Molecular Basis of the Attenuation Exhibited by Molecularly Cloned Highly Passaged Chicken Anemia Virus Isolates

Abstract

Chimeric virus experiments indicated that the pathogenicity and monoclonal antibody reactivity differences between two molecularly cloned, highly passaged chicken anemia virus isolates could be attributed to the VP1 amino acid change at residue 89. The introduction of this change into a pathogenic cloned low-passage isolate was not sufficient to cause attenuation.