Figure 2

Model of MDV infectious life cycle in resistant birds. MDV infection of naive host occurs via inhalation of dust or skin dander encapsulated viral particles into the respiratory tract. 1 Primary infection occurs when virus particle breaks mucosal tolerance in the lungs, site of entry into the epithelial cells. Local viral replication establishes infection and initiates viral immediate-early gene, viral Interleukin-8 (vIL-8), transcription and translation. Inflammatory responses in the underlying tissue recruit innate immune system cells which result in uptake of infectious virus particle by macrophages. Infiltration of lymphocytes via action of vIL-8 follows resulting in MDV infection of B-cells. 2 Viral replication in B cells initiates Semi Production Lytic Viral Infection and disease progression. MDV infected B cells secret vIL-8 that acts as a chemotactic factor for and gains access to T-cells. This specific lymphotropism (B cells and T cells) enables systemic disseminated viraemia. Viral replication causes apoptosis of B and T lymphocytes in a hallmark of immunosuppression. MDV integrates specifically into the genome of CD4+ T cells enabling escape from immune detection and initiates Latent Viral Infection. Early latently infected and activated CD4+ T cells have not been phenotypically characterised by cell surface markers. a Early latently infected and activated CD4+ T cells migrate to cutaneous sites of replication namely feather follicle. 3 Infection of feather follicle epithelium enables fully productive viral replication. Viral replication results in syncytia formation. Infection of feather epithelium leads to secretion of mature virion in skin danders and dust that act as the major source of infectious materials. Horizontal transmission is the only recognized form for environmental persistence and infection in field conditions. Systemic infection and neoplastic transformation of CD4+ T cells in susceptible birds is further discussed (Figure 3).