Abstract

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.

Highlights

  • Infectious bursal disease (IBD), caused by infectious bursal disease virus (IBDV), is a very acute and highly contagious disease which leads to great loss in poultry

  • Results showed that the viral titer significantly increased in chicken Hsp70 (cHsp70) overexpressed DF-1 cells, suggesting that cHsp70 promotes the production of IBDV (Figure 4c). These results showed that cHsp70 plays a positive role in IBDV infection

  • Overexpression of cHsp70 in DF-1 cells increased IBDV titer, indicating that cHsp70 plays a positive role in IBDV infection (Figure 4)

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Summary

Introduction

Infectious bursal disease (IBD), caused by infectious bursal disease virus (IBDV), is a very acute and highly contagious disease which leads to great loss in poultry. IBDV targets chicken B lymphocytes primarily, disrupts the function of the bursa of Fabricius, leads to immunosuppression and makes chickens susceptible to other pathogens. Serotype 1 strains of IBDV are widely propagated in chicken embryo fibroblast cells, such as DF-1 cells and chicken embryo fibroblasts (CEF) [5]. Vp and vp are structural proteins of IBDV particles, and the binding between vp or vp with dsRNA is very important to maintain the stability of virions [7]. Many processes in the viral propagation rely on host factors to facilitate, such as adsorption, stripping, genome replication and transcription, viral protein synthesis, virus particle packaging and so on [8,9,10,11,12]. Study of virus–host protein interactions is critical for understanding viral pathogenesis and development of antiviral drugs

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