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PMID: 7504739 Published · ppublish English Journal Article

Apoptosis induced in CD4+ cells expressing gp160 of human immunodeficiency virus type 1.

Journal of virology ·Vol. 68 ·No. 1 ·1994-01-00 ·Pages 390-9

Lu YY, Koga Y, Tanaka K, Sasaki M, Kimura G, Nomoto K

Abstract

In a previous study (Y. Koga, M. Sasaki, H. Yoshida, H. Wigzell, G. Kimura, and K. Nomoto, J. Immunol. 144:94-102, 1990), we demonstrated that the expression of gp160, a precursor form of envelope glycoprotein of human immunodeficiency virus type 1, in CD4+ cells causes the downregulation of surface CD4 and single-cell killing by forming intracellular gp160-CD4 complex. In the present study we investigated the events that lead to cell death in CD4+ cells expressing gp160. We found that apoptosis is induced in cells undergoing single-cell death. Moreover, even the cell clone, which expresses so little gp160 that it does not exhibit any apparent cytopathic effects, such as the inhibition of cell growth, was found to be highly susceptible to the apoptosis induction by the anti-Fas monoclonal antibody.

MeSH Terms
Antigens, Surface/pharmacology Apoptosis/drug effects Base Sequence CD4 Antigens/biosynthesis CD4-Positive T-Lymphocytes/cytology,immunology,ultrastructure Cell Line Cytopathogenic Effect, Viral DNA Damage Down-Regulation Gene Products, env/biosynthesis,pharmacology HIV Envelope Protein gp160 HIV-1/physiology Humans Molecular Sequence Data Protein Precursors/biosynthesis,pharmacology Recombinant Proteins/biosynthesis Transfection fas Receptor
Chemicals
Antigens, Surface CD4 Antigens Gene Products, env HIV Envelope Protein gp160 Protein Precursors Recombinant Proteins fas Receptor
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Lu Y Y
Department of Immunology, Kyushu University, Fukuoka, Japan.
Koga Y
Tanaka K
Sasaki M
Kimura G
Nomoto K
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
Published
1994-01-00
Pages
390-9
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC236299
Subset
IM
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