HPAIV-induced heat shock protein expression in chickens and its potential NF-κB-mediated transcriptional regulation.

During infection with highly pathogenic Avian Influenza virus (HPAIV), heat shock proteins (HSPs) play roles in host immune responses by interacting with various regulators of cell signaling pathways and in mediating cellular homeostasis. However, the tissue-specific regulation of these chaperones, particularly their potential association with the NF-κB pathway, remains poorly defined in avian species. Chickens were infected with HPAIV (A/chicken/Vietnam/NA01/2019 (H5N1), and the expression patterns of a comprehensive range of HSPs (small HSPs to canonical classes) were analyzed in lung and spleen at 1 and 3 days post-infection (dpi). As a result, HPAIV infection induced significant temporal up-regulation of mRNA of small sHSPs (sHSPs; HSPB7, HSPB9), HSPE1, and a collagen-specific molecular chaperone, SERPINH1, in both tissues. To investigate transcriptional regulation, DF-1 cells were stimulated with Poly(I: C) in the presence or absence of NF-κB inhibitors. Notably, NF-κB inhibition was associated with an up-regulation of HSPB9 and a depression of SERPINH1 in PIC-treated DF-1. These results suggest that specific HSPs may be influenced by pro-inflammatory signaling during viral infection, with NF-κB signalling potentially contributing to their negative regulation during viral stress response. Collectively, these findings provide preliminary insights into the complex molecular dynamics of HPAIV pathogenesis and highlight the importance of host-mediated signaling pathways in modulating the host cellular stress response in poultry.