Divergent IFITM1 regulation is associated with resistance and susceptibility to duck hepatitis A virus genotype 3 in Pekin ducks
- 1Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, No. 2 Yuanmingyuan West Road, Haidian district, Beijing, 100193, People's Republic of China
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.
Related
- Divergent regulation of STING-mediated innate immune responses by CBP and p300
- Divergent evolutionary paths of vancomycin resistance operons reveal the transition from mobility to genomic stabilization in Enterococcus faecium
- Sustained hypoxia induces divergent response patterns in cardiac metabolic-immune adaptation and circadian rhythm regulation
- Rapid enhancement of antibiotic resistance and divergent remodeling of gene expression in single cells of bacteria
- MeSRT1 Interacts with MeNF-YC15 and Negatively Mediates Resistance to Cassava Bacterial Blight via Regulation of Gibberellin Metabolism in Manihot esculenta Crantz
BibTeX
@article{liang2026divergent,
title = {{Divergent IFITM1 regulation is associated with resistance and susceptibility to duck hepatitis A virus genotype 3 in Pekin ducks}},
author = {Suyun Liang and Meixi Lu and Huihui Li and Yi Tang and Shuisheng Hou},
journal = {Poultry Science},
year = {2026},
month = oct,
doi = {10.1016/j.psj.2026.107936},
url = {https://doi.org/10.1016/j.psj.2026.107936},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Divergent IFITM1 regulation is associated with resistance and susceptibility to duck hepatitis A virus genotype 3 in Pekin ducks
AU - Suyun Liang
AU - Meixi Lu
AU - Huihui Li
AU - Yi Tang
AU - Shuisheng Hou
PY - 2026
DA - 2026/10/11
JO - Poultry Science
DO - 10.1016/j.psj.2026.107936
UR - https://doi.org/10.1016/j.psj.2026.107936
AB - 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.
SN - 0032-5791
SN - 1525-3171
ER -