Membrane-interactive phospholipids inhibit HIV type 1-induced cell fusion and surface gp160/gp120 binding to monoclonal antibody. NLM AIDSLINE Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.

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Membrane-interactive phospholipids inhibit HIV type 1-induced cell fusion and surface gp160/gp120 binding to monoclonal antibody.

AIDS Res Hum Retroviruses. 1995 Jun;11(6):705-12. Unique Identifier : AIDSLINE MED/96078231
Krugner-Higby L; Goff D; Edwards T; Iyer N; Neufeld J; Kute T; Morris-Natschke S; Ishaq K; Piantadosi C; Kucera LS; Department of Comparative Medicine, Wake Forest University; Medical Center, Winston-Salem, North Carolina 27157-1064, USA.

Abstract: Membrane-interactive phospholipids (PLs), previously evaluated for activity against HIV-1 in vitro, are known to affect late steps in viral replication. Studies were done to determine the effects of PL analogs on post-translational processing of HIV-1 proteins, binding of viral surface gp160/gp120 to CD4 receptor, and HIV-1-induced cell fusion. Results of this investigation indicated that PL alone (1-octadecanamido-2-ethoxypropyl-rac-3-phosphocholine, CP-51) and PL-AZT conjugate (1-octadecanamido-2-ethoxypropyl-rac-3-phospho-3'- azido-3'-deoxythymidine, CP-92) have no effect on HIV-1-induced syntheses or processing of gp160/gp120, pr51, p24, or p17 (including myristoylation) in infected cells. Progeny HIV-1 particles made in CP-92-treated H9IIIB cells contained gp120, pr51, and p24; however, these virus particles had reduced capacity to bind to CD4+ cells. Both CP-51 and CP-92 inhibited syncytium (cell fusion) formation between treated HIV-1-infected cells and uninfected CD4+ cells, and, they reduced HIV-1 gp160/gp120 binding to CD4+ cells and monoclonal antibody. These results suggest that anti-HIV-1 activity of PL compounds involves alteration of cell surface membranes and viral envelopes. Phospholipid compounds are a novel class of membrane interactive compounds with potential use in blocking the spread of HIV-1 infection and pathogenesis in AIDS.
Keywords: Antibodies, Monoclonal/METABOLISM Cell Fusion/*DRUG EFFECTS Cell Membrane/DRUG EFFECTS/VIROLOGY CD4-Positive T-Lymphocytes/VIROLOGY Gene Products, env/*METABOLISM HIV Antibodies/METABOLISM HIV Envelope Protein gp120/*METABOLISM HIV-1/*DRUG EFFECTS Indolizines/PHARMACOLOGY Myristic Acids/METABOLISM Phospholipid Ethers/CHEMICAL SYNTHESIS/PHARMACOLOGY Phospholipids/CHEMICAL SYNTHESIS/*PHARMACOLOGY Protein Precursors/*METABOLISM Protein Processing, Post-Translational/DRUG EFFECTS Support, U.S. Gov't, P.H.S. Viral Proteins/BIOSYNTHESIS/METABOLISM Virion/METABOLISM Zidovudine/ANALOGS & DERIVATIVES/CHEMICAL SYNTHESIS/PHARMACOLOGY JOURNAL ARTICLEKWDantibodies,monoclonal/metabolismcellfusion/KWDdrugeffectscellmembrane/drugeffects/virologycd4-positivet-lymphocytes/virologygeneproducts,env/KWDmetabolismhivantibodies/metabolismhivenvelopeproteingp120/KWDmetabolismhiv-1/KWDdrugeffectsindolizines/pharmacologymyristicacids/metabolismphospholipidethers/chemicalsynthesis/pharmacologyphospholipids/chemicalsynthesis/KWDpharmacologyproteinprecursors/KWDmetabolismproteinprocessing,post-translational/drugeffectssupport,uKWDsKWDgov't,pKWDhKWDsKWDviralproteins/biosynthesis/metabolismvirion/metabolismzidovudine/analogs&derivatives/chemicalsynthesis/pharmacologyjournalarticle
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