Survival phenotypes and lipid metabolic responses to DHAV-3 infection in Pekin duck hybrids with differential resistance.

Host metabolic reprogramming is increasingly recognized as a determinant of viral pathogenesis, yet its role in genetic disease resistance remains elusive. This study investigated the survival and lipid metabolic dynamics of Pekin duck combinations-pure resistant (RR), pure susceptible (SS), and reciprocal crosses (RS: R♀ × S♂; SR: S♀ × R♂)-following DHAV-3 infection. Phenotypic analysis revealed striking maternal inheritance in disease resistance: RS females exhibited the lowest mortality (22.7%), significantly outperforming SR females (51.4%) and even the resistant RR pure line (27.0%). To uncover the underlying mechanisms, we analyzed pre- and post-infection lipid profiles. Pre-infection liver biochemistry identified baseline cholesterol (CHOL) and LDL-C as robust predictors of viral susceptibility, with the highly susceptible SS group exhibiting the highest levels. Following viral challenge, plasma lipid dynamics and liver function indicators (ALT, AST) fluctuated significantly depending on cross-combination, sex, and time. Furthermore, the dynamic expression of key lipid metabolism genes, particularly cholesterol efflux regulators (ABCA1, ABCG1), was tightly orchestrated by genetic background and sex interactions. Overall, these findings demonstrate that baseline lipid profiles and post-infection lipid network reshuffling dictate the disease resistance differences among hybrid combinations. The exceptional resistance of the RS combination highlights the critical role of maternal effects and offers a metabolic perspective for strategic crossbreeding in poultry.