Abstract
The coexpression of human immunodeficiency virus type 1 (HIV-1) envelope glycoproteins and receptors leads to the lysis of single cells by a process that is dependent upon membrane fusion. This cell lysis was inhibited by low-molecular-weight compounds that interfere with receptor binding or with receptor-induced conformational transitions in the envelope glycoproteins. A peptide, T20, potently inhibited cell-cell fusion but had no effect on single cell lysis mediated by the HIV-1 envelope glycoproteins. Thus, critical events in the lysis of single cells by the HIV-1 envelope glycoproteins occur in intracellular compartments accessible only to small inhibitory compounds.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Cell Line
-
Cytopathogenic Effect, Viral / drug effects
-
Dogs
-
Enfuvirtide
-
Ethers / pharmacology*
-
Gene Products, env / metabolism*
-
HIV Envelope Protein gp41 / pharmacology
-
HIV-1 / drug effects*
-
HIV-1 / pathogenicity*
-
Humans
-
Hydrocarbons, Fluorinated / pharmacology*
-
Membrane Fusion / drug effects*
-
Molecular Weight
-
Peptide Fragments / pharmacology
-
Piperazines / pharmacology*
Substances
-
BMS 806
-
Ethers
-
Gene Products, env
-
HIV Envelope Protein gp41
-
Hydrocarbons, Fluorinated
-
Peptide Fragments
-
Piperazines
-
Enfuvirtide
-
fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether