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Divergent IFITM1 regulation is associated with resistance and susceptibility to duck hepatitis A virus genotype 3 in Pekin ducks

Year: 2026
Type: article
Abstract: Duck viral hepatitis (DVH), caused by duck hepatitis A virus genotype 3 (DHAV-3), is a highly lethal infectious disease in ducklings, yet the key host determinants underlying differential resistance remain unclear. Using previously established DHAV-3-resistant (Z7R) and -susceptible (Z7S) Pekin duck models, we investigated the molecular mechanisms driving host resistance to DHAV-3. Resistant ducks exhibited significantly lower viral load and reduced viral replication compared to susceptible ducks, while heightened interferon-induced transmembrane protein 1 (IFITM1) expression levels in susceptible ducks were associated with severe hepatic tissue damage. Strikingly, functional analyses revealed that IFITM1-mediated resistance is not solely dependent on its expression level but involves regulation of host cell cycle progression at the G1 phase during viral infection. Mechanistically, we identified a novel interaction between IFITM1, the host antiviral sensor IFIT5, and the viral capsid protein VP1, which together form a regulatory axis that modulates antiviral defense and cell-cycle control. Among DHAV-3 structural proteins, VP1 was the only component showing differential expression between resistant and susceptible ducks. These findings identify IFITM1 as an essential host factor that mediates antiviral defense against DHAV-3 and provide mechanistic insights into the IFITM1-IFIT5-VP1 axis, linking innate immunity, cell-cycle regulation, and viral pathogenesis.
DOI: 10.1016/j.psj.2026.107936
Language: English
Subfield: Immunology
Open Access status: gold
Estimated APC paid: $2,600
OpenAlex ID: W7221443011
FWCI:
Cites: 27
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Related to: 10