Journal of General Virology (1997), 78, 1907–1911
1Department of Immunology/Microbiology, Rush University, 1653 West Congress Parkway, Chicago, IL 60612, USA
2Department of Medicine, Washington University School of Medicine, 660 South Euclid Ave., St Louis, MO 63110, USA
3Division of Hematology/Oncology, University of Utah School of Medicine and the Veteran Affairs Medical Center, 500 Foothill Blvd, Salt Lake City, UT 84148, USA
Author for correspondence: Mohammed Saifuddin
Fax +1 312 942 2808. e-mail msaifudd@rush.edu
Human immunodeficiency virus type 1 (HIV-1) can be either resistant or sensitive to complement-mediated destruction depending on the host cells. Incorporation of different levels of host cell CD46, CD55 and CD59 may account for this differential sensitivity to complement. However, it has not been determined whether CD46, CD55 and CD59 can all be incorporated at levels which protect virions. To determine whether each of these proteins can protect HIV-1, virions were derived from CHO cells expressing either human CD46, CD55 or CD59. Virions were shown to incorporate both glycosyl phosphatidylinositol (GPI)-anchored CD55 and CD59 as well as transmembrane CD46. Importantly, all three virus preparations were significantly more resistant to complement lysis than control virus. This study demonstrates that HIV-1 incorporates both transmembrane and GPI-anchored complement control proteins from host cells and that both types of protein increase complement resistance of virus.
Received 27 January 1997; Accepted 25 April 1997.
© 1997 Society for General Microbiology