Transcriptomic Characterization of a Chicken Embryo Model Infected With Duck Hepatitis A Virus Type 1

Xie, Jinyan; Zeng, Qiurui; Wang, Mingshu; Ou, Xumin; Ma, Yunchao; Cheng, Anchun; Zhao, Xinxin; Liu, Mafeng; Zhu, Dekang; Chen, Shun; Jia, Renyong; Yang, Qiao; Wu, Ying; Zhang, Shaqiu; Liu, Yunya; Yu, Yanling; Zhang, Ling; Chen, Xiaoyue

doi:10.3389/fimmu.2018.01845

Cited by 18 publications

(20 citation statements)

References 60 publications

(47 reference statements)

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“…In the susceptible ducklings, the apoptosis rate was significantly higher than that in the resistant group. Previous studies found that duck hepatitis A virus type 1 (DHAV-1) caused apoptosis in the liver after infection (38)(39)(40). In agreement with previous studies, the DHAV-1 infection drove apoptosis in the liver and the inflammatory response to viral infection could have exacerbated the level of apoptosis.…”

Section: Discussionsupporting

confidence: 82%

Dynamic Transcriptome Reveals the Mechanism of Liver Injury Caused by DHAV-3 Infection in Pekin Duck

et al. 2020

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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.

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Section: Discussionsupporting

confidence: 82%

Dynamic Transcriptome Reveals the Mechanism of Liver Injury Caused by DHAV-3 Infection in Pekin Duck

et al. 2020

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“…Previous studies have shown that chicken embryos can be used as an animal model for DHAV-1 (16). However, there is no report of DHAV-1 infection in CEFs.…”

Section: Resultsmentioning

confidence: 99%

“…The changes in attenuated vaccines and virulent strains in the host before and after adaptation are also worthy of attention. Through transcriptome sequencing, we have found that attenuated vaccines induce type I and II interferon responses, activate innate immune responses, and simultaneously enhance the expression of SOCS1 and SOCS3 (16). We suspected that the adaptation of attenuated vaccines during the process of serial passage is related to high expression of SOCS proteins.…”

Section: Discussionmentioning

confidence: 99%

“…Intensive research has found that incompatible host translational selection pressure is one of the main mechanisms of viral attenuation and adaptation in chicken embryos (15). In addition, transcriptome sequencing has revealed that infection of chicken embryo livers with the CH60 strain is associated with enhanced type I and II interferon responses, activated innate immune responses, and abundant expression of cytokine signaling molecules 1 and 3 (SOCS1 and SOCS3) (16). Some structural and functional information about genes involved in host interactions with DHAV-1 has been reported recently (17–23).…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, SOCS3 also plays a role in mediating the ubiquitination and subsequent proteasome degradation of cytokine/growth factor/hormone receptor (26). Previous studies have revealed that the CH60 strain significantly enhances SOCS1 and SOCS3 mRNA levels in the liver, activates the JAK-STAT signaling pathway and induces type I and II interferon responses (16). However, the role of SOCS proteins in viral attenuation and adaptation in chicken embryos remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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DHAV-1 Inhibits Type I Interferon Signaling to Assist Viral Adaption by Increasing the Expression of SOCS3

et al. 2019

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Duck hepatitis A virus type 1 (DHAV-1) is one of the most lethal pathogens in the duck industry. The attenuated vaccine (the CH60 strain) is cultivated through serial passage in chicken embryos and is widely used for the prevention and control of the disease. However, the specific mechanism underlying its adaptation in chicken embryos has not been fully elucidated. In this study, we first infected chicken embryo fibroblasts (CEFs) with the DHAV-1 CH60 strain. The peak of viral proliferation occurred within 36–48 h post-infection. The different DHAV-1 strains significantly induced the expression of IFNα, IFNγ, and Suppressor of cytokine signaling 3 (SOCS3) in CEFs, and we found that SOCS3 overexpression significantly promoted viral replication. Furthermore, SOCS3 overexpression significantly inhibited the expression of IFNα but promoted the expression of IFNγ. In addition, SOCS3 overexpression clearly decreased the mRNA levels of STAT1 and STAT3 in the Janus kinase (JAK)-STAT signaling pathway and inhibited the expression of the antiviral proteins MX1 and OASL. Immune-precipitation assays indicated that SOCS3 and IFNα do not physically interact. Subcellular localization of SOCS3 and IFNα revealed that SOCS3 was mainly located in the nucleus and cytoplasm, while IFNα was located only in the cytoplasm. Co-localization of these two proteins was not observed in the cytoplasm. In conclusion, the DHAV-1 CH60 strain may inhibit the expression of IFNα by increasing the SOCS3 protein and SOCS3 can in turn decrease STAT1 and STAT3 mRNA levels, thereby inhibiting the antiviral protein MX1 and ultimately promoting viral proliferation, indirectly assisting in viral adaptation in chicken embryos.

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RNA-seq and microRNA association analysis to explore the pathogenic mechanism of DHAV-1 infection with DEHs

Wang

Zhang

et al. 2023

Funct Integr Genomics

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Transcriptomic Characterization of a Chicken Embryo Model Infected With Duck Hepatitis A Virus Type 1

Cited by 18 publications

References 60 publications

Dynamic Transcriptome Reveals the Mechanism of Liver Injury Caused by DHAV-3 Infection in Pekin Duck

Dynamic Transcriptome Reveals the Mechanism of Liver Injury Caused by DHAV-3 Infection in Pekin Duck

DHAV-1 Inhibits Type I Interferon Signaling to Assist Viral Adaption by Increasing the Expression of SOCS3

RNA-seq and microRNA association analysis to explore the pathogenic mechanism of DHAV-1 infection with DEHs

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