scholarly journals Determination of antiviral action of long non-coding RNA loc107051710 during infectious bursal disease virus infection due to enhancement of interferon production

Virulence ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 68-79 ◽  
Author(s):  
Xuewei Huang ◽  
Yigang Xu ◽  
Qingyu Lin ◽  
Weilong Guo ◽  
Dongfang Zhao ◽  
...  
Keyword(s):  
Virus Infection ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Antiviral Action ◽  
Interferon Production ◽  
Non Coding Rna ◽  
Bursal Disease ◽  
Long Non Coding Rna

scholarly journals Genome-wide analysis of differentially expressed mRNAs, lncRNAs, and circRNAs in chicken bursae of Fabricius during infection with very virulent infectious bursal disease virus

BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Xuewei Huang ◽  
Junyan Zhang ◽  
Zengsu Liu ◽  
Meng Wang ◽  
Xiaolong Fan ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Expression Profiles ◽  
Circular Rna ◽  
Differentially Expressed ◽  
Bursa Of Fabricius ◽  
Infectious Bursal Disease ◽  
Non Coding Rna ◽  
Bursal Disease

Abstract Background Infectious bursal disease virus (IBDV) causes acute, highly contagious, immunosuppressive, and lethal infectious disease in young chickens and mainly infects the bursa of Fabricius (BF). To investigate interactions between IBDV and its host, RNA sequencing was applied to analyze the responses of the differentially expressed transcriptional profiles of BF infected by very virulent IBDV (vvIBDV). Results In total, 317 upregulated and 94 downregulated mRNAs were found to be significantly differentially expressed in infected chickens, compared to controls. Long non-coding RNA (lncRNA) and circular RNA (circRNA) alterations were identified in IBDV-infected chickens, and significantly different expression was observed in 272 lncRNAs and 143 circRNAs. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed to assess the functions of significantly dysregulated genes, which showed that the JAK-STAT signaling pathway, the NOD-like receptor signaling pathway, and apoptosis may be activated by IBDV infection. We predicted interactions between differentially expressed genes and produced lncRNA-mRNA and circRNA-miRNA-mRNA regulator network. Conclusions The present study identified the expression profiles of mRNAs, lncRNAs, and circRNAs during vvIBDV infection and provides new insights into the pathogenesis of IBDV and antiviral immunity of the host.

scholarly journals Western blot detection of infectious bursal disease virus infection

1998 ◽  
Vol 31 (5) ◽  
pp. 671-674 ◽  
Author(s):  
S.R.F.G. Pereira ◽  
C.E.P.F. Travassos ◽  
A. Huguenim ◽  
A.C.C. Guimarães ◽  
A.G. Silva ◽  
...  
Keyword(s):  
Virus Infection ◽  
Western Blot ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Bursal Disease

scholarly journals Nonstructural Protein of Infectious Bursal Disease Virus Inhibits Apoptosis at the Early Stage of Virus Infection

2006 ◽  
Vol 80 (7) ◽  
pp. 3369-3377 ◽  
Author(s):  
Meihong Liu ◽  
Vikram N. Vakharia
Keyword(s):  
Virus Infection ◽  
Dna Fragmentation ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Early Stage ◽  
Nonstructural Protein ◽  
Infectious Bursal Disease ◽  
Knockout Mutant ◽  
Bursal Disease ◽  
Induced Apoptosis

ABSTRACT Infectious bursal disease virus (IBDV), the causative agent of a highly contagious disease in chickens, carries a small nonstructural protein (NS). This protein has been implicated to play a role in the induction of apoptosis. In this study, we investigate the kinetics of viral replication during a single round of viral replication and examine the mechanism of IBDV-induced apoptosis. Our results show that it is caspase dependent and activates caspases 3 and 9. Nuclear factor kappa B (NF-κB) is also activated and is required for IBDV-induced apoptosis. The NF-κB inhibitor MG132 completely inhibited IBDV-induced DNA fragmentation, caspase 3 activation, and NF-κB activation. To study the function of the NS protein in this context, we generated the recombinant rGLS virus and an NS knockout mutant, rGLSNSΔ virus, using reverse genetics. Comparisons of the replication kinetics and markers for virally induced apoptosis indicated that the NS knockout mutant virus induces earlier and increased DNA fragmentation, caspase activity, and NF-κB activation. These results suggest that the NS protein has an antiapoptotic function at the early stage of virus infection.

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