Concentration-dependent differential induction of necrosis or apoptosis by HIV-1 lytic peptide 1

• Published in: Peptides (New York, N.Y. : 1980) Vol. 20; no. 11; pp. 1275 - 1283
• Main Authors: Plymale, Douglas R, Comardelle, Alla M, Fermin, Cesar D, Martin, Dale S, Costin, Joshua M, Norris, Charles H, Burroughs Tencza, Sarah, Mietzner, Timothy A, Montelaro, Ronald C, Garry, Robert F
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-11-1999
• Subjects: AIDS; AIDS/HIV; Amino Acid Sequence; Apoptosis; Apoptosis - physiology; CD4-Positive T-Lymphocytes - cytology; HIV-1 - physiology; HIV-1 cytopathology; HIV-1 lytic peptide; Human immunodeficiency virus 1; Humans; lytic peptide 1; Microscopy, Electron; Molecular Sequence Data; Necrosis; Spectrometry, Fluorescence; AIDS; HIV-1 lytic peptide; HIV-1 cytopathology; Apoptosis; Necrosis
• ISSN: 0196-9781; 1873-5169
• DOI: 10.1016/S0196-9781(99)00132-1

The mechanism by which human immunodeficiency virus type 1 induces depletion of CD4
+ T-lymphocytes remains controversial, but may involve cytotoxic viral proteins. Synthetic peptides (lentivirus lytic peptide type 1) corresponding to the carboxyl terminus of the human immunodeficiency virus type 1 transmembrane glycoprotein induce cytopathology at concentrations of 100 nM and above. At these concentrations lentivirus lytic peptide type 1 disrupts mitochondrial integrity of CD4
+ T-lymphoblastoid cells and induces other changes characteristic of necrosis. In contrast, at concentrations of 20 nM, lentivirus lytic peptide type 1 potently induces apoptosis. Thus, the mechanism by which human immunodeficiency virus type 1 mediates cell death, necrosis or apoptosis, may depend, in part, on the tissue concentration of transmembrane glycoprotein.