Novel goose-origin astrovirus infection in geese: the effect of age at infection

Abstract

Since 2017, a serious infectious disease characterized by visceral gout has emerged in China's main goose-producing regions. The disease has caused huge economic losses to China's goose industry. In our previous study, we determined that the pathogen causing gout in goslings is a novel goose-origin astrovirus, designated as AStV/SDPY/Goose/1116/17 (AStV-SDPY) strain. To investigate the effect of host age on the outcome of novel goose-origin astrovirus infection, 200 1-day-old healthy goslings were selected to be experimentally infected at 1, 5, 15, 25, and 35 D of age. It was shown in experimental infection that the AStV-SDPY strain was highly pathogenic in goslings aged 1 to 15 D, causing growth repression, severe visceral urate deposition, and even death, whereas goslings infected at 25 and 35 D of age showed mild symptoms. Histopathologic examination indicated that lesions occurred mainly in the kidney and liver of infected goslings, which is correlated to the severity of clinical signs and gross lesions. Viral RNA was detected in all representative tissues, and virus shedding was detected continuously within 15 D after inoculation. Higher viral copy number, especially in vital organs such as the liver and kidney, was developed in the goslings infected at 1 to 15 D of age than older geese. In addition, clinical chemistry and inflammatory cytokines showed that younger geese are more sensitive to AStV infection. Overall, our study demonstrates that the pathogenicity of AStV-SDPY in goslings is partly associated with the age of infection, laying a foundation for further study of the pathogenic mechanism of this virus.

Keywords: age; goose; histopathology; novel goose-origin astrovirus; viral load.

Figure 1

Gross lesions of goslings infected with AStV-SDPY at 5 different ages. (A–C) Urate deposits on the surface of the liver and heart in groups S1, S2 and S3, whereas there were no obvious urate in the S4 (D) and S5 (E) groups; urate deposits on the surface of the proventriculus in groups S1 (F) and S2 (G), no urate deposition were observed in S3 (H), S4 (I), and S5 (J) groups; Severe hemorrhage and swellings appeared in the kidneys of geese in groups S1 (K), S2 (L), mild swellings of kidneys in group S3 (M), no obvious lesions were observed in groups S4 (N) and S5 (O); white urate appeared in joints of goslings in groups S1 (P), S2 (Q), and S3 (R), whereas the joints in the S4 (S) and S5 (T) groups had smooth mucosa and no urate deposits.

Figure 2

Pathologic changes of the AStV-SDPY infected goslings at 5 different ages. (A–C) Urate deposits (black arrow) on the liver (H&E) observed in groups S1, S2 and S3. (D, E) Liver (H&E) in groups S4 and S5, no urate deposits. (F, G) Kidney (H&E) in groups S1 and S2, renal tubular epithelial cell severe exfoliation (black arrow). (H) Renal tubular epithelial cell exfoliation (black arrow) in group S3. (I, J) H&E-stained kidney in groups S4 and S5, renal tubular epithelial cells intact. (K) H&E-stained spleen, S1 group, severe hemorrhage of splenocyte. (L) Spleen (H&E), S2 group, diffuse hemorrhage of splenocyte. (M) Spleen (H&E), S3 group, mild bleeding. (N, O) Spleen (H&E), S4 and S5 groups, goslings infected at 25 and 35 d of age, no microscopic lesions were observed. Abbreviation: H&E, hematoxylin and eosin.

Figure 3

Normalized AStV copy numbers (log10) per 1 μg total RNA in the internal organs of experimentally infected goslings collected at 3 (A), 6 (B), 9 (C), 12 (D), and 15 (E) dpi. Statistically significant differences (P < 0.05) of viral loads in kidney between 1-day-old infected group and the other 4 age groups. (F) Cloacal virus shedding after the goslings in S1–S5 groups were infected with the AStV-SDPY. Note: Each sample was analyzed in triplicate. Error bars were expressed as SD of the means (n = 3). Abbreviation: dpi, days postinfection.

Figure 4

Weight changes of goslings after infected with AStV-SDPY. (A) 1-day-old (S1) group (1–15 dpi); (B) 5-day-old (S2) group (1–15 dpi); (C) 15-day-old (S3) group (1–15 dpi); (D) 25-day-old (S4) group (1–15 dpi); (E) 35-day-old (S5) group (1–15 dpi). Note: All values are presented as the mean BW ±SD. Asterisks indicate statistically significant differences compared with the control group. ∗P < 0.05; ∗∗P < 0.01. Abbreviation: dpi, days postinfection.

Figure 5

Dynamics of ALT, AST, and UA in serum of the geese after artificially beinginfected with AStV-SDPY. (A, D, G, J, M) Levels of ALT in infected groups (S1–S5) and control groups (C1–C5) (3–15 dpi). (B, E, H, K, N) Levels of AST in infected groups (S1–S5) and control groups (C1–C5) (3–15 dpi). (C, F, I, L, O) Levels of UA in infected groups (S1–S5) and control groups (C1–C5) (3–15 dpi). Note: Data are expressed as the mean ± SD. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001. Abbreviations: ALT, alanine aminotransferase; AST, aspartate aminotransferase; dpi, days postinfection; UA, uric acid.

Figure 6

Dynamics of IL-6 and interferon alpha in serum of the geese after being artificially infected with AStV-SDPY. (A–E) Levels of IL-6 in groups S1–S5 compared with C1–C5 groups (3–15 dpi); (F–J) levels of interferon alpha in groups S1–S5 compared with C1–C5 groups (3–15 dpi). Note: Data are expressed as the mean ± SD. Asterisks indicate statistically significant differences compared with the control group. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001. Abbreviations: dpi, days postinfection; IFN, interferon.