Immune responses to avian influenza viruses in chickens.

Abstract

Chickens are a key species in both the manifestation of avian influenza and the potential for zoonotic transmission. Avian influenza virus (AIV) infection in chickens can range from asymptomatic or mild disease with low pathogenic AIVs (LPAIVs) to systemic fatal disease with high pathogenic AIVs (HPAIVs). During AIV infection in chickens, Toll-like receptor 7 and melanoma differentiation-associated gene 5 are upregulated to detect the single-stranded ribonucleic acid genomes of AIV, triggering a signaling cascade that produces interferons (IFNs) and pro-inflammatory cytokines. These inflammatory mediators induce the expression of antiviral proteins and recruit immune system cells, such as macrophages and dendritic cells, to the infection site. AIV evades these antiviral responses primarily through its non-structural protein 1, which suppresses type I IFNs, influencing viral pathogenicity. The uncontrolled release of pro-inflammatory cytokines may contribute to the pathogenicity and high mortality associated with HPAIV infections. AIV modulates apoptosis in chicken cells to enhance its replication, with variations in apoptosis pathways influenced by viral strain and host cell type. The presentation of AIV antigens to T and B cells leads to the production of neutralizing antibodies and the targeted destruction of infected cells by CD8⁺ T cells, respectively, which enhances protection and establishes immunological memory. This review explores the diverse innate and adaptive immune responses in chickens to different AIVs, focusing on the dynamics of these responses relative to protection, susceptibility, and potential immunopathology. By understanding these immune mechanisms, informed strategies for controlling AIV infection and improving chicken health can be developed.