Modulation of the immune responses in chickens by low-pathogenicity avian influenza virus H9N2
Zheng Xing1, Carol J Cardona2, Jinling Li2
1Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA.
Abstract:
Most low-pathogenicity avian influenza (LPAI) viruses cause no or mild disease in avian species. Little is known about the mechanisms of host defence and the immune responses of avian influenza-infected birds. This study showed that chicken macrophages are susceptible to infection with LPAI H9N2 and H6N2 viruses and that infection led to apoptosis. In H9N2 virus-infected chicken macrophages, Toll-like receptor 7 responded to infection and mediated the cytokine responses. Whilst pro-inflammatory cytokines were largely upregulated, the interferon (IFN) response was fairly weak and IFN-inducible genes were differentially regulated. Among the regulated genes, major histocompatibility complex (MHC) antigens II were downregulated, which also occurred in the lungs of H9N2-infected chickens. Additionally, interleukin (IL)-4, IL-4 receptor and CD74 (MHC class II invariable chain) were also downregulated, all of which are pivotal in the activation of CD4+ helper T cells and humoral immunity. Remarkably, in H9N2 virus-infected chickens, the antibody response was severely suppressed. This was in contrast to the robust antibody response in chickens infected with H6N2 virus, in which expression of MHC class II antigens was upregulated. These data suggest that neutralizing antibodies and humoral immunity may not be developed efficiently in H9N2-infected chickens. These findings raise questions about how some LPAI viruses differentially regulate avian immune responses and whether they have similar effects on mammalian immune function.
Insights
Low-pathogenicity avian influenza (LPAI) viruses like H9N2 can suppress chicken immune responses, hindering antibody production. This contrasts with H6N2, highlighting differential immune regulation by LPAI viruses.
Area of Science:
- Immunology
- Virology
- Avian Health
Background:
- Low-pathogenicity avian influenza (LPAI) viruses typically cause mild avian disease, but their immune evasion mechanisms remain poorly understood.
- Understanding host defense and immune responses in LPAI-infected birds is crucial for disease management and control.
Purpose of the Study:
- To investigate the immune responses of chicken macrophages and tissues infected with LPAI H9N2 and H6N2 viruses.
- To elucidate the mechanisms by which LPAI viruses differentially regulate avian immune responses, particularly humoral immunity.
Main Methods:
- Infection of chicken macrophages and lung tissues with LPAI H9N2 and H6N2 viruses.
- Analysis of Toll-like receptor 7 (TLR7) activation, cytokine profiles, and interferon (IFN) responses.
- Quantification of major histocompatibility complex (MHC) class II antigen expression and antibody responses.
Main Results:
- Chicken macrophages are susceptible to H9N2 and H6N2 infection, leading to apoptosis.
- H9N2 infection induced weak IFN responses and downregulated MHC class II antigens, IL-4, IL-4 receptor, and CD74, impairing CD4+ T cell activation.
- H9N2 infection severely suppressed antibody responses, while H6N2 infection led to upregulated MHC class II and a robust antibody response.
Conclusions:
- LPAI H9N2 virus differentially regulates avian immune responses, potentially inhibiting the development of neutralizing antibodies and humoral immunity.
- The distinct immune profiles observed between H9N2 and H6N2 infections suggest varied immune evasion strategies among LPAI viruses.
- Further research is needed to determine if these differential immune effects extend to mammalian systems.
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