Authors
Qinqin Sun, Lianshun Zhang, Yutong Liu, Junze Chen, Siting Zheng, Lijin Liu, Honglin Xie, Qiang Fu
Published in
Poultry science. Volume 105. Issue 12. Pages 107965. Oct 15, 2026. Epub Oct 15, 2026.
Abstract
Fowl adenovirus serotype 4 (FAdV-4) causes hepatitis-hydropericardium syndrome in poultry, yet viral subversion of host autophagy remains unclear. Here, we investigated the role of the viral structural protein Fiber-2 in modulating the host autophagy-lysosome pathway. Transcriptomic profiling of LMH cells expressing Fiber-2 revealed coordinated upregulation of autophagy-related genes, validated by quantitative PCR. Functional assays demonstrated that Fiber-2 expression leads to autophagosome accumulation and impaired autophagic flux, as shown by LC3-II/p62 analysis, tandem fluorescent LC3 reporter imaging, Bafilomycin A1 treatment, and transmission electron microscopy. Fiber-2 predominantly localizes to late endosomes and lysosomes, and GFP-Galectin-3 reporter assays indicate that it disrupts lysosomal membrane integrity rather than blocking autophagosome-lysosome fusion. Co-immunoprecipitation (Co-IP) and enrichment analyses identified BECN1, a key autophagy regulator, as a Fiber-2-interacting protein, and associated host proteins were enriched in autophagy-related pathways. Finally, CRISPR/Cas9-mediated deletion of Fiber-2 significantly reduced FAdV-4 replication at later stages of infection, consistent with a proviral role for Fiber-2. These findings indicate that Fiber-2 disrupts autophagic flux by inducing lysosomal dysfunction and membrane damage, thereby promoting FAdV-4 replication and uncovering a previously unrecognized mechanism of viral subversion of host degradative pathways.
PMID:
42913222
Bibliographic data and abstract were imported from PubMed on 24 Oct 2026.
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