Molecular basis of the attenuation exhibited by molecularly cloned highly passaged chicken anemia virus isolates.
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.
Department of Agriculture and Rural Development for Northern Ireland, Veterinary Sciences Division, the Queen's University of Belfast, Stormont, United Kingdom. Daniel.Todd@dardni.gov.uk
Daniel
D
Todd
Alistair N J
AN
Scott
Neris W
NW
Ball
Borghert J
BJ
Borghmans
Brian M
BM
Adair
D000818:Animals; D000911:Antibodies, Monoclonal; D002213:Capsid / Q000235:genetics; D036022:Capsid Proteins; D017727:Chicken anemia virus / Q000235:genetics* / Q000276:immunology / Q000302:isolation & purification / Q000472:pathogenicity*; D002645:Chickens; D002678:Chimera / Q000235:genetics / Q000276:immunology; D018173:Circoviridae Infections / Q000276:immunology / Q000517:prevention & control; D003001:Cloning, Molecular; D004279:DNA, Viral / Q000235:genetics; D016679:Genome, Viral; D008969:Molecular Sequence Data; D014613:Vaccines, Attenuated / Q000235:genetics; D014765:Viral Vaccines / Q000235:genetics; D014774:Virulence / Q000235:genetics
D000911:Antibodies, Monoclonal; D036022:Capsid Proteins; D004279:DNA, Viral; C091717:VP3 protein, Chicken anemia virus; D014613:Vaccines, Attenuated; D014765:Viral Vaccines