ArticlePoultry science2026
Comparative pathogenesis, tissue tropism, and immune dynamics of infectious bronchitis virus genotypes GI‑1 and GI‑24 in broiler chickens.
Article in Poultry science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Infectious bronchitis (IB) is an acute and highly contagious respiratory and renal disease of poultry caused by infectious bronchitis virus (IBV). This study comparatively evaluated the pathogenesis, tissue tropism, viral shedding, cytokine dynamics, and humoral immune responses induced by the recently characterized GI-1 and GI-24 variant strains of IBV in broiler chickens. Birds (n = 90) were experimentally inoculated intranasally and intraocularly with 10⁶ EID₅₀/0.1 ml of either GI-1 (n = 30) or GI-24 (n = 30), while control birds (n = 30) received uninoculated allantoic fluid and were monitored for 21 days post-infection (dpi). Both IBV variants induced pronounced clinical disease characterized by pyrexia, reduced weight gain, severe respiratory and renal manifestations. Gross and histopathological examinations revealed marked congestion, hemorrhage, tubular degeneration, and necrosis in lungs and kidneys of infected birds. Real-time RT-PCR analysis demonstrated high viral loads and prolonged viral shedding in both respiratory and renal tissues, persisting through 21 dpi (P < 0.001) accompanied by distinct tissue-specific inflammatory and pro-inflammatory cytokine responses representing the first characterization of organ-specific and swab-associated cytokine dynamics following GI-24 infection. The GI‑1 variant consistently induced higher and more sustained expression of pro‑inflammatory cytokines; IL‑1β and TNF‑α (P < 0.001 and P < 0.01), antiviral interferons; IFN‑γ and IFN‑β (P < 0.01), and the regulatory cytokine IL‑10 (P < 0.01) compared with GI‑24. Both infected groups developed robust humoral immune responses with seroconversion by 14 dpi and peak antibody titers at 21 dpi. Overall, GI-1 exhibited greater pathogenicity and more persistent lesions than GI-24, whereas the emerging GI-24 variant showed dual respiratory and renal tropism and induced distinct tissue-specific cytokine responses, representing the first detailed characterization of its immunopathogenesis and highlighting the need for continuous surveillance and strain-matched vaccination strategies.
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