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 e€ects
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
AbstractThe immunopathogenesis of chicken anemia virus (CAV) infection is reviewed. The virus causes a disease inyoung chicks which is characterised by generalised lymphoid atrophy, increased mortality and severe anemia. Thevirus appears to target erythroid and lymphoid progenitor cells in the bone marrow and thymus respectively. The Bcells in the chicken are not susceptible to CAV infection and are not directly affected by the virus. Destruction oferythroid 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 e€ectson susceptibility to, and enhancement of, the pathogenicity of secondary infectious agents, and sub-optimalantibody responses. Apoptosis appears to be a feature of the lymphocyte depletion in the thymic cortex, which maybe mediated by one of the non-structural viral proteins
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