Introduction
Chicken anemia virus (CAV)-induced disease normally occurs in chickens derived from breeder flocks which become infected with CAV for the first time during egg production . In this situation, vertical transmission of virus through the egg to the progeny chicks results in a severe disease characterised by a generalised lymphoid atrophy, increased mortality, usually around 10%, severe anemia, and the development of subcutaneous and intramuscular hemorrhages. Experimental infection of young chickens or chicken embryos with CAV gives rise to a disease which is similar in many respects to that seen in the field, and current understanding of the immunopathogenesis of CAV infection is based largely on sequential virological, pathological, immunocytochemical, and immunological studies of experimentally infected birds [1]. These studies suggest that the hemocytoblasts in the bone marrow and precursor lymphocytes in the thymus are important targets for the virus infection. Infected chickens appear to exhibit an increased incidence of secondary bacterial infections and evidence of decreased responsiveness to vaccines, suggesting that the virus was likely to be immunosuppressive, and this has been confirmed by immunological studies [4,5]. The effects of the virus on the immune system and the subsequent immunosuppression have been studied in some detail and will be dealt with in depth in this review.