Introduction
Chicken anemia virus (CAV)-induced disease
normally occurs in chickens derived from breeder
¯ocks which become infected with CAV for the
®rst time during egg production [1]. In this situ-
ation, vertical transmission of virus through the
egg to the progeny chicks results in a severe dis-
ease characterised by a generalised lymphoid
atrophy, increased mortality, usually around
10%, severe anemia, and the development of sub-
cutaneous and intramuscular hemorrhages [1].
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 ®eld, and current understanding of the immu-
nopathogenesis of CAV infection is based largely
on sequential virological, pathological, immuno-
cytochemical, and immunological studies of ex-
perimentally infected birds [1]. These studies
suggest that the hemocytoblasts in the bone mar-
row 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
[1±3], suggesting that the virus was likely to be
immunosuppressive, and this has been con®rmed
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.
IntroductionChicken anemia virus (CAV)-induced diseasenormally occurs in chickens derived from breeder¯ocks which become infected with CAV for the®rst time during egg production [1]. In this situ-ation, vertical transmission of virus through theegg to the progeny chicks results in a severe dis-ease characterised by a generalised lymphoidatrophy, increased mortality, usually around10%, severe anemia, and the development of sub-cutaneous and intramuscular hemorrhages [1].Experimental infection of young chickens orchicken embryos with CAV gives rise to a diseasewhich is similar in many respects to that seen inthe ®eld, and current understanding of the immu-nopathogenesis of CAV infection is based largelyon sequential virological, pathological, immuno-cytochemical, and immunological studies of ex-perimentally infected birds [1]. These studiessuggest that the hemocytoblasts in the bone mar-row and precursor lymphocytes in the thymusare important targets for the virus infection.Infected chickens appear to exhibit an increasedincidence of secondary bacterial infections andevidence of decreased responsiveness to vaccines[1±3], suggesting that the virus was likely to beimmunosuppressive, and this has been con®rmedby immunological studies [4,5]. The effects of thevirus on the immune system and the subsequentimmunosuppression have been studied in somedetail and will be dealt with in depth in thisreview.
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