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Journal of Virology, January 2006, p. 912-919, Vol. 80, No. 2
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.2.912-919.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Immune Response to Individual Maedi-Visna Virus gag Antigens

Inderpal Singh,{dagger} Ian McConnell, and Barbara Blacklaws*

Centre for Veterinary Science, Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge, United Kingdom CB3 0ES

Received 4 October 2005/ Accepted 17 October 2005

The lesions caused by maedi-visna virus (MVV) are known to be immune mediated with a presumed contribution by the response to viral antigens. However, very little is known about the T-cell response to individual viral proteins. We have therefore expressed the three individual gag antigens of MVV strain EV1 (p16, p25, and p14) in a bacterial expression system and used the purified recombinant proteins to analyze the antibody and CD4+ T-cell response to MVV. Plasma samples were taken from sheep after 1 year of infection with MVV. The titers for antibodies in these samples were determined by indirect enzyme-linked immunosorbent assays and were as follows: anti-p25 antibody, 1:400 to >1:3,200; anti-p16 antibody, 1:400 to 1:3,200; and anti-p14 antibody, 1:<100 to 1:3,200. When the induction of antibodies was followed over time postinfection (p.i.), samples positive for anti-p25 were seen by day 24 p.i., followed by anti-p16 by day 45 p.i., and lastly anti-p14 by day 100 p.i. T-cell proliferative responses to all three gag antigens were detected in persistently infected sheep peripheral blood lymphocytes. The antigens were therefore used to raise T-cell lines from persistently infected sheep. These T-cell lines were shown to be specific for the recombinant gag antigens and for viral antigen expressed on infected macrophages. The proliferative response was restricted to major histocompatibility complex class II HLA-DR and so was due to CD4+ T lymphocytes. All three gag antigens may therefore play a role in immune-mediated lesion formation in MVV disease by presentation on infected macrophages in lesions.

* Corresponding author. Mailing address: Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge, United Kingdom CB3 0ES. Phone: 44 1223 337609. Fax: 44 1223 337610. E-mail: bab2{at}cam.ac.uk.

{dagger} Present address: Division of Infectious Diseases, Tufts University Cummings School of Veterinary Medicine, 200 Westborough Road, North Grafton, MA 01536.

Journal of Virology, January 2006, p. 912-919, Vol. 80, No. 2
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.2.912-919.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.





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