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1 Department of Tumor Biology, Karolinska Institutet, 104 01 Stockholm, Sweden
2 Department of Medical and Physiologic Chemistry, Uppsala Universitet, 751 23 Uppsala, Sweden
3 Laboratory for Immunology, Department of Pathology and the Norwegian Cancer Society
and4 Department of Biophysics, Norsk Hydro's Institute for Cancer Research, The Norwegian Radiumhospital, Montebello, Oslo 3, Norway
The relationship between the receptors for the EpsteinBarr virus (EBV) and the C3d fragment of complement was investigated at the molecular level. In the presence of cell-bound C3, virus binding was enhanced in EBV genome-carrying lines. An identical effect could be elicited by C3d at one-quarter the weight amount; C3b and methylamine-treated C3 had no effect on virus binding. The minimum concentration of C3 which produced significant enhancement was 25 µg/ml. Virus binding increases were observed only after 20 min of complement-cell co-incubation. The response was not noted with EBV-negative lines and was independent of virus strain assayed (B95-8 and P3HR-1). These studies suggest that the binding sites for the two moieties are distinct, although they both involve the same cell surface complex. The two receptors are believed to display cooperativity.
Keywords: EBV, complement, receptors
Present address: Department of Microbiology, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama 700, Japan.
Present address: First Department of Internal Medicine, Okayama University Medical School, 2-5-1 Shikatacho, Okayama 700, Japan.
Present address: Department of Immunology, Scripps Clinic and Research Foundation, 10666 North Torrey Pines Road, La Jolla, California 92037, U.S.A.
Received 23 September 1983;
accepted 25 November 1983.
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