Chicken anemia virus (CAV) causes cytopathogenic effects in chicken th
ymocytes and cultured transformed mononuclear cells via apoptosis. Ear
ly after infection of chicken mononuclear cells, the CAV-encoded prote
in VP3 exhibits a finely granular distribution within the nucleus. At
a later stage after infection, VP3 forms aggregates. At this point, th
e cell becomes apoptotic and the cellular DNA is fragmented and conden
sed. By immunogold electron microscopy VP3 was shown to be associated
with apoptotic structures. In vitro, expression of VP3 induced apoptos
is in chicken lymphoblastoid T cells and myeloid cells, which are susc
eptible to CAV infection, but not in chicken embryo fibroblasts, which
are not susceptible to CAV. Expression of a C-terminally truncated VP
3 induced much less pronounced apoptosis in the chicken lymphoblastoid
T cells.