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Journal of Virology, June 2004, p. 5805-5811, Vol. 78, No. 11
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.11.5805-5811.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Porcine Endogenous Retrovirus Transmission Characteristics of Galactose {alpha}1-3 Galactose-Deficient Pig Cells

Gary Quinn, James C. Wood, David J. J. Ryan, Kristen M. Suling, Kathleen M. Moran, Donna L. Kolber-Simonds, Julia L. Greenstein, Henk-Jan Schuurman, Robert J. Hawley, and Clive Patience*

Immerge BioTherapeutics Inc., Cambridge, Massachusetts 02139

Received 11 November 2003/ Accepted 27 January 2004

Galactose {alpha}1-3 galactose (Gal) trisaccharides are present on the surface of wild-type pig cells, as well as on viruses particles produced from such cells. The recognition of Gal sugars by natural anti-Gal antibodies (NAb) in human and Old World primate serum can cause the lysis of the particles via complement-dependent mechanisms and has therefore been proposed as an important antiviral mechanism. Recently, pigs have been generated that possess disrupted galactosyl-transferase (GGTA1) genes. The cells of these pigs do not express Gal sugars on their surface, i.e., are Gal null. Concerns have been raised that the risk of virus transmission from such pigs may be increased due to the absence of the Gal sugars. We investigated the sensitivity of porcine endogenous retrovirus (PERV) produced from Gal-null and Gal-positive pig cells to inactivation by purified NAb and human serum. PERV produced in Gal-null pig cells was resistant to inactivation by either NAb or human serum. In contrast, although Gal-positive PERV particles were sensitive to inactivation by NAb and human serum, they required markedly higher concentrations of NAb for inactivation compared to the Gal-positive cells from which they were produced. Complete inactivation of Gal-positive PERV particles was not achievable despite the use of high levels of NAb, indicating that NAb-mediated inactivation of cell-free PERV particles is an inefficient process.

* Corresponding author. Mailing address: Immerge BioTherapeutics Inc., 300 Technology Sq., Cambridge, MA 02139. Phone: (617) 250-5587. Fax: (617) 241-0539. E-mail: clive.patience{at}immergebt.com.

Journal of Virology, June 2004, p. 5805-5811, Vol. 78, No. 11
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.11.5805-5811.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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