Chicken Origin Tribasic H9N2 Avian Influenza Virus Induces Potent Early Antiviral Response With Low Pathogenicity in Japanese Quails.

Abstract

BACKGROUND: Low-pathogenic avian influenza (LPAI) virus H9N2 has been endemic in Bangladesh since 2006. While the molecular epidemiology and pathogenicity of circulating tribasic H9N2 viruses are well-documented in chickens, data on pathogenicity in quails remain limited. Given the fact that quails serve as potential mixing vessels for avian influenza viruses, understanding of currently circulating tribasic H9N2 viruses' pathobiology is crucial. OBJECTIVES: The aim of this work was to observe pathogenicity, including clinicopathological changes, virus shedding, and cytokine expression of the recent circulating tribasic H9N2 virus-infected Japanese quails in Bangladesh. METHODS: A total of 64 quails were randomly assigned into two groups: an infected group (n = 32) and a control group (n = 32). Infected quails (at 4 weeks) received 500 µL of virus (10EID/mL) via the oculo-nasal route. Quails were subsequently monitored for clinicopathological changes, virus shedding, and cytokine expression at various intervals until 70 days of age. RESULTS: Infected quails exhibited decreased egg production (7%-24%) and reduced weight gain (5%-12%) compared to controls, though no mortality was observed. Gross lesions included congestion and mild-to-moderate haemorrhages in the trachea, lungs, intestine, and kidney until 10 days post-infection (dpi). Histopathology revealed mild tracheitis, pneumonia, slight haemorrhages and degenerative kidney changes at different dpi. The virus replicated prominently in the trachea, lungs, intestine, and kidney up to 5 dpi, with peak shedding via the oropharyngeal route. Following infection, IL-8, TNF-α, IFN-β, and IFN-γ were expressed in the trachea, lungs, intestine, and lymphoid organs at 2, 5, 10, and 15 dpi. Proinflammatory cytokine TNF-α was upregulated to the significantly higher levels (p ≤ 0.001) in trachea and lungs at 10 dpi in tribasic H9N2-infected quails compared to non-infected control group. Notably, quails exhibited a robust early antiviral response (IFN-β and IFN-γ on 2 dpi) against H9N2 infection except for lymphoid tissues regarding IFN-γ. CONCLUSIONS: This study gives valuable insights into host-pathogen interaction and confirms that the circulating tribasic H9N2 virus remains phenotypically low pathogenic in Japanese quails in Bangladesh but cause long-term impairment of important productivity parameters (weight gain, laying rates).