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Journal of Virology, August 2002, p. 8472-8474, Vol. 76, No. 16
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.16.8472-8474.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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

Daniel Todd,1* Alistair N. J. Scott,2 Neris W. Ball,1 Borghert J. Borghmans,1 and Brian M. Adair1

Department of Agriculture and Rural Development for Northern Ireland,1 Department of Veterinary Science, Veterinary Sciences Division, the Queen's University of Belfast, Stormont, Belfast BT4 3SD, United Kingdom2

Received 19 February 2002/ Accepted 10 May 2002

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.

* Corresponding author. Mailing address: Department of Agriculture and Rural Development for Northern Ireland, Veterinary Sciences Division, the Queen's University of Belfast, Stormont, Belfast BT4 3SD, United Kingdom. Phone: 44-2890-525814. Fax: 44-2890-525773. E-mail: Daniel.Todd{at}dardni.gov.uk.

Journal of Virology, August 2002, p. 8472-8474, Vol. 76, No. 16
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.16.8472-8474.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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