Immunopathogenesis of chicken anemia virus infection

Abstract

The immunopathogenesis of chicken anemia virus (CAV) infection is reviewed. The virus causes a disease in young chicks which is characterised by generalised lymphoid atrophy, increased mortality and severe anemia. The virus appears to target erythroid and lymphoid progenitor cells in the bone marrow and thymus respectively. The B cells in the chicken are not susceptible to CAV infection and are not directly affected by the virus. Destruction of erythroid progenitors in bone marrow results in severe anemia, and depletion of granulocytes and thrombocytes. Destruction of precursor T cells results in depletion of mature cytotoxic and helper T cells with consequent effects on susceptibility to, and enhancement of, the pathogenicity of secondary infectious agents, and sub-optimal antibody responses. Apoptosis appears to be a feature of the lymphocyte depletion in the thymic cortex, which may be mediated by one of the non-structural viral proteins, VP3 (apoptin).