Fiber-1, Not Fiber-2, Directly Mediates the Infection of the Pathogenic Serotype 4 Fowl Adenovirus via Its Shaft and Knob Domains.

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  • Additional Information
    • Source:
      Publisher: American Society For Microbiology Country of Publication: United States NLM ID: 0113724 Publication Model: Electronic-Print Cited Medium: Internet ISSN: 1098-5514 (Electronic) Linking ISSN: 0022538X NLM ISO Abbreviation: J Virol Subsets: MEDLINE
    • Publication Information:
      Publication: Washington Dc : American Society For Microbiology
      Original Publication: Baltimore, American Society for Microbiology.
    • Subject Terms:
      Adenoviridae/*genetics ; Adenoviridae/*metabolism ; Adenoviridae Infections/*virology ; Capsid Proteins/*genetics ; Capsid Proteins/*metabolism ; Poultry Diseases/*virology; Adenoviridae/pathogenicity ; Adenoviridae Infections/immunology ; Adenoviridae Infections/pathology ; Adenoviridae Infections/prevention & control ; Animals ; Antibodies, Viral ; Cell Line ; Chickens/virology ; Disease Models, Animal ; Female ; Mice ; Mice, Inbred BALB C ; Poultry Diseases/immunology ; Poultry Diseases/pathology ; Poultry Diseases/prevention & control ; Protein Domains ; Serogroup ; Viral Vaccines/immunology
    • Abstract:
      Recently, the disease of hepatitis-hydropericardium syndrome (HPS) caused by serotype 4 fowl adenovirus (FAdV-4) has spread widely and resulted in huge economic losses to the poultry industry. Although the genome of FAdV-4 has two fiber genes (fiber-1 and fiber-2), the exact role of the genes in the infection of FAdV-4 is barely known. In this study, through superinfection resistance analysis and an interfering assay, we found that fiber-1, but not fiber-2, was the key factor for directly triggering the infection of FAdV-4. The truncation analysis further revealed that both of the shaft and knob domains of fiber-1 were required for the infection. Moreover, the sera against the knob domain were able to block FAdV-4 infection, and the knob-containing fusion protein provided efficient protection against the lethal challenge of FAdV-4 in chickens. All the data demonstrated the significant roles of fiber-1 and its knob domain in directly mediating the infection of FAdV-4, which established a foundation for identifying the receptor of FAdV-4 and developing efficient vaccines against FAdV-4. IMPORTANCE Among 12 serotypes of fowl adenovirus (FAdV), FAdV-1, FAdV-4, and FAdV-10 all carry two fiber genes (i.e., fiber-1 and fiber-2), whereas other serotypes have only one. As important viral surface proteins, the fibers play vital roles in the infection and pathogenesis of FAdV. However, the importance of the fibers to the infection and pathogenesis of FAdV may be different from each other. Recent studies reveal that fiber-2 is identified as a determinant of virulence, but which fiber triggers the infection of FAdV-4 remains unknown. In this study, fiber-1 was identified as a key factor for directly mediating the infection of FAdV-4 through its shaft and knob domains, whereas fiber-2 did not play a role in triggering FAdV-4 infection. The results suggest that fiber-1 and its knob domain may serve as a target for identifying the receptor of FAdV-4 and developing efficient drugs or vaccines against FAdV-4.
      (Copyright © 2020 American Society for Microbiology.)
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    • Contributed Indexing:
      Keywords: FAdV-4; fiber-1; hepatitis-hydropericardium syndrome; infection; knob domain; vaccine
    • Accession Number:
      0 (Antibodies, Viral)
      0 (Capsid Proteins)
      0 (Viral Vaccines)
      0 (hexon capsid protein, Adenovirus)
    • Publication Date:
      Date Created: 20200703 Date Completed: 20201130 Latest Revision: 20210217
    • Publication Date:
      20221213
    • Accession Number:
      PMC7431794
    • Accession Number:
      10.1128/JVI.00954-20
    • Accession Number:
      32611755