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

Fig. 1. Experimental design, population composition, and mortality kinetics of F₁ duck crosses following viral challenge. (A) The resistant ducks and susceptible ducks were used as parents for crossbreeding, resulting in four F₁ hybrid combinations: RR (R♀ × R♂), RS (R♀ × S♂), SS (S♀ × S♂), and SR (S♀ × R♂). The number of male and female offspring from each F₁ hybrid group has been indicated. The live ducks in the pictures represent the resistant ducks, while the dead ducks represent the susceptible ducks. (B) Cumulative mortality curves (hours post-infection, hpi) of the four crosses, stratified by sex. (C) Final mortality rates at the conclusion of the observation period, compared by cross and sex. (D) Comparative analysis of cumulative mortality between hybrids (RS, SR) and purebred lines (RR, SS). (E) Direct comparison of mortality kinetics between reciprocal hybrids (RS vs. SR), highlighting sex-dependent survival patterns.

Fig. 2. Basal hepatic biochemical profiles in F₁ duck crosses prior to viral challenge. Concentrations of (A) alanine aminotransferase (ALT), (B) aspartate aminotransferase (AST), (C) total cholesterol (CHOL), (D) triglycerides (TG), (E) high-density lipoprotein cholesterol (HDL-C), and (F) low-density lipoprotein cholesterol (LDL-C) were measured in liver tissues of RR, SS, RS, and SR crosses (n = 6). Data are presented as mean ± SD. *P < 0.05, **P < 0.01.

Fig. 3. Correlation analysis, PCA, and post-infection plasma enzyme kinetics. (A) Spearman rank correlation heatmap between pre-infection biochemical parameters and final mortality-related traits. Blue and red scales represent positive and negative correlations, respectively; color intensity indicates the strength of the correlation. (B) PCA variable contribution plot based on pre-infection hepatic biochemical data. Arrow direction and length represent the correlation with Dim1/Dim2 and the contribution magnitude of each indicator, respectively. (C) Comparison of the integrated optical density (IOD) of hepatic Oil Red O staining among different cross-combinations at 36, 48 and 72 hpi. (D) Gender-differentiated IOD of hepatic Oil Red O staining among combinations at 36, 48 and 72 hpi. (E) Representative images of Oil Red O-stained liver sections at 48 hpi.

Fig. 4. Spatiotemporal dynamics of plasma biochemical and lipid profiles across F₁ duck crosses, sexes, and infection phases. Temporal changes in plasma levels of (A) aspartate aminotransferase (AST), (B) alanine aminotransferase (ALT), (C) triglycerides (TG), (D) total cholesterol (CHOL), (E) high-density lipoprotein cholesterol (HDL-C), and (F) low-density lipoprotein cholesterol (LDL-C) at 36, 48, and 72 hpi. Within each panel, data are stratified by hybrid combinations (RR, SS, RS, SR) and sex (males: blue/solid lines; females: red/dashed lines) to illustrate three-dimensional variations. Significant differences between specific groups at a given time point are indicated by corresponding color-coded symbols. Data are presented as mean ± SD. *P < 0.05, **P < 0.01.

Fig. 5. Schematic model illustrating the proposed mechanism of resistance versus susceptibility in Pekin duck hybrids after DHAV‑3 infection. This conceptual diagram, created with BioRender.com, depicts a metabolic balance model comparing the RS (resistant) and SR (susceptible) hybrid combinations. The central balance scale represents lipid metabolic homeostasis as the key determinant of disease outcome.