proteins associated with viral species or serotypes. However, the epitopes of Hexon protein remain largely unknown. In this study, a monoclonal antibody (mAb) specific to Hexon protein of FAdV-4, designated as 3G8, was generated. Subsequently, the linear peptide recognized by 3G8 was mapped and identified as 213AYGAYVK219 using a series of overlapping peptides generated from Hexon protein. Amino acid sequence analysis revealed that the epitope recognized by 3G8 was highly conserved across all the FAdVs. The epitope was immunogenic and could be recognized by FAdV-4 positive chicken serum samples. These findings will enrich our knowledge regarding the epitope on Hexon and provide valuable information for further characterization of the antigenicity of Hexon protein.
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