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Objective To investigate the pathogenesis and immunogenicity of H9N2 influenza virus A/Guangzhou/333/99 (a reassortant of G1 and G9 viruses isolated from a female patient in 1999) in a mouse model of infection.Methods Mice were infected with increasing virus titers.Viral load in the lungs and trachea was determined by EID50 assay.Pulmonary histopathology was assessed by hematoxylin‐eosin staining.Anti‐HI antibody titers and T‐cell responses to viral HA were determined by ELISPOT and confirmed by flow cytometry.Results Mice presented a mild syndrome after intranasal infection with A/Guangzhou/333/99 (H9N2) influenza virus.Virus was detected in the trachea and lungs of mice harvested on days 3,6,and 9 post‐infection.A T‐cell response to viral HA was detected on day 6 and H9 HA‐specific CD 4+ T‐cells predominated.Seroconversion was detected after 14 days and antibody persisted for at least 28 weeks.Conclusion Our results suggest that H9N2 (A/Guangzhou/333/99) can replicate in the murine respiratory tract without prior adaptation,and both humoral and cell‐mediated immunity play an important role in the immune response.
Objective To investigate the pathogenesis and immunogenicity of H9N2 influenza virus A / Guangzhou / 333/99 (a reassortant of G1 and G9 viruses isolated from a female patient in 1999) in a mouse model of infection. Methods Mice were infected with increasing virus titers. Viral load in the lungs and trachea was determined by EID50 assay. Pulmonary histopathology was assessed by hematoxylin-eosin staining. Anti-HI antibody titers and T-cell responses to viral HA were determined by ELISPOT and confirmed by flow cytometry. Results Mice presented a mild syndrome after intranasal infection with A / Guangzhou / 333/99 (H9N2) influenza virus. Virus was detected in the trachea and lungs of mice harvested on days 3,6, and 9 post-infection. detected on day 6 and H9 HA-specific CD 4+ T-cells predominated. Seroconversion was detected after 14 days and antibody persisted for at least 28 weeks. Conlusion Our results suggest that H9N2 (A / Guangzhou / 333/99) can replicate i n the murine respiratory tract without prior adaptation, and both humoral and cell-mediated immunity play an important role in the immune response.