Regulatory T cell infiltration precedes early events associated with persistent infectious bronchitis virus (IBV) infection in the cecal tonsils of chickens.

Abstract

Infectious bronchitis (IB) is a contagious respiratory disease in chickens caused by infectious bronchitis virus (IBV). While initially affecting the respiratory tract, IBV has evolved to infect other body systems. Notably, the Delmarva (DMV)/1639 genotype of IBV has been shown to persist in the cecal tonsils (CT), potentially facilitating viral transmission to naïve birds. This study aimed to uncover the early immunological mechanisms leading up to IBV persistence in the CT, compared to the spleen and to evaluate the persistence patterns among different genotypes of IBV. An animal experiment was conducted using three IBV genotypes, with samples collected at 3, 8, 10, and 14 days post-infection (dpi). Across all IBV infected groups, viral genome loads were significantly higher in the CT than that in the spleen. Recruitment of B cells and cluster of differentiation (CD)8T cells, crucial for viral clearance, was significantly lower in the CT. Regulatory T (Treg) cells-which suppress immune responses via interleukin (IL)-10 and transforming growth factor (TGF)-β-were expected to peak early, their abundance in the CT was significantly higher only at the later time points. Among all genotypes, DMV/1639 exhibited increased potential for persistence in the CT associated with higher levels of Treg cells and viral genome load at 14 dpi. These findings suggest that delayed Treg cell infiltration, reduced effector cell recruitment, and a suppressive cytokine environment may precede to IBV persistence in the CT. Further studies are needed to explore the potential role of anti-inflammatory cytokines and other immunological factors in IBV persistence in the CT.