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

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.

CD4+CD25+ Cells Are Essential for Maintaining Immune Tolerance in Chickens Inoculated with Bovine Serum Albumin at the Late Stage of Embryonic Development.

In this study, the role of chicken CD4+CD25+ cells during induced immunotolerance was tested. Properties of chicken CD4+CD25+ cells sorted by flow cytometry were analyzed. Results showed that chicken CD4+CD25+ cells express IL-10, TGF-ß highly and suppress proliferation of CD4+CD25- cells in vitro. To induce immunotolerance, embryos were inoculated with bovine serum albumin (BSA) via an intravascular route on embryo incubation day 20 (EID20), and after hatching chicks experienced BSA immunization four times at 7-day intervals. Serum anti-BSA antibodies and CD4+CD25+ cell ratio was analyzed. Results showed that humoral tolerance was obtained and the CD4+CD25+ cell percentage in peripheral blood lymphocytes increased along with this progress. Injection of anti-chicken CD25 antibody via an intravascular route on EID16 is applied to block CD4+CD25+ cells, and the CD4+CD25+ cell ratio decreased significantly up to 35 d post-hatch. Based on the above, injections of anti-chicken CD25 antibody on EID16 and BSA on EID20 were carried out sequentially, and tolerance level was contrasted to the BSA-injection group. Data revealed the anti-BSA antibodies increased significantly in the CD4+CD25+ cell-blocked groups indicating that immune tolerance level was weakened. In conclusion, chicken CD4+CD25+ cells are essential in maintaining induced immune tolerance.