scholarly journals Transcriptome Analysis of Duck Liver and Identification of Differentially Expressed Transcripts in Response to Duck Hepatitis A Virus Genotype C Infection

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e71051 ◽  
Author(s):  
Cheng Tang ◽  
Daoliang Lan ◽  
Huanrong Zhang ◽  
Jing Ma ◽  
Hua Yue
2020 ◽  
Vol 248 ◽  
pp. 108813
Author(s):  
Suyun Liang ◽  
Ming Xie ◽  
Jing Tang ◽  
Minghang Wang ◽  
Dabing Zhang ◽  
...  

Gene ◽  
2020 ◽  
Vol 748 ◽  
pp. 144710
Author(s):  
Suyun Liang ◽  
Jing Tang ◽  
Xiaoyan Wang ◽  
Zhiguo Wen ◽  
Ming Xie ◽  
...  

PLoS ONE ◽  
2017 ◽  
Vol 12 (6) ◽  
pp. e0178993 ◽  
Author(s):  
Xumin Ou ◽  
Sai Mao ◽  
Jingyu Cao ◽  
Anchun Cheng ◽  
Mingshu Wang ◽  
...  

Viruses ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 80
Author(s):  
Minghang Wang ◽  
Lili Chai ◽  
Suyun Liang ◽  
Junfeng Lv ◽  
Lixin Yang ◽  
...  

Among the causative agents of duck viral hepatitis, duck hepatitis A virus genotype 1 (DHAV-1) is the most common virus reported in most outbreaks worldwide. How to propagate DHAV-1 in cell cultures efficiently remains a problem to be explored. Here, we aimed to test the effect of serum type on DHAV-1 replication in duck embryo fibroblast (DEF) cells. Comparative studies involved virus culture and passage, observation of cytopathic effect (CPE), virus quantification, and plaque formation assay. From the results of these investigations, we conclude that use of chicken serum (CS) in maintenance medium allows DHAV-1 to establish productive, cytocidal infection in DEF cells, whereas FCS exerts inhibitory effects on DHAV-1 replication, CPE development, and plaque formation. By using a neutralization test, we found that the direct action of FCS on virions is likely to play a key role in inhibiting DHAV-1 replication in DEF cells. Mechanism analyses revealed that FCS inhibits DHAV-1 replication at virus adsorption and reduces extracellular virus yields. The present work may shed light on a new perspective for antiviral agent development, and have provided a virus–host cell system for further studies on molecular mechanism involved DHAV-1 replication and pathogenesis.


Author(s):  
Nana Sui ◽  
Ruihua Zhang ◽  
Yue Jiang ◽  
Honglei Yu ◽  
Guige Xu ◽  
...  

Duck hepatitis A virus 1 (DHAV-1) is a highly contagious etiological agent that causes acute hepatitis in young ducklings. MicroRNAs (miRNAs) play important regulatory roles in response to pathogens. However, the interplay between DHAV-1 infection and miRNAs remains ambiguous. We characterized and compared miRNA and mRNA expression profiles in duck embryo fibroblasts cells (DEFs) infected with DHAV-1. In total, 36 and 96 differentially expressed (DE) miRNAs, and 4110 and 2595 DE mRNAs, were identified at 12 and 24 h after infection. In particular, 126 and 275 miRNA–mRNA pairs with a negative correlation were chosen to construct an interaction network. Subsequently, we identified the functional annotation of DE mRNAs and target genes of DE miRNAs enriched in diverse Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, which may be important for virus resistance, cell proliferation, and metabolism. Moreover, upregulated miR-222a could negatively regulate DHAV-1 replication in DEFs and downregulate integrin subunit beta 3 (ITGB3) expression by targeting the 3′ untranslated region (3′UTR), indicating that miR-222a may modulate DHAV-1 replication via interaction with ITGB3. In conclusion, the results reveal changes of mRNAs and miRNAs during DHAV-1 infection and suggest miR-222a as an antiviral factor against DHAV-1.


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