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J Gen Virol 77 (1996), 2015-2023; DOI 10.1099/0022-1317-77-9-2015
© 1996 Society for General Microbiology

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Human Immunodeficiency Virus Grown in CD4-Expressing Cells is Associated with CD4

Carol A. Hartley1, Mark J. Gilbert2, Luis Brigido3,4,, Tarek Elbeik2,3,, Jay A. Levy5, Suzanne M. Crowe1 and John Mills1,2,3,

1 Macfarlane Burnet Centre for Medical Research, PO Box 254, Fairfield, Victoria, Australia 3078
2 Department of Medicine, University of California, San Francisco, USA
3 Medical Service and Division of Infectious Diseases, San Francisco General Hospital, San Francisco, USA
4 Institute Adolfo Lutz, Division of Medical Biology, San Paulo, Brazil
5 Cancer Research Institute, University of California, San Francisco, USA

Author for correspondence: John Mills. Fax + 61 39 282 2100, e-mail mills{at}burnet.mbcmr.unimelb.edu.au

Using a CD4-capture immunoassay for gp120, several strains of human immunodeficiency virus type 1 (HIV-1) grown in CD4-expressing T lymphoblastoid cells were found to contain little CD4-reactive gp120 (0·3–1·0 ng/ml) relative to virus titre (103·2–105·0 TCID50/ml) and p24 antigen (80–1000 ng/ml). The measured CD4-reactive gp120 concentrations of HIV-1 suspensions grown in CD4-negative human neuroblastoma cells were 100- to 10000-fold greater than those of HIV-1 grown in CD4-positive lymphoblastoid cells, even though both virus suspensions contained abundant viral gp120 as shown by immunoblot assay. It was postulated that CD4 derived from host cells might be associated with virions, concealing the binding domains of gp120. CD4 association with HIV-1 virions grown in CD4-positive cells was demonstrated directly by immunoblot assay of sucrose gradient-purified virus suspensions and by specific co-sedimentation of 125I-labelled OKT4 with virions propagated in CD4-expressing cells. CD4 coating of primary HIV-1 isolates grown in peripheral blood mononuclear cells was also observed. The biological significance of CD4 coating of HIV particles remains to be determined.

Received 8 January 1996; accepted 17 April 1996.





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