Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 18, 1995
Publication Date: N/A
Interpretive Summary: This paper identifies an important host defense mechanism to viral diseases in chickens. The arm of the immune system that rejects viral infection was discovered using chicken cells engineered to express both viral and chicken proteins required for immune system activation. Using these cells, a powerful immune response that rejects viral infection was shown to be highly active in infected chickens 10 days after viral infection occurred. Specialized cells in the chickens blood were shown to be responsible for this strong immune response. The characterization of this highly effective host viral defense mechanism will provide new insights into vaccine research and development and reduce economic loss for poultry producers.
Technical Abstract: Cytotoxic T lymphocytes (CTL) can control some viral infections and may be important in the control of avian retroviruses, including avian leukosis virus (ALV). Cytolysis by major histocompatibility complex (MHC)-restricted CD8+ lymphocytes to ALV was studied using target cells which had chicken MHC class I gene sequences inserted. The MHC class I genes were inserted using a retroviral vector resulting in target cells which expressed both the class I glycoproteins and the ALV viral antigens on their surface. Peripheral blood monocytes (PBMC) from chickens with two different haplotypes and with or without endogenous retroviruses (ev) were used as effector cells in a 51CR-release assay. The ALV-specific activity was MHC-restricted by determined by assaying allogeneic target cells and was mediated by CD8+ T lymphocytes as determined by depleting these cells using a panning procedure using an anti-DC8 monoclonal antibody. In addition, Line 0 chickens which have the BF IV-B21 MHC haplotype and lack ev were significantly more cytolytic with syngeneic target cells than congenic chickens of the same MHC haplotype which contained ev suggesting the presence of ev genes induces tolerance to ALV.