Chicken anaemia virus infection: Molecular basis of pathogenicity

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Abstract
Chicken anaemia virus (CAV) is a small virus of a unique type with a particle diameter of 23 to 25 nm and a genome consisting of a circular single‐stranded (minus‐strand) DNA. This DNA multiplies in infected cells via a circular double‐stranded replicative intermediate, which was recently cloned. DNA analysis of CAV strains isolated in different continents revealed only minor differences among the various isolates. Apparently, all CAV isolates belong to a single serotype. CAV is not related to other known animal single‐stranded circular‐DNA viruses, such as porcine circovirus and psittacine beak‐and‐feather‐disease virus. The major transcript from the CAV genome is an unspliced polycistronic mRNA of about 2100 nucleotides encoding three proteins of 51.6 kDa (VP1), 24.0 kDa (VP2) and 13.6 kDa (VP3 or apoptin). All three predicted CAV proteins are synthesized in CAV‐infected cells. Immunization with (recombinant) VP1 and VP2 synchronously synthesized in the same cells elicits a protective response and can be used as subunit vaccine against chicken infectious anaemia. CAV causes clinical and subclinical disease in chickens, and is recognized as an important avian pathogen worldwide. In young chickens, CAV causes a transient severe anaemia due to destruction of erythroblastoid cells in the bone marrow and immunodeficiency due to depletion of cortical thymocytes. The depletion of the cortical thymocytes is considered to cause a (transient) immunodeficiency resulting in enhanced concurrent infections and to vaccination failures. The depletion of thymocytes and most likely also of erythroblastoid cells occurs via CAV‐induced apoptosis. The CAV‐encoded protein apoptin is the main inducer of this phenomenon.