Monoclonal antibody development and antigenic epitope identification of chicken pro-IL-1β.

Pro-IL-1β is an important inflammatory factor and is also a biomarker for detecting early pro-inflammatory immune responses. However, commercially available antibodies against chicken inflammatory factors are lacking, which prohibits an in-depth exploration of the mechanism of chicken inflammation. This study cloned and expressed chicken pro-IL-1β, and developed a hybridoma cell line 1E12 capable of stably secreting chicken pro-IL-1β monoclonal antibody (mAb).

Monoclonal antibody development and antigenic epitope identification of infectious bursal disease virus VP5.

Infectious bursal disease (IBD) is an important immunosuppressive disease affecting chickens and is caused by infectious bursal disease virus (IBDV) infection. VP5 is a non-essential protein for IBDV replication but plays a critical role in IBDV pathogenesis. A deeper understanding of the biological functions of VP5 is lacking.

Loop P of viral capsid protein is involved in immune escape of the emerging novel variant infectious bursal disease virus.

Infectious bursa disease (IBD) is an acute, highly contactable, lethal, immunosuppressive infectious disease caused by the Infectious bursa disease virus (IBDV). Currently, the emerged novel variant IBDV (nVarIBDV) and the sustainedly prevalent very virulent IBDV (vvIBDV) are the two most prevalent strains of IBDV in China. The antigenic properties of the two prevalent strains differed significantly, which led to the escape of nVarIBDV from the immune protection provided by the existing vvIBDV vaccine.

Infectious bursal disease virus VP5 triggers host shutoff in a transcription-dependent manner.

Viruses have evolved intricate mechanisms to evade host antiviral responses and exploit cellular resources by manipulating the expression profile of host genes. During infection, viruses encode proteins with shutoff activity to globally inhibit host protein synthesis, which is an effective strategy for immune evasion. In this study, compelling evidence shows that infectious bursal disease virus (IBDV) infection triggers the suppression of host protein synthesis.