scholarly journals Cyclophilin A Interacts with Viral VP4 and Inhibits the Replication of Infectious Bursal Disease Virus

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Nian Wang ◽  
Lizhou Zhang ◽  
Yuming Chen ◽  
Zhen Lu ◽  
Li Gao ◽  
...  
Keyword(s):  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Nonstructural Protein ◽  
Chicken Embryo Fibroblast ◽  
Cyclophilin A ◽  
Host Cells ◽  
Infectious Bursal Disease ◽  
Cell Protein ◽  
Small Interfering Rnas ◽  
Bursal Disease

Nonstructural protein VP4, a serine protease of infectious bursal disease virus (IBDV) that catalyzes the hydrolysis of polyprotein pVP2-VP4-VP3 to form the viral proteins VP2, VP4, and VP3, is essential to the replication of IBDV. However, the interacting partners of VP4 in host cells and the effects of the interaction on the IBDV lifecycle remain incompletely elucidated. In this study, using the yeast two-hybrid system, the putative VP4-interacting partner cyclophilin A (CypA) was obtained from a chicken embryo fibroblast (CEF) expression library. CypA was further confirmed to interact with VP4 of IBDV using co-immunoprecipitation (CO-IP), GST pull-down, and confocal microscopy assays. Moreover, we found that the overexpression of CypA suppressed IBDV replication, whereas the knock-down of CypA by small interfering RNAs promoted the replication of IBDV. Taken together, our findings indicate that the host cell protein CypA interacts with viral VP4 and inhibits the replication of IBDV.

scholarly journals Chicken Heat Shock Protein 70 Is an Essential Host Protein for Infectious Bursal Disease Virus Infection In Vitro

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 664
Author(s):  
Yufang Meng ◽  
Xiaoxue Yu ◽  
Chunxue You ◽  
Wenjuan Zhang ◽  
Yingfeng Sun ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Disease Virus ◽  
Heat Shock Protein 70 ◽  
Infectious Bursal Disease Virus ◽  
Host Protein ◽  
Infectious Bursal Disease ◽  
Economic Losses ◽  
Small Interfering Rnas ◽  
Bursal Disease

Infectious bursal disease virus (IBDV) infection causes pathogenicity and mortality in chickens, leading to huge economic losses in the poultry industry worldwide. Studies of host-virus interaction can help us to better understand the viral pathogenicity. As a highly conservative host factor, heat shock protein 70 (Hsp70) is observed to be involved in numerous viral infections. However, there is little information about the role of chicken Hsp70 (cHsp70) in IBDV infection. In the present study, the increased expression of cHsp70 was observed during IBDV-infected DF-1 cells. Further studies revealed that Hsp70 had similar locations with the viral double-stranded RNA (dsRNA), and the result of pull-down assay showed the direct interaction between cHsp70 with dsRNA, viral proteins (vp)2 and 3, indicating that maybe cHsp70 participates in the formation of the replication and transcription complex. Furthermore, overexpression of cHsp70 promoted IBDV production and knockdown of cHsp70 using small interfering RNAs (siRNA) and reducedviral production, implying the necessity of cHsp70 in IBDV infection. These results reveal that cHsp70 is essential for IBDV infection in DF-1 cells, suggesting that targeting cHsp70 may be applied as an antiviral strategy.

scholarly journals Immunogenicity and Efficacy Evaluation of Vero Cell-Adapted Infectious Bursal Disease Virus LC-75 Vaccine Strain in Ethiopia 

2021 ◽  
Author(s):  
Wakjira Kebebe ◽  
Molalegne Bitew ◽  
Fufa Dawo ◽  
Bedaso Mammo ◽  
Hawa Mohammed ◽  
...  
Keyword(s):  
Vero Cell ◽  
Disease Virus ◽  
Vaccine Strain ◽  
Infectious Bursal Disease Virus ◽  
Chicken Embryo Fibroblast ◽  
Vero Cells ◽  
Infectious Bursal Disease ◽  
Efficacy Evaluation ◽  
Viral Pathogen ◽  
Bursal Disease

Abstract Background: Infectious bursal disease virus (IBDV) is an avian viral pathogen that causes infectious bursal disease (IBD) of chickens. The disease is endemic in Ethiopia since 2002 and vaccination is the major means of disease prevention and control. IBD vaccine is produced in Ethiopia using primary chicken embryo fibroblast (CEF) cell; which is time-consuming, laborious, and uneconomical. The present study was carried out to develop cell-based IBDV LC-75 vaccine using Vero cells, and to evaluate the immunogenicity and protection level.Results: Identity of the vaccine seed was confirmed using gene-specific primers using reverse transcription polymerase chain reaction. Confluent monolayer of Vero cells was infected with vaccine virus and serial passage continued till passage ten. Characteristic virus induced cytopathic effect was observed starting from passage 2 on the third day post-infection. The infectious titer of adapted virus showed a linear increment along the passage level. Virus induced specific antibody was determined using indirect ELISA after vaccination of 14 days old chicks through ocular route. Accordingly, the antibody titer measured from Vero cells vaccinated chicks revealed similar level with the currently available CEF cell-based vaccine. Chicks vaccinated with Vero cell adapted virus showed complete protection against very virulent IBDV, while unvaccinated group had 60% morbidity and 25% mortality.Conclusions: The IBDV vaccine strain well adapted on Vero cells and found to be immunogenic induces antibodies development and successfully protects chicks against challenging with the circulating field IBDV isolate. Hence, it is recommended to produce IBD vaccine using Vero cell culture with enough quantity to conquer the limitations using CEF cells and thus to vaccinate chicks to protect against IBDV infection.

scholarly journals Complete Genome Sequence of a Chicken Embryo Fibroblast-Adapted Attenuated Infectious Bursal Disease Virus Isolate from India

2016 ◽  
Vol 4 (3) ◽  
Author(s):  
T. M. A. Senthilkumar ◽  
C. V. Priyadharsini ◽  
P. Raja ◽  
K. Kumanan
Keyword(s):  
Disease Virus ◽  
Genome Sequence ◽  
Complete Genome Sequence ◽  
Complete Genome ◽  
Infectious Bursal Disease Virus ◽  
Chicken Embryo Fibroblast ◽  
Infectious Bursal Disease ◽  
Avian Pathogen ◽  
Bursal Disease ◽  
Commercial Broiler

Infectious bursal disease virus is an avian pathogen that causes huge morbidity and mortality in the poultry sector all over the world. Here, we report the full-length genome sequence of an Indian strain, MB11/ABT/MVC/2016, isolated from a commercial broiler flock. This is a first report of a complete genome sequence of infectious bursal disease virus from India.

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.

scholarly journals VP1 and VP3 Are Required and Sufficient for Translation Initiation of Uncapped Infectious Bursal Disease Virus Genomic Double-Stranded RNA

2017 ◽  
Vol 92 (2) ◽  
Author(s):  
Chengjin Ye ◽  
Yu Wang ◽  
Enli Zhang ◽  
Xinpeng Han ◽  
Zhaoli Yu ◽  
...  
Keyword(s):  
Disease Virus ◽  
Translation Initiation ◽  
Infectious Bursal Disease Virus ◽  
Binding Protein ◽  
Viral Proteins ◽  
Host Cells ◽  
Infectious Bursal Disease ◽  
Genomic Rna ◽  
Sense Strand ◽  
Bursal Disease

ABSTRACTInfectious bursal disease virus (IBDV) is a bisegmented double-strand RNA (dsRNA) virus of theBirnaviridaefamily. While IBDV genomic dsRNA lacks a 5′ cap, the means by which the uncapped IBDV genomic RNA is translated effectively is unknown. In this study, we describe a cap-independent pathway of translation initiation of IBDV uncapped RNA that relies on VP1 and VP3. We show that neither purified IBDV genomic dsRNA nor the uncapped viral plus-sense RNA transcripts were directly translated and rescued into infectious viruses in host cells. This defect in translation of the uncapped IBDV genomic dsRNA was rescued bytrans-supplementation of the viral proteins VP1 and VP3 which was dependent on both the intact polymerase activity of VP1 and the dsRNA binding activity of VP3. Deletion analysis showed that both 5′ and 3′ untranslated regions (UTRs) of IBDV dsRNA were essential for VP1/VP3-dependent translation initiation. Significantly, VP1 and VP3 could also mediate the recovery of infectious IBDV from the authentic minus-sense strand of IBDV dsRNA. Moreover, downregulation or inhibition of the cap-binding protein eIF4E did not decrease but, rather, enhanced the VP1/VP3-mediated translation of the uncapped IBDV RNA. Collectively, our findings for the first time reveal that VP1 and VP3 compensate for the deficiency of the 5′ cap and replace eIF4E to confer upon the uncapped IBDV RNA the ability to be translated and rescued into infectious viruses.IMPORTANCEA key point of control for virus replication is viral translation initiation. The current study shows that the uncapped IBDV RNA cannot be translated into viral proteins directly by host translation machinery and is thus noninfectious. Our results constitute the first direct experimental evidence that VP1 and VP3 are required and sufficient to initiate translation of uncapped IBDV genomic RNA by acting as a substitute for cap and replacing the cap-binding protein eIF4E. Significantly, VP1/VP3 mediate the recovery of infectious IBDV not only from the plus-sense strand but also from the minus-sense strand of the IBDV dsRNA. These findings provide not only new insights into the molecular mechanisms of the life cycle of IBDV but also a new tool for an alternative strategy for the recovery of IBDV from both the plus- and the minus-sense strands of the viral genomic dsRNA.

scholarly journals Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus

2007 ◽  
Vol 7 (3) ◽  
pp. 612-625 ◽  
Author(s):  
Xiaojuan Zheng ◽  
Lianlian Hong ◽  
Lixue Shi ◽  
Junqing Guo ◽  
Zhen Sun ◽  
...  
Keyword(s):  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Host Cells ◽  
Infectious Bursal Disease ◽  
Proteomics Analysis ◽  
Bursal Disease

scholarly journals MicroRNA gga-miR-130b Suppresses Infectious Bursal Disease Virus Replication via Targeting of the Viral Genome and Cellular Suppressors of Cytokine Signaling 5

2017 ◽  
Vol 92 (1) ◽  
Author(s):  
Mengjiao Fu ◽  
Bin Wang ◽  
Xiang Chen ◽  
Zhiyuan He ◽  
Yongqiang Wang ◽  
...  
Keyword(s):  
Disease Virus ◽  
Viral Genome ◽  
Infectious Bursal Disease Virus ◽  
Host Cells ◽  
Infectious Bursal Disease ◽  
Cytokine Signaling ◽  
Type I ◽  
Bursal Disease ◽  
Suppressors Of Cytokine Signaling

ABSTRACTMicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression posttranscriptionally through silencing or degrading their targets, thus playing important roles in the immune response. However, the role of miRNAs in the host response against infectious bursal disease virus (IBDV) infection is not clear. In this study, we show that the expression of a series of miRNAs was significantly altered in DF-1 cells after IBDV infection. We found that the miRNA gga-miR-130b inhibited IBDV replication via targeting the specific sequence of IBDV segment A and enhanced the expression of beta interferon (IFN-β) by targeting suppressors of cytokine signaling 5 (SOCS5) in host cells. These findings indicate that gga-miR-130b-3p plays a crucial role in host defense against IBDV infection.IMPORTANCEThis work shows that gga-miR-130b suppresses IBDV replication via directly targeting the viral genome and cellular SOCS5, the negative regulator for type I interferon expression, revealing the mechanism underlying gga-miR-130-induced inhibition of IBDV replication. This information will be helpful for the understanding of how host cells combat pathogenic infection by self-encoded small RNA and furthers our knowledge of the role of microRNAs in the cell response to viral infection.

Sign in / Sign up

Export Citation Format

Share Document