Abstract
Since 2015, severe outbreaks of hepatitis-hydropericardium syndrome (HHS), caused by hypervirulent fowl adenovirus serotype 4 (FAdV-4), have emerged in several provinces in China, posing a great threat to poultry industry. So far, factors contributing to the pathogenesis of hypervirulent FAdV-4 have not been fully uncovered. Elucidation of the pathogenesis of FAdV-4 will facilitate the development of effective FAdV-4 vaccine candidates for the control of HHS and vaccine vector. The interaction between pathogen and host defense system determines the pathogenicity of the pathogen. Therefore, the present review highlights the knowledge of both viral and host factors contributing to the pathogenesis of hypervirulent FAdV-4 strains to facilitate the related further studies.
Highlights
Fowl adenovirus serotype 4 (FAdV-4), belonging to the FAdV-C species of the Aviadenovirus genus, the Adenoviridae family, is a non-enveloped, double-stranded DNA virus
Given the great threat posed by hypervirulent FAdV-4 strains to poultry industry, elucidating the pathogenesis of FAdV-4 will facilitate the development of effective FAdV-4 vaccine candidates for the control of hepatitis-hydropericardium syndrome (HHS) and vaccine vector
Mortality patterns showed that seamlessly replacing 1966 bp deletion region of highly pathogenic FAdV-4 with non-pathogenic counterpart did not change the hypervirulent characteristics; the pathogenicity of viruses with substituted fiber-2 or hexon gene significantly changed, compared to that of parental strain. These results strongly suggested that the increased virulence of hypervirulent FAdV-4 was independent of 1966 bp deletion, but closely associated with the fiber-2 and hexon genes [27,28]
Summary
Fowl adenovirus serotype 4 (FAdV-4), belonging to the FAdV-C species of the Aviadenovirus genus, the Adenoviridae family, is a non-enveloped, double-stranded DNA virus. The FAdV-4 capsid consists of three main exposed structural proteins, hexon, fiber and penton base, with the fiber being noncovalently linked to the penton base. The FAdV-4 capsid is characterized by two separate fiber proteins (fiber-1 and fiber-2) associated with each penton base [1]. The prevalence of HHS in China was relatively low with only sporadic outbreaks before 2015. A dramatic increase in HHS outbreaks began in various broiler-raising provinces of China in May 2015. Accumulating data demonstrated that the HHS in China was caused by a novel genotype FAdV-4, and reproduction experiment with SPF chickens revealed its high pathogenicity [14,15,16,17,18,19,20,21,22]. A comprehensive description of the current understanding in the pathogenesis of FAdV-4 is provided
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