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Enhancement of human immunodeficiency virus type 1 infection by cationic liposomes: the role of CD4, serum and liposome-cell interactions

Charles E. Larsen^1,

Nejat Düzgüne^1,2,3,

¹ Cancer Research Institute
and² Department of Pharmaceutical Chemistry, University of California, San Francisco, California 94143-0128
³ Department of Microbiology, University of the Pacific, School of Dentistry, San Francisco, California 94115
and⁴ Medical Research Institute of San Francisco at California Pacific Medical Center, San Francisco, California 94115, U.S.A.

We have reported previously the enhancement of the infectivity of human immunodeficiency virus type 1 (HIV-1) by liposomes composed of the cationic lipid N-[2,3-(dioleyloxy) propyl]-N,N,N-trimethylammonium chloride (DOTMA). To determine the mechanism by which this process occurs, we have investigated the role of CD4, serum concentration and liposome-cell interactions in the DOTMA-mediated stimulation of HIV-1 infection of A3.01 cells. Serum alone significantly inhibited the binding and infectivity of HIV-1, but DOTMA-mediated enhancement of infectivity was more pronounced in the presence of serum than in its absence. HIV-1 binding to cells was increased in the presence of DOTMA liposomes, DEAE-dextran and polybrene, all of which also enhanced infectivity to a similar extent at comparable concentrations. Fluorescence dequenching measurements indicated that DOTMA liposomes fused with HIV-1, but not with cell membranes, in the presence of serum. The enhancing effect of DOTMA liposomes on HIV-1 infectivity was CD4-dependent, and appeared to involve virus-liposome fusion and liposome binding to the cell surface. DOTMA liposomes did not mediate infection of the CD4^- K562 and Raji cell lines.

Present address: Department of Bioscience and Biotechnology, Drexel University, Philadelphia, Pennsylvania 19104, U.S.A.

Received 26 April 1991; accepted 29 July 1991.

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