Abstract
Duck hepatitis A virus 3 (DHAV-3) is a wild endemic virus, which seriously endangers the duck industry in China. The present study aims to elucidate the mechanism of duck resistance to DHAV-3 infection. Both resistant and susceptible ducks were challenged with DHAV-3 in this experiment. The histopathological features and serum biochemical indices (ALT and AST) were analyzed to estimate liver injury status at 6, 12, 15, and 24 h post-infection (hpi). The dynamic transcriptomes of liver were analyzed to explain the molecular regulation mechanism in ducks against DHAV-3. The result showed that the liver injury in susceptible ducks was more serious than that in the resistant ducks throughout the four time points. A total of 2,127 differentially expressed genes (DEGs) were identified by comparing the transcriptome of the two populations. The expression levels of genes involved in innate immune response increased rapidly in susceptible ducks from 12 hpi. Similarly, the expression of genes involved in cytokine regulation also increased at the same time points, while the expression levels of these genes in resistant ducks remained similar between the various time points. KEGG enrichment analysis of the DEGs revealed that the genes involved in cytokine regulation and apoptosis were highly expressed in susceptible ducks than that in resistant ducks, suggesting that excessive cytokine storm and apoptosis may partially explain the mechanism of liver injury caused by DHAV-3 infection. Besides, we found that the FUT9 gene may contribute to resistance towards DHAV-3 in resistant ducklings. These findings will provide insight into duck resistance and susceptibility to DHAV-3 infection in the early phases, facilitate the development of a strategy for DHAV-3 prevention and treatment, and enhance genetic resistance via genetic selection in animal breeding.
Highlights
Duck hepatitis A virus 3 (DHAV-3) is a threat to the duck industry in China [1]
Livers were collected at 6, 12, 15, and 24 hpi, and we found that the gross lesions in the susceptible ducklings underwent dynamic changes and peaked at 24 hpi (Figures 1B1–B4)
At 6, 12, 15, and 24 hpi, liver damage and apoptosis were observed, at the same time, 46, 205, 545, and 1,954 differentially expressed genes (DEGs) were obtained through RNA-seq analysis
Summary
Duck hepatitis A virus 3 (DHAV-3) is a threat to the duck industry in China [1]. For ducklings aged below 14 days, the mortality rate caused by DHAV-3 infection will reach almost 90% [2]. DHAV-3 is characterized by its rapid transmission. Opisthotonos posturing and severe liver multiple ecchymoses occur in dead ducklings. There are three serotypes of DHAV, DHAV-3 is more epidemic in China than the other two serotypes (DHAV-1, -2) [3,4,5,6]. According to the epidemiological investigations, DHAV-3 strain has been the predominant viral type in China since 2013, with high morbidity and mortality, causing economic loss to the intensive duck production farms [7, 8]. DHAV-3 has become one of the major pathogens harming the development of the duck industry
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